| 'AF4 bodies' - a named subnuclear compartment that is non-nucleolar and coincident with no known nuclear structure, and the one place a KMT2A fusion has been shown to move a partner | Mechanism | 3 | 3/5 |
| 'AFF1-only' is a property of mid-activity promoters: zero in the bottom three deciles, zero in the top decile, and 81% of the 332 in deciles 6-8 | Analysis | 1 | 4/5 |
| 'Four consecutive beats found 40-50% of their genes anti-selective' was the null expectation, not a pattern - and the real test shows the curated set IS enriched for selectivity, p = 0.0016 | Analysis | 2 | 3/5 |
| 'Not expressed on normal haematopoietic cells' is a claim about blood, and it has been read for thirty years as a claim about the body | Explainer | 4 | 4/5 |
| 'Transcriptional memory' means two different things in this literature, and both of them are used about MLL leukaemia | Explainer | 4 | 5/5 |
| "Dispensable for haematopoiesis" is a summary of a real phenotype: halved white counts, perturbed HSC and progenitor numbers, and failing serial replating | Mechanism | 4 | 4/5 |
| "Diverse models of MLL-rearranged leukaemia" is one mouse cell line: the RNF20 H2Bub requirement resolves to murine RN2 (MLL-AF9/NrasG12D) | Analysis | 3 | 4/5 |
| "ENL" returns 1,109 PubMed records of which about 30% are the protein: a measured alias-precision failure | Analysis | 2 | 4/5 |
| "Menin was lost" and "menin did not move" are both true of the same experiment: a target-gene-restricted signal measure and a genome-wide peak-presence measure answer different questions, and the majority of the genome that does not move is exactly what the second one is made of | Explainer | 1 | 4/5 |
| "Seen in MLL-AF4 and no other bait" excludes AFF1, AFF4 and ELL — the three most AFF1-specific proteins in the experiment — and keeps ACADM and GLUD1 | Analysis | 2 | 4/5 |
| "SWI/SNF" is three different machines: cBAF, PBAF and ncBAF - and only one of them looks KMT2A-selective | Explainer | 5 | 4/5 |
| "Zero called peaks" is a statement about a reproducibility threshold, not about whether the protein was there - and in this graph the difference was worth a whole cycle's conclusion | Explainer | 2 | 4/5 |
| [CORRECTED cycle 110 - F2 not F1, and the floor spans ~20x across arms] Measuring the same-condition histone-mark noise floor from replicates already binned on local disk, zero downloads: 15.97% at the peaks and 3.03% at D1, so the borrowed 10% floor was 3.3x too generous in the bulk - independently reproducing, in a different deposit, cell system, mark and antibody, what the GSE299100 beat measured at 9.4% and 2.4% | Analysis | 1 | 3/5 |
| [CORRECTED cycle 117 - the columns were not scaled] [CORRECTED cycle 110 - the gradient is NOT an artefact] Grading this project's own stratified-share statistic on data where the truth is known: it is not blind to a global collapse, it is DISTORTING - a pure 5.84x genome-wide loss with no redistribution whatsoever is rendered as a monotone gradient rising from the peaks into the sparse deciles, reporting a 9.70x INCREASE at D10 where the absolute change is 1.66x, and 62 of 66 strata are confidently outside the measured noise floor | Analysis | 1 | 4/5 |
| [CORRECTED cycle 117 - the columns were not scaled] Correcting yesterday's correction: share(s) = absolute(s)/G is an exact identity, so a within-sample share reproduces the true SHAPE faithfully and misstates only the LEVEL - but that is the worse failure, because 34 of 66 strata lost up to 68% of their signal while reading as gains of up to +440% | Analysis | 1 | 4/5 |
| `absence_class` is one token per ENTRY while the entries carry seven to eleven distinct gaps each, so it is a summary label - and inside gene-nbn it hid a verifiably false ENCODE claim for three cycles | Analysis | 2 | 5/5 |
| 0.2% of profiled sarcomas, median age 38, and every number here has a denominator that is not the population | Epidemiology | 5 | 3/5 |
| 124 entries already write NOT APPLICABLE as a category statement on the localization dimension, and the epigenetics dimension has no equivalent - so a correctly-annotated Golgi enzyme and an unwritten chromatin protein are indistinguishable in the epigenetics figure | Analysis | 1 | 4/5 |
| 14-3-3 theta binds AF4 at Ser588 and rides into the MLL-AF4 complex - the phospho-gated contact the fusion really does carry | Interface | 3 | 3/5 |
| 148752 and 152985 are one patient before and during revumenib, not two treated patients - so the drug-free arm this corpus said did not exist is sample 148752 | Analysis | 2 | 4/5 |
| 172 adults with KMT2A-r AML: translocation subtype did not predict survival, so treat all KMT2A-r as adverse | Epidemiology | 4 | 3/5 |
| 18% of this graph's evidence is the same finding said again | Analysis | 1 | 3/5 |
| 2-hydroxyglutarate competitively inhibits the alpha-KG dioxygenases - and it hits the TET demethylases AND the KDM histone demethylases, which is why its net effect on a CXXC reader is not predictable | Mechanism | 3 | 4/5 |
| 21.6% of this project's 19,404 promoter windows contain another gene's TSS, so an attribution caveat is corpus-wide and not an IRX2 peculiarity | Analysis | 3 | 4/5 |
| 22 of the 37 promoters in the published B-ALL-specific peak class are the clustered protocadherin gamma locus - one 23.8 kb interval at chr5:141,473,710-141,497,491 - and it reads below an average promoter in all 27 samples | Analysis | 2 | 4/5 |
| 3,288 papers are 2,025 research groups, the per-entry overcount is 11.7% and barely moved while the graph doubled - and TWO entries now rest on three papers from a single laboratory, where the first run of this analysis found none | Analysis | 4 | 0/5 |
| 4,589 genes with no prior, and menin comes first (run) | Analysis | 2 | 3/5 |
| 42.5% of every node in this corpus names a histone mark, so 'names a mark' is a weak instrument - but it is not noise, and the two types where it collapses are the ones that tell you it is measuring something | Analysis | 1 | 4/5 |
| 42% of every gene-body occupancy call is at a locus where wild-type MLL1 is also bound - but the AFF1-exclusive class is not, HOXA9 and MEIS1 are not, and SPAG7 is | Analysis | 3 | 4/5 |
| 43 of the 62 discussed-but-unwritten interactome partners (69%) are genuinely draftable from the committed corpus, so cycle 93's decision to work them before the 34 never-read ones has a real cost basis - but the clause that decided it was the citation clause I thought was safe, not the proxy I flagged as weak, and the 12 RNA-processing failures turn out to be a promiscuity census that should NOT be promoted partner by partner | Analysis | 1 | 5/5 |
| 43.9% of every occupancy call this project's rule makes is at a shared window it cannot attribute - twice the 21.6% base rate, in 27 of 27 samples | Analysis | 2 | 3/5 |
| 465 KMT2A-r B-ALL cases from 1 month to 89 years: partner predicts MRD clearance independently of age | Epidemiology | 3 | 3/5 |
| 49 of 91 proteins in this graph have never had a drug-like molecule bound to them | Analysis | 1 | 4/5 |
| 56 of KMT2A's 130 observed phosphosites survive the translocation, and the retained fragment is phospho-denser than the part that is lost | Analysis | 2 | 4/5 |
| 577 citations carried a bare PMID with no title, so the audit built to catch a fabricated title could not see them: the third dropped denominator in this project | Analysis | 3 | 4/5 |
| 6-Mercaptopurine - two years of a nightly tablet whose lethal dose is a genotype, given as a liquid to a baby who cannot swallow it and must not have it with milk | Drug | 5 | 3/5 |
| 6-Thioguanine - the drug a 1,498-child randomised trial removed from maintenance and left in intensification, which is exactly where Interfant-06 uses it | Drug | 5 | 4/5 |
| 756 children with 11q23/MLL-rearranged AML: 5-year EFS runs from 11% to 92% depending on the partner | Epidemiology | 3 | 4/5 |
| 78% of the noncoding beat rests on a claim that nobody has done something | Analysis | 1 | 4/5 |
| A 109-transcription-factor BioID network puts KMT2A next to MYC, YY1 and the ETS and KLF families - and AF10 next to ERG and KLF5 | Analysis | 3 | 3/5 |
| A 2026 preprint puts XPO1 upstream of the menin interface itself: XPO1 reported to stabilise menin on chromatin and menin's binding to KMT2A and KMT2A::MLLT3 | Mechanism | 2 | 2/5 |
| A binary peak call cannot see a two-fold change, so 'the peaks are still there' is not 'the protein is still there' | Explainer | 3 | 4/5 |
| A BioID hit is a neighbour, not a complex member - and the two methods are known to disagree | Explainer | 5 | 5/5 |
| A bulk normal-tissue expression value includes the white blood cells living inside that tissue - which is why CD19 'failed' a normal-tissue safety filter at 31.2 nTPM in small intestine | Explainer | 2 | 4/5 |
| A caveat that weakened the index fusion, wrongly: the MLL-AF4 spreading deposition is 30 SEM samples plus six other lines, all human | Analysis | 3 | 5/5 |
| A CD number names a reagent cluster, not a molecule - and four different things can sit behind one | Explainer | 6 | 5/5 |
| A CD19 CAR that secretes a CLEC12A bridge: aimed squarely at lineage switch, and it inherits both antigens' failure modes | Target | 2 | 3/5 |
| A cell that cannot deposit H2AK119ub is still evicted normally by a menin inhibitor and silences its vacated sites less - so a fusion-occupancy pharmacodynamic marker reads FULL ENGAGEMENT in exactly the genotype that responds worst, and this is now the fourth independent reason this corpus distrusts its own candidate markers | Resistance | 2 | 3/5 |
| A checker for the error the citation checker cannot see | Analysis | 2 | 0/5 |
| A child who made a KMT2A fusion during chemotherapy, lost it again, and never got leukaemia in 12.8 years | Patient story | 2 | 4/5 |
| A ChIP-seq series of 158 samples that names no antibody anywhere in its metadata: the string 'antibod' occurs ZERO times in GSE260742's 419,824-character SOFT dump, and the reagents are in a supplementary spreadsheet the full text never quotes | Analysis | 2 | 4/5 |
| A chromatin-occupancy readout has one dimension and the question has three: eviction, degradation and relocation all lower the signal at a target gene | Explainer | 3 | 4/5 |
| A claim-to-paper overlap score measures where a citation's support lives, not whether it exists - so its zero is a pointer to a supplement, not a verdict against the citation | Explainer | 2 | 4/5 |
| A cohort median is a summary of many nulls and the null of none of them | Explainer | 2 | 4/5 |
| A congress abstract book is one indexed document containing thousands of unrelated abstracts, so it matches almost any conjunction: across 18 Europe PMC full-text intersections read to completion, 83 of 321 records (25.9%) are proceedings, ranging 0% to 50% per query | Analysis | 2 | 4/5 |
| A counted PubMed absence is bounded by ABSTRACTS, not by papers - and the measurement you are looking for is usually a supporting figure | Explainer | 2 | 4/5 |
| A cross-partner absence is a rule-of-three bound, and the denominator must be the samples that could have shown it | Explainer | 1 | 5/5 |
| A detector for cross-paper contradictions, and the measurement that says it does not work | Analysis | 3 | 0/5 |
| A dimension can be saturated in the corpus and empty in the entry named for it, and the reporter that measures coverage cannot tell the difference | Explainer | 1 | 4/5 |
| A documented absence: not one endocrine outcome measure across the three lead menin-inhibitor trials | Explainer | 4 | 5/5 |
| A DOT1L inhibitor DOUBLES H3K79me2's mid-occupancy share (1.89-2.01) and a menin inhibitor CUTS it (0.69-0.78), in THREE murine samples one of which is a replicate (corrected cycle 97; the id still says four) with no overlap between the ranges, while the FLAG and MLL1-N channels sit at 0.905-0.929 under both drugs - so the two drugs do not act on one axis and 'a fraction of the achievable effect' presumes they do | Analysis | 1 | 3/5 |
| A DOT1L inhibitor, which does not touch the menin-KMT2A interface, removes 70% of the fusion's enrichment from its own strongest sites - two thirds of what a menin inhibitor removes - so fusion chromatin residency is partly downstream of H3K79 methylation rather than only of menin | Analysis | 3 | 3/5 |
| A drug that fixes diabetes in mice, and neither label contains the word glucose | Explainer | 2 | 5/5 |
| A failure-mode atlas for drugging the KMT2A::AFF1 axis: 90 modes over a 10 x 11 grid of layers and mechanisms, 46 cells argued not applicable, and eight modes the corpus has no entry for | Analysis | 1 | 2/5 |
| A falsifier written and scored inside Q118 last cycle, cashed again in the second cell line one cycle later: H3K79me2 at the MLL1-N held bins is 0.7008 in RS4;11 (does not fire, threshold 0.75) and 0.9980 in MOLM13 (FIRES) - the same pre-registered clause, opposite verdicts, and nothing in the clause names a cell line | Analysis | 1 | 4/5 |
| A filter-free promoter ranking with no peak caller and no target list recovers 40 of the top 50 published oncoprotein-target genes in the drug-free infant sample, and 0 of 50 in the drug-exposed one | Analysis | 3 | 4/5 |
| A five-year-old with KMT2A::USP2 ALL whose MRD would not clear until blinatumomab, then transplant, then more blinatumomab | Patient story | 2 | 2/5 |
| A full 2x2 on the MLL1 channel in one run - DMSO, EPZ5676 1 uM, VTP-50469 100 nM and both - closes cycle 83's thirty-cycle-old threat: at the fusion's strongest MLL1 sites the menin inhibitor removes 58.3% against the DOT1L inhibitor's 17.5%, a 3.33-fold separation at TEN TIMES the DOT1L dose Q136 could test, with sequencing depth running opposite to the effect in every arm | Analysis | 1 | 3/5 |
| A fusion-versus-rest expression difference can be pure morphology composition - I published one at p below 1e-12 and it dissolved inside every FAB stratum | Explainer | 1 | 4/5 |
| A gene-set permutation is anti-conservative for a protein complex, and the fix is to permute the other margin | Risk | 2 | 4/5 |
| A genome-wide DAMAGE-STATE occupancy dataset for CtIP and MRE11 does exist and is public - GSE218590, 58 samples, +/- 4-OHT and a light-activated Cas9 time course - and it cannot answer the KMT2A question, because there is not one AsiSI site in the 90,377 bp of the gene | Analysis | 3 | 4/5 |
| A genome-wide gene-body occupancy matrix over 133 libraries costs one fragment BED of peak disk, not 133 - stream, bin in flight, delete | Explainer | 1 | 4/5 |
| A genome-wide null flatters any interval that belongs to an enriched class: the KMT2A promoter ranked in the top 0.07% of the genome and is 1.24x an ordinary housekeeping promoter, and the exon-11 element ranked in the top 3% and sits BELOW the median CTCF anchor | Explainer | 2 | 4/5 |
| A genome-wide peak-call census is the wrong pharmacodynamic assay for a menin inhibitor, in two independent ways | Risk | 3 | 4/5 |
| A genuine small-molecule disruptor of an oncogenic oligomer DOES exist - 7.44 against the RUNX1::RUNX1T1 NHR2 tetramer - which corrects this graph's record; and its eighteen-year potency curve says the class is a chemistry problem, which is what this graph concluded for the wrong reason | Analogy | 3 | 4/5 |
| A GEO cell-type field can name the patient's clinical course rather than the aliquot's exposure, and the two readings differ by an entire control arm | Explainer | 2 | 4/5 |
| A GEO deposit can name two different cell lines for the same four samples in two different metadata fields, and reading only the filename - which is what every automated pipeline does - shows you neither: the case where my dispatch brief was right, my correction of it was wrong, and the deposit supports neither of us | Explainer | 1 | 4/5 |
| A group of four cannot support a correlation at any effect size: name it, do not compute it | Explainer | 1 | 5/5 |
| A housekeeping normalisation defines the global change to be zero, so only redistribution is measurable | Explainer | 3 | 4/5 |
| A Jaccard index is not a result until its null knows that active promoters cluster | Explainer | 3 | 4/5 |
| A junction-specific monoclonal antibody against a paediatric leukaemia fusion oncoprotein exists: clone TEL 6F2, raised against a 12-mer spanning the ETV6::RUNX1 fusion site and used for genome-wide ChIP | Explainer | 4 | 4/5 |
| A KMT2A fusion acquired at seventy-three: KMT2A::ELL AML arising out of polycythaemia vera, and a menin inhibitor used to hold the line | Patient story | 1 | 3/5 |
| A KMT2A fusion is necessary but not sufficient: the cell it lands in decides whether there is a disease and which one | Hypothesis | 4 | 3/5 |
| A long non-coding RNA binds DOT1L's catalytic domain and turns its activity up - and blocking it makes the fusion protein itself get eaten | Mechanism | 3 | 3/5 |
| A mass-spectrometry protein group's leading identifier is not the interactor, and curating it puts dubious isoforms and unreviewed accessions into the interaction databases | Explainer | 3 | 4/5 |
| A menin degrader removes six surfaces; a pocket inhibitor blocks one and touches a second - and in a child receiving TOP2 poisons that difference is a repair-competence difference nobody has measured | Risk | 4 | 3/5 |
| A menin inhibitor does not only take something away - it causes PRC1.1 to put something on, and the drug needs the cell's own silencing machinery to work | Mechanism | 3 | 3/5 |
| A menin inhibitor is a partial LXR agonist, and no trial in the class has looked | Hypothesis | 4 | 1/5 |
| A menin inhibitor is not a fusion degron, so watching menin leave chromatin under one cannot identify what was holding it there - every model predicts the same result | Explainer | 3 | 4/5 |
| A menin inhibitor may release RELA from menin's restraint — and released RELA is what keeps MLL fusions on chromatin. Prior 0.20 | Hypothesis | 5 | 1/5 |
| A menin inhibitor's chromatin signature is organised by how much fusion it removed from each site, so every mark's response is a GRADIENT in eviction depth - and any readout that averages over a fusion-occupancy set is underpowered by construction, sometimes to exactly 1.000 | Hypothesis | 3 | 3/5 |
| A menin peak that keeps its call has still lost a sixth of its enrichment - and only where the fusion was | Analysis | 3 | 3/5 |
| A methionine rescue arm, which separates SAM limitation from ordinary cytotoxicity | Experiment | 1 | 0/5 |
| A nine-month-old with AML whose fusion was found only after every standard test failed | Patient story | 2 | 3/5 |
| A noncoding element has no HGNC symbol, so every rule in this brief for resolving an identifier fails on it - worked on the one MYC enhancer that matters | Explainer | 3 | 5/5 |
| A null that costs one command, run first rather than afterwards - and SSRP1 is genuinely LESS required in KMT2A-rearranged lines, while the rest of the chaperone layer is not much of anything | Analysis | 3 | 0/5 |
| A panel of many antigens in one cell type is the input track the deposit did not provide: eight H3K9-axis proteins in MCF-7 all read the whole KMT2A locus elevated (six-non-anchor medians 49.8-72.4) and all read the KMT2A promoter at the 87.6th-99.9th percentile - so the shared component has to be subtracted before any single antigen's number means anything | Explainer | 2 | 3/5 |
| A partial resolution: the leptin-LEPR chemoresistance model is murine MLL-AF9, but the two AML arms were never separated and the proteomics deposition is unreachable | Analysis | 3 | 3/5 |
| A partner-exclusive promoter set needs a label-permutation null, not an independence one | Explainer | 1 | 4/5 |
| A partner's 'normal' compartment is usually read off a different tissue, and for at least two KMT2A partners that reading is wrong in blood cells | Explainer | 4 | 3/5 |
| A PCGF1-null cell - a published resistance genotype - loses H3K79me2 at the most-evicted sites exactly as a control cell does (0.6123 against 0.5860), so the new stratified readout scores it as fully drug-engaged, and stratification does NOT close the resistance blind spot it was hoped to close | Resistance | 3 | 3/5 |
| A per-sample parameter nobody reads: MACS's fragment-size estimate varies 822-1112 bp across ten ChIPs from one sequencing run, and within the DOT1L arm peak count correlates +0.7 with fragment size and -0.8 with library depth - so the obvious confound is not the operating one, and the non-obvious one is | Analysis | 2 | 4/5 |
| A phosphosite on a menin target predicts who responds to a menin inhibitor | Mechanism | 1 | 3/5 |
| A plateau criterion of the form 'the last interval contributes at most 10% of the total' fires when the last interval is NEGATIVE, so it reports a plateau for a series that reversed - and the guard that caught it was a separate monotonicity check written for a different reason | Explainer | 1 | 4/5 |
| A pocketless fusion already had its protein-protein-interface drug taken to phase I/II - and TK216 turned out to be a microtubule destabiliser, not an EWS::FLI1 antagonist. This is the closest thing the field has to a controlled failure of the interface hypothesis. | Analogy | 4 | 4/5 |
| A pre-registered gate of the form 'signal at the top sites / median of random tiles >= 5' returns inf and PASSES on any sparse track, because the median of random 147 bp tiles in a CUT&RUN file is exactly 0.0 - the control was degenerate in three of four tracks and nothing in the output said so | Explainer | 2 | 4/5 |
| A pre-registered, institution-matched serial-pair replication: does a patient's own target set predict itself better than another child's does? | Experiment | 2 | 3/5 |
| A promoter neighbour goes missing two ways - absent from the table, or present under a different one of its own TSSs - and both return the same clean negative | Explainer | 4 | 4/5 |
| A promoter window is not a gene: what it means to say a protein 'sits on gene X's switch' | Explainer | 3 | 4/5 |
| A published Kd is a property of five experimental choices, and this beat measured how much each one is worth | Explainer | 3 | 4/5 |
| A published MLL leukaemia stem-cell programme immortalises progenitors WITHOUT Hoxa or Meis - Myb, Hmgb3 and Cbx5 - and nobody has ever asked what a menin inhibitor does to it, although this graph reads the drug's effect almost entirely through HOXA9 and MEIS1 | Hypothesis | 2 | 1/5 |
| A quantile calling rule and an absolute one answer different questions, and on the same data they can order the same pairs oppositely | Explainer | 2 | 4/5 |
| A quarter of this graph's gene entries have a UniProt localization that nobody measured - and the subnuclear vocabulary UniProt does carry avoids the genes we care about most | Analysis | 2 | 4/5 |
| A quarter of this graph's load-bearing evidence is under twelve months old, and the year field is right in a way a checker would call wrong | Analysis | 2 | 3/5 |
| A ratio-of-ratios combines four independent tracks and a pair ratio combines two, so its noise floor is wider by a factor of root two in log space - and cycles 101 and 102 scored two ratio-of-ratios against a pair floor. Applying the correction to the measured 9.4% peak floor gives 13.5%: VTP's 1.3% stays comfortably inside, and SGC0946's 22.8% stays outside but its margin falls from '2-6x outside' to 1.7x | Analysis | 2 | 3/5 |
| A real defect in a committed scan, computed three days ago and never written up: `depmap-kmt2a-selective-scan-full` fixes both comparison arms from the FIRST gene that returns data, so five of sixteen eligible KMT2A-rearranged lines are excluded from all 17,728 gene comparisons - including the genes where they were screened | Analysis | 2 | 4/5 |
| A reciprocal-negative t(11;19) patient was documented in 1995 by a different mechanism entirely - the 3' half of KMT2A was simply deleted | Explainer | 2 | 3/5 |
| A residue axis for menin, derived from coordinates: three spatial lobes, not four named ones, and the sharpest seam in the protein runs through the drug pocket | Analysis | 5 | 4/5 |
| A resource status has three values - verified-present, verified-absent, unreachable - and an HTTP 200 from depmap.org is a 5,175-byte bot wall titled 'DepMap - Verification' | Explainer | 2 | 4/5 |
| A reversed genomic interval returns a plausible low number and no error — the coordinate gate caught mine | Explainer | 3 | 5/5 |
| A second brake, unconnected to JunD: menin is a TEAD1 corepressor with VGLL4 in the beta cell | Mechanism | 1 | 3/5 |
| A second disease finds the same DOT1L-to-non-canonical-PRC1 axis in the same year - and the mark moves the opposite way | Mechanism | 3 | 3/5 |
| A second sample id is not a second patient: three of the interesting pairs in GSE252378 are one patient twice, and reading them as independent doubles the apparent n | Explainer | 2 | 5/5 |
| A sharper test than complex enrichment: is the claimed partner's OBLIGATE partner also there? — and its fourth failure is the one protein the source paper named as its own non-selectivity control | Analysis | 4 | 2/5 |
| A six-month-old with a week of coughing: KMT2A::AFF1 pro-B ALL presenting with extreme hyperleukocytosis | Patient story | 1 | 3/5 |
| A sixth paper systematically measured every human CXXC domain's DNA binding, deposited the MLL co-crystal, and failed all five retrieval routes | Explainer | 1 | 2/5 |
| A Spearman over exact zeros is tie-degenerate, and argsort-of-argsort silently picks one value from a range | Explainer | 1 | 5/5 |
| A Spearman over four quartiles has 24 orderings and 11 attainable values: rho = +1.000 is 1/24 = 0.042, |rho| = 1.000 is 2/24 = 0.083, and a +-20% band around 0.80 contains exactly one attainable value - so a perfect monotone over four strata is a weak statistic and must never be scored alone | Explainer | 3 | 5/5 |
| A statistic whose denominator contains its numerator cannot test a magnitude claim, and the tell is that its between-sample spread sits near 1 whatever the biology does | Explainer | 2 | 5/5 |
| A surfaceome-first screen for KMT2A::AFF1: 2,404 surface proteins, 169 expressed in the fusion's own cell lines, 15 fusion-enriched, 3 clean in normal tissue - and the two sets do not intersect | Analysis | 8 | 3/5 |
| A sweep for the failure that cost two cycles: of 234 analysis directories holding a non-empty results file, only 5 are cited by no entry at all - so the backlog is real but small, and one of the five contains a defect in a committed scan | Analysis | 1 | 4/5 |
| A target map read off the diagnostic sample does not describe the same child's disease after a lineage switch | Risk | 2 | 3/5 |
| A tempting second finding that does NOT survive its control: about half of each treated sample's peaks are absent from DMSO, but the two independent VTP-50469 libraries share only 10.5% of their gained sites - against 7.7%, 8.1% and 10.6% for the DOT1L-inhibitor arms - so the gained peaks are threshold noise and there is no evidence of redistribution | Analysis | 2 | 3/5 |
| A ten-residue export signal is the 5' partner's whole contribution - and the field disagrees about which direction it pushes | Mechanism | 5 | 4/5 |
| A tested negative: neither fusion product alters DNA double-strand break repair | Explainer | 2 | 4/5 |
| A third of the papers we said we could not read were free to read in full | Analysis | 5 | 0/5 |
| A three-question triage to detect subtraction mechanisms, applied to every KMT2A partner in the graph | Analysis | 2 | 2/5 |
| A tighter CXXC domain fails and a weaker one works: affinity rank does not predict function in the MLL-AF9 swap series | Analysis | 3 | 4/5 |
| A time-resolved BRG1/RING1B/H2AK119ub CUT&RUN at BENC under menin inhibition - the inv(16) experiment, run on the right disease | Experiment | 4 | 1/5 |
| A two-compartment switch for a SEC cargo: nucleolar retention versus AFF4-induced nucleoplasmic droplets, set by one methylated arginine | Mechanism | 3 | 3/5 |
| A uniform permutation null and a coverability-matched one disagreed on 18 of 23 samples for the same gene set - the null, not the data, decided the verdict | Explainer | 1 | 4/5 |
| A width-matched panel of loci that cannot be occupied is a usable per-locus floor; IgG in this deposit is not | Explainer | 1 | 5/5 |
| A within-sample share cancels an unknown scale factor but it does NOT make two studies comparable - the same eviction reads as 0.20 over a genome-wide denominator and 0.67 over a promoter-only one, in the same cells on the same day | Explainer | 1 | 4/5 |
| A73051 has the lowest oncoprotein share of the 25 untreated samples, and its sequencing depth is mid-range (37th-39th percentile), so the reading is not a depth artefact - the coordinator's cycle-135 qualification misidentified enrichment as coverage and was reversed in cycle 138 | Analysis | 2 | 4/5 |
| A73051 is the one HOXA-negative non-AFF1 sample in GSE252378, and it is IRX1-negative too | Analysis | 1 | 3/5 |
| ABI1 (Abl interactor 1 / e3B1) — WAVE-complex cytoskeletal adaptor, KMT2A partner, and an ENL-binding protein | Protein | 4 | 3/5 |
| ABL1 — domain architecture and residue coordinates (with the 1a/1b numbering trap) | Protein | 8 | 5/5 |
| About one KMT2A-rearranged patient in twenty has no direct fusion at all - only the reciprocal one | Explainer | 4 | 3/5 |
| Absence claims: 93% are unbounded in prose, but the evidence claims are 71% bounded - and the query that tested them was itself broken | Analysis | 3 | 3/5 |
| Absence: the tissue with the clinical signal is the one tissue nobody has put under a menin inhibitor and measured - one record in the whole literature, and it is a review | Analysis | 4 | 4/5 |
| ACADM is a mitochondrial matrix beta-oxidation enzyme with an experimentally coded matrix-only localisation, recovered on 8 spectra from a nuclear-extract pulldown whose specific tail is 14.5% mitochondrial — declined | Interface | 5 | 2/5 |
| ACER1 is on the list of in-frame reciprocal KMT2A partners - and ACER1 is the gene the 'reciprocal-negative' breakpoints fall next to | Explainer | 4 | 3/5 |
| Acetylation is a cycle, not a mark - and this graph holds one complete cycle, on a residue the fusion throws away | Mechanism | 5 | 3/5 |
| ACIN1 (Acinus) - a splicing/apoptosis protein whose only domain is the 35-residue module the leukaemic fusion keeps, and whose entire localization record is uncoded | Protein | 5 | 3/5 |
| ACIN1::NUTM1 - the commonest NUTM1 fusion in infants, cryptic to cytogenetics, and the only one with a human cell line | Fusion | 6 | 3/5 |
| Across 21 stopped trials of menin, DOT1L, BET, CDK9 and LSD1 inhibitors in acute leukaemia, 12 (57%) were stopped for sponsor or enrolment reasons, and the only two risk-benefit stops are one molecule - failure here has mostly been structural | Analysis | 3 | 3/5 |
| Across all seven MLL-fusion baits, how deep a bait's fixed top-300 list runs into non-significance predicts how many "specific" partners it appears to have — Spearman +0.821, exact p = 0.034, and MLL-AF4 is the extreme on both axes | Analysis | 3 | 4/5 |
| Across eight murine contrasts and two human stratifications, the H3K79me2 eviction span separates a menin inhibitor from a DOT1L inhibitor 22-fold with no overlap AND detects menin engagement in a human cell whose aggregate reads 0.998 - two properties the aggregate has one of and one of | Analysis | 3 | 3/5 |
| Across every same-condition H2AK119ub replicate pair in GSE260742 - nine pairs, three arms, both pairing shapes - rank concordance over the shared bin universe runs 0.6481 to 0.8796 and never reaches 0.88. The floors this thread scores against are all computed from pairs that are only moderately concordant. | Analysis | 1 | 3/5 |
| Across four VTP timepoints the within-sample share at a fixed top-0.1% set ranks perfectly inversely to the track's non-zero bin count (Spearman -1.000 over a 2.2-fold spread), so this project's standard instrument is confounded with ChIP enrichment - and the confound cannot be removed from inside one sample | Explainer | 1 | 3/5 |
| Across one infant's B-ALL to AML lineage switch, HOXA occupancy collapses ~28-fold and IRX1 falls only ~2.2-fold | Analysis | 2 | 2/5 |
| ACSL4 - a CRISPR-screen-derived, functionally validated KMT2A-selective vulnerability in myeloid disease, and a gene whose loss normally protects cells from ferroptosis | Protein | 3 | 4/5 |
| ACTB / beta-actin (P60709) as a SUBJECT, not a loading control - the dirtiest negative control in the pan-MLL-fusion 42, and the one the paper's authors kept | Gene | 3 | 2/5 |
| Adaptive, non-genetic resistance — the leukemia keeps the fusion and rewires how it is maintained | Resistance | 5 | 3/5 |
| Adjudicated: CTCF does not do opposite things at KMT2A - it does one thing, and this graph's contradiction is an untested premise about whether a break becomes a rearrangement | Explainer | 9 | 3/5 |
| Adjudicating the unwritten-gene queue by claim membership diverges from it at Spearman 0.36 - and then puts four acronym collisions in its own top five, so divergence was not improvement | Analysis | 2 | 4/5 |
| ADJUDICATION: the SvID and the gamma-H2A.X motif are OVERLAPPING BUT NOT THE SAME SURFACE - and the premise that made the question urgent, that the SvID is distinct from the MLL cavity, is FALSE at the SvID's own boundary | Analysis | 4 | 4/5 |
| AF10 fusions recruit and stabilise JAK1 - a kinase bound to the fusion with no phosphosite on the fusion | Interface | 2 | 3/5 |
| AF10/MLLT10 fusions drive aberrant self-renewal of non-stem progenitors — found only by opening the paper | Mechanism | 3 | 3/5 |
| AF9's nuclear residence is chaperone-dependent, the Hsp90 site is the SAME C-terminal region the fusion keeps, and UniProt records no cytoplasmic pool at all | Mechanism | 4 | 3/5 |
| AFDN (AF6): nothing is discarded from the fusion, yet this is the clearest subtraction in the set — the fusion steals wild-type AF6 out of the cytoplasm | Mechanism | 4 | 3/5 |
| AFDN / AF6 — domain architecture and residue coordinates | Protein | 5 | 4/5 |
| AFF1 / AF4 — domain architecture and residue coordinates | Protein | 10 | 3/5 |
| AFF1 / AF4 — the 3' half of the fusion, and a target with almost no structural footing | Protein | 13 | 3/5 |
| AFF1 AF4_int motif to AF9/ENL AHD: the index fusion's only documented elongation interface, and it competes with DOT1L | Interface | 7 | 4/5 |
| AFF1 and fusion occupancy transfer between infants at Spearman 0.82-0.92, but H3K4me3 transfers better at 0.93-0.97 - so the transferable part is mostly promoter structure, not fusion targeting | Analysis | 2 | 4/5 |
| AFF1 as the subtraction control: the refutation is WITHDRAWN - the degron is lost, not retained | Mechanism | 4 | 2/5 |
| AFF1 is NOT peptide-poor - it yields 49 detectable tryptic peptides against menin's 28, and menin cleared the identity threshold while AFF1 scored zero - but the two groups do not separate on peptide yield at all, so the driver is abundance | Analysis | 2 | 4/5 |
| AFF1 occupancy does not distinguish fusion-occupied promoters from wild-type KMT2A promoters in primary infant KMT2A::AFF1 - reproduced at promoter resolution, and the corpus should stop reading a partner ChIP as a fusion readout | Analysis | 3 | 4/5 |
| AFF1 reaches P-TEFb only through AFF4, and the index fusion's elongation phenotype is therefore a claim about AFF4 availability | Hypothesis | 3 | 1/5 |
| AFF1- and AFF4-containing super elongation complexes occupy physically distinct neighbourhoods in living cells, and KMT2A::AFF1 inherits the AFF1 one | Hypothesis | 3 | 1/5 |
| AFF1-AFF4 heterodimerisation through the C-terminal homology domain: the one SEC interface KMT2A::AFF1 certainly keeps, defined by a 2.2 A structure of the wrong subunit | Interface | 3 | 3/5 |
| AFF1-AS1 - the antisense RNA 151 bp from the index fusion partner's TSS, which Ensembl does not recognise and this project's promoter table cannot see | Gene | 6 | 3/5 |
| AFF1-exclusivity describes 378 of 719 genes and 72% of them rest on one patient - and the MEIS1 comparison I used to call IRX1 indistinguishable was an artefact of scoring MEIS1 with the weaker instrument | Analysis | 2 | 4/5 |
| AFF1-NPM1 proximity: nucleophosmin is the only bait in any published proximity experiment whose neighbourhood contains AFF1, KMT2A and menin together | Interface | 4 | 2/5 |
| AFF1-RBM15 proximity: the m6A-complex adaptor, itself a paediatric leukaemia fusion partner, has AFF1 in its BioID neighbourhood | Interface | 4 | 2/5 |
| AFF1, the fusion's 3-prime partner, carries 126 genome-wide-significant in-gene SNPs across 505 traits in one contiguous 201 kb block (98.9th length-matched percentile), 631 of 849 rows lipid-related and 68 red-cell indices | Analysis | 2 | 3/5 |
| AFF1::KMT2A (AF4-MLL), the der(4) product: what it is made of, residue by residue | Protein | 5 | 4/5 |
| AFF1's modern proximity neighbourhood is four RNA-binding proteins - NPM1, RBM15, SBDS, ZRANB2 - and it barely overlaps AFF4's | Analysis | 3 | 3/5 |
| AFF1's own promoter window is occupied in 20 of 27 samples - top 4% of the whole table - and the call cannot be attributed to AFF1 | Analysis | 3 | 3/5 |
| AFF1's promoter window is 92.5% AFF1-AS1's - worse than IRX2's 89.2% - and the project's promoter table has no row for the neighbour at all | Analysis | 3 | 4/5 |
| AFF1/AFF4-CAMKV - DECLINED, and it is a LABELLED REDISCOVERY: data/symbol-collisions.json already holds a CAMKV row saying BioPlex 2017 and 2021 are one programme and that CAMKV is deposited under split isoform accessions | Interface | 4 | 2/5 |
| AFF2 (FMR2) — the SEC-L2 scaffold, and the AFF-family member with no dependency anywhere | Protein | 2 | 3/5 |
| AFF3 (LAF4) — the AFF-family scaffold of SEC-L3, and a KMT2A fusion partner in its own right | Protein | 5 | 3/5 |
| AFF4 — the textbook SEC scaffold that KMT2A::AFF1 cells need LESS than other leukemias | Protein | 8 | 4/5 |
| AFF4 has never been placed in a haematopoietic cell state — every SEC cell-state result is in another tissue | Analysis | 4 | 4/5 |
| AFF4-BTK - DECLINED. One osteosarcoma AP-MS row, and it is the only partner in the uncovered prey-only tail with an approved drug against it, which is exactly why the decline is written down | Interface | 2 | 2/5 |
| AFF4-CDK15: AFF4 is prey in a systematic CMGC-kinase TAP interactome - a kinase adjacent to the complex CDK9 works in, and nobody has followed it up | Interface | 2 | 2/5 |
| AFF4-FMR1 - DECLINED, and the provenance is the finding: the 'publication' behind this IntAct row is HENA, an Alzheimer's data-integration dataset, not an experiment on AFF4 | Interface | 2 | 2/5 |
| AFF4-MED10: AFF4 is prey in a 2004 Mediator MudPIT purification - a lead with an independent mechanistic reason to be true, and no experiment that tests it | Interface | 3 | 2/5 |
| AFF4-SDCBP (syntenin): the only prey-only row in this census typed 'direct interaction' - a proteomic phage-display hit on AFF4's C-terminal peptide, in vitro | Interface | 3 | 2/5 |
| AFG2A / SPATA5 (Q8NB90) - a 55LCC replisome-proteostasis ATPase that co-purifies with KMT2A and menin, and whose CURRENT symbol cannot retrieve its own source paper or any of its function literature | Gene | 7 | 2/5 |
| AFG2B / SPATA5L1 (Q9BVQ7) - the second 55LCC ATPase, the only read-queue member with an annotated nuclear pool, pan-essential in 95.5% of lines, and the one that touches PSIP1 | Gene | 6 | 2/5 |
| After lineage switch, KMT2A-rearranged AML does not merely lose CD19 - it acquires a monocytic myeloid-derived suppressor cell phenotype and actively suppresses T cells | Mechanism | 2 | 3/5 |
| Against a chromatin-machinery name list written before the intersection, only 8 of 151 symbols have an entry with no mark, no epigenetics field and no chromatin concept at all - and 7 of the 8 are the P-TEFb brake and the AFF paralogues | Analysis | 1 | 4/5 |
| Against a correctly measured same-condition floor, a menin inhibitor's effect on H3K4me3, H3K79me2 and H3K27me3 is a genome-wide redistribution - up in the decile below the peaks, down monotonically to the sparsest decile - while its effect on the FUSION stays confined to the top 0.1%. The drug displaces the complex at the peaks and moves the marks everywhere | Hypothesis | 2 | 1/5 |
| Agency law — actual authority, apparent authority, and what revocation cannot undo | Analogy | 4 | 1/5 |
| AGGF1 - an angiogenic G-patch protein whose BioID neighbourhood contains ELL, KMT2A, LEDGF, WDR5, KAT7 and RNA polymerase II | Gene | 3 | 2/5 |
| AHDC1 (Gibbin) - an AT-hook chromatin-architecture factor that is already a cofactor of a DIFFERENT sarcoma fusion oncoprotein, and whose KMT2A breakpoint lands in an untranslated exon | Gene | 8 | 3/5 |
| AK_7_3, a KMT2A::AFF1-derived fusion circRNA that holds down mitochondrial respiration and ROS in t(4;11) B-ALL - the only mitochondrial mechanism in this beat measured in the index fusion | Mechanism | 2 | 3/5 |
| AKAP8 (AKAP95) - the only nuclear A-kinase anchoring protein, and the one that turned out to be required for MLL-rearranged leukaemia | Gene | 7 | 4/5 |
| AKAP8::ZNF384 - the same protein that MLL-rearranged leukaemia depends on is itself a rare B-ALL fusion partner, on the 5' side, donating its condensate-forming IDR | Fusion | 3 | 3/5 |
| AKAP95 binds the Pol II CTD directly and nascent RNA gates the condensate - a feed-forward loop where transcription recruits the factor that sustains transcription | Mechanism | 2 | 3/5 |
| AKAP95 directly enhances H3K4 mono-, di- and tri-methylation - by the KMT2B complex, and ONLY by the KMT2B complex; the paper's own discussion says the MLL1/KMT2A case was never tested | Mechanism | 3 | 4/5 |
| AKAP95 IDR1 co-condenses with the KMT2A N-terminal fragment - the one AKAP95 contact that lands inside the region every KMT2A fusion retains | Interface | 3 | 3/5 |
| AKAP95 is phenotypically silent at steady state and required only when a cell is changing state - the same shape in ATRA differentiation and in MLL-AF9 transformation, thirteen years apart | Cell state | 2 | 4/5 |
| AKAP95 reaches this disease by two separate routes - through WRAD/DPY30 and through the retained KMT2A fragment - and only the second one survives the fusion | Explainer | 3 | 3/5 |
| AKAP95-DPY30: a direct contact whose binding determinant two groups map to OPPOSITE ends of AKAP95, and neither has been structurally resolved | Interface | 4 | 3/5 |
| AKAP95's requirement in KMT2A-rearranged leukaemia runs entirely through IDR co-condensation with the retained fragment, and not at all through DPY30 - so a DPY30-binding-dead AKAP95 will fully rescue | Hypothesis | 2 | 1/5 |
| AKAP95's subnuclear addresses - nuclear matrix, nucleolus, and dynamic foci - and the finding that the famous one is the one its MLL-linked function does not need | Mechanism | 4 | 4/5 |
| AKT and ATM push ELL between two complexes: K355 acetylation sends it to SEC, ATM phosphorylation sends it to LEC | Mechanism | 2 | 3/5 |
| ALDH1L2 (Q3SY69) - the second-largest fall in the serine/one-carbon panel (-3.40), named nowhere in this graph, zero of 1,258 DepMap lines require it, and a tumour SUPPRESSOR where it has been studied | Gene | 5 | 3/5 |
| ALK (anaplastic lymphoma kinase) domain architecture | Protein | 1 | 4/5 |
| ALKBH5 — the second m6A eraser: a cancer-stem-cell self-renewal role elsewhere, one incidental KMT2A record, and a flat dependency row | Gene | 5 | 2/5 |
| All 39 bounded absences in this graph, classified by WHAT BOUNDS THEM: 23 rest on an abstract-level literature search, 7 on a threshold or a query filter, and only 2 on reading the primary source | Analysis | 6 | 4/5 |
| All 46 comparator lines screened: the two we tripped over are the only two we can find | Analysis | 3 | 3/5 |
| All 46 patient phosphosites sit outside folded domains, none of LEDGF's twelve is in the clamp that holds KMT2A, and six of KMT2A's eleven are not on the fusion protein | Analysis | 3 | 0/5 |
| All 56 core-complex partners that anyone deliberately fished for already have an entry: the unwritten interactome is 100% by-product | Analysis | 2 | 4/5 |
| All four input samples explicitly titled to the MLLAF9 ChIP arm of GSE260742 carry supplementary_file = NONE, so no input-referenced peak call is possible from the processed deposit - and the only deposited batch-1 inputs are two BAMs filed under a different arm's title with the same cell line and the same F3 filename prefix | Analysis | 3 | 5/5 |
| All four murine VTP-50469 H3K79me2 contrasts in GSE260742 give Spearman -1.000 against eviction depth, and all four SGC0946 contrasts are flat: the sign reproduces four times out of four, the span only to within a factor of 1.99, and the replicate pair that establishes this was already binned on disk from cycle 82 | Analysis | 3 | 3/5 |
| All nine unwritten MEN1 partners trace to exactly two publications, neither of which mentions menin outside an antibody catalogue row | Analysis | 6 | 4/5 |
| All three pre-registered branches came out of the same numbers under four defensible floors - the expressed/silent binary was measuring the ruler, not the gene | Explainer | 1 | 4/5 |
| All three withdrawn mechanism-targeted trials admit infants and none of the 52 trials that do not has been withdrawn (exact p = 0.0032, noticed after looking), but the stated reasons are business and administrative and all three are 2025-2026 registrations | Analysis | 1 | 2/5 |
| ALL-PO (CVCL_1069) — an infant KMT2A::AFF1 line that is already in DepMap and has never been screened | Explainer | 4 | 4/5 |
| Alu repeats and nuclear-matrix anchors in the KMT2A breakpoint region — the genome-feature side of the break | Mechanism | 6 | 3/5 |
| aml_stjude_2024 - 887 paediatric AML cases with per-sample KMT2A fusion-partner structural-variant calls for all 180 KMT2A-rearranged cases, plus mRNA-seq and FAB morphology | Analysis | 1 | 4/5 |
| AMLSG 23-14 / Palbo-AL-1 (NCT02310243) — the only trial ever run in MLL-rearranged acute leukemia with a CDK4/6 inhibitor, and it reported nothing | Trial | 2 | 5/5 |
| An activity-stratified permutation null for promoter-set overlap, and the check that its hypergeometric shortcut is not an instrument bug | Analysis | 2 | 4/5 |
| An anchored comparison keeps the nuisance sample on both sides, which is how you ask whether a PAIR is special rather than whether a SAMPLE is unusual | Explainer | 2 | 4/5 |
| An anti-MLL-C antibody in a t(4;11) cell is looking at two proteins at once | Explainer | 6 | 4/5 |
| An anti-MLL-N antibody sees the wild-type allele and the direct fusion, and nothing else - and cannot rank them | Explainer | 3 | 4/5 |
| An assay that cannot separate me2a from me2s cannot test the arginine switch - the two states are isobaric and predict OPPOSITE things, so a non-discriminating readout returns no information rather than an imprecise answer | Explainer | 6 | 4/5 |
| An ENCODE-only archive bound systematically undercounts chromatin-modifying enzymes, because ENCODE's target catalogue is transcription-factor-shaped - measured 3-for-3 on the H3K9 machinery, with ratios of infinity, 2.8x and 7.3x | Hypothesis | 2 | 1/5 |
| An expression subgroup is not an occupancy subgroup — and this project keeps reading one as the other | Explainer | 3 | 4/5 |
| An H3K4me3-reading PHD finger fused to NUP98 makes a potent leukaemia oncoprotein; the H3K4me3-reading PHD finger of KMT2A is deleted from every KMT2A fusion and reinstating it abolishes transformation. Same module class, opposite sign - and the one NUP98 fusion that carries KMT2A's PHD cassette is the weakest member of its family. | Analogy | 3 | 3/5 |
| An independence null OVERSTATES partner-exclusive recurrence 16-fold here - it is not a lower bound, and the brief that dispatched this beat said it was | Analysis | 2 | 4/5 |
| An MLL1 N-terminus ChIP sees the fusion and wild-type MLL1 in one track, and a menin ChIP has the same problem from the other side - so the standard reagents of the menin-inhibitor literature cannot attribute occupancy to the fusion, and the masking factor is now measured at 3.5 to 4.0-fold | Explainer | 2 | 5/5 |
| An NG2-directed therapy meets pericytes - and unlike B-cell aplasia there is no replacement therapy for a damaged vascular wall | Risk | 4 | 3/5 |
| An occupancy readout returned background in every channel of the only drug-exposed patient sample it has been tried in - so a negative from such an assay cannot currently be told apart from an assay failure | Risk | 3 | 3/5 |
| An occupancy-matched floor built from ~8,600 mid-occupancy promoter windows per track closes a gap Q117 named in its own memo - and it was necessary, because GAPDH and ACTB GAIN share in two of three human lines while Q117 measured them LOSING share in mouse | Analysis | 1 | 4/5 |
| An unstated system is not a coin flip: four out of five resolve away from the index disease, so silence in this graph is systematically optimistic | Explainer | 3 | 4/5 |
| Analysis (planned) — comparative druggability scan of every obligate fusion-partner interface in the atlas | Analysis | 5 | 3/5 |
| Analysis (planned): is CLEC12A a selective dependency in KMT2A-rearranged lines in DepMap, lineage-split and reported as raw effect? | Analysis | 2 | 1/5 |
| Analysis (runnable): build a methylome cell-of-origin score for infant KMT2A-rearranged ALL and test it as a predictor of lineage destination | Analysis | 4 | 3/5 |
| Analysis (runnable): build the first correlation matrix of menin-inhibitor resistance routes, from screens and from patient cohorts | Analysis | 4 | 3/5 |
| Analysis (runnable): can a menin ligand tell KMT2A from JUND? A structural and co-folding selectivity profile of the whole inhibitor class | Analysis | 4 | 3/5 |
| Analysis (runnable): do KMT2A partners rank by nuclear contact frequency in the same order as they rank in patients? | Analysis | 4 | 3/5 |
| Analysis (runnable): does product viability leave a signature in the KMT2A breakpoint map once DNA fragility is controlled for? | Analysis | 2 | 3/5 |
| Analysis (runnable): does the infant methylome predict HOXA status once age and breakpoint are controlled? | Analysis | 4 | 3/5 |
| Analysis (runnable): fit the relapse hazard function in KMT2A-rearranged infant ALL and test whether the cohort is a mixture | Analysis | 3 | 3/5 |
| Analysis (runnable): is anything actually enriched at KMT2A breakpoints? The test has never been run against a background that could say no | Analysis | 8 | 3/5 |
| Analysis (runnable): is there a shared cell-state signature behind non-genetic menin-inhibitor and BET-inhibitor resistance? | Analysis | 4 | 3/5 |
| Analysis (runnable): mine the KMT2A junction sequences for repair-pathway signature, and count the one junction class with a genetic control behind it | Analysis | 8 | 3/5 |
| Analysis (runnable): value a menin inhibitor as a short-duration instrument — cohort meta-regression plus a discrete-event model of remission months | Analysis | 5 | 3/5 |
| Analysis: cross-validating the single-group non-menin KMT2A-fusion dependencies in one framework | Analysis | 5 | 3/5 |
| Analysis: does the fusion's target set sit at lamina-associated domain borders? A free overlay of published LAD maps on published fusion occupancy | Analysis | 3 | 3/5 |
| Analysis: is the KMT2A genomic breakpoint a prognostic variable? A reanalysis of data Interfant and Frankfurt already hold | Analysis | 2 | 3/5 |
| Analysis: score fetal, myeloid-priming and differentiation-stage signatures across public KMT2A-r datasets | Analysis | 5 | 3/5 |
| Analysis: separate loss-of-protein from loss-of-occupancy by comparing degron-depletion and menin-inhibition transcriptional time courses | Analysis | 2 | 3/5 |
| Analysis: test whether published KMT2A::AFF1 occupancy is enriched at scaffold-attachment and cruciform-prone DNA beyond what CpG islands explain | Analysis | 3 | 3/5 |
| Another fusion family did the experiment this beat wants: in FUS::ERG and CBFA2T3::GLIS2 AML, MHC class I and II are absent at diagnosis, EZH2 drives it, and an EZH2 inhibitor restores presentation | Analogy | 3 | 3/5 |
| ANP32E - the eviction chaperone: the only protein in this beat whose job is to take a histone variant OUT of chromatin | Gene | 3 | 3/5 |
| ANSWERED from the paper's own methods, not from the corresponding author: the `dsgf` token that splits GSE139196's four SUV39H1 tracks into the two high and the two low ones is DSG-plus-formaldehyde double crosslinking - so the 44.5-percentile spread Q114 reported is a protocol variable, not replicate noise | Explainer | 2 | 3/5 |
| Answering a question three cycles filed and none ran: H3K79me2 also has two channels in GSE260742 - rep1 and rep2, 199 numeric leaves each - so cycle 104 quoted one of two available numbers without saying so. Unlike H2AK119ub they never materially disagree, 0 of 18 comparable ratios, and H3K27me3 and H3K4me3 were never scored under any second channel at all | Analysis | 1 | 3/5 |
| Anthracycline cardiotoxicity: the heart an infant keeps for sixty years | Risk | 5 | 4/5 |
| Anti-AF9 antibodies see three proteins, not two - and the third is an internal-promoter isoform discovered in 2025 | Explainer | 3 | 3/5 |
| Anti-AFF1 antibodies: attributable on a gel, not attributable in a microscope, and the classic localisation result shows exactly why | Explainer | 3 | 4/5 |
| Anti-ELL antibodies carry a confound the other partners do not: two paralogues and a protein whose abundance is actively regulated | Explainer | 3 | 3/5 |
| Anti-ENL antibodies are the cleanest partner reagent in this disease and sit on top of the worst confound | Explainer | 3 | 3/5 |
| Anti-thymocyte globulin - a rabbit antibody against human T cells, given to infants at a fixed mg/kg dose against a T-cell mass that nobody measures | Drug | 3 | 3/5 |
| AP2B1 (beta-2-adaptin) - the only one of AFF4's four two-hybrid partners that is not a hub, and the only one with an echo in this graph's endocytosis biology | Protein | 4 | 2/5 |
| Apoptotic nucleases cut KMT2A, and cells that survive the attempt can carry a translocation | Mechanism | 3 | 3/5 |
| Applied symmetrically, the criteria that were never applied make IRX1 the weakest member of the class it won - and MEIS1, a canonical fusion target, is indistinguishable from it, so the deposit cannot separate the two | Analysis | 2 | 4/5 |
| AQR (Aquarius) - a spliceosomal RNA helicase whose loss impairs MLL-rearranged leukaemia stem cells | Gene | 4 | 3/5 |
| AR / androgen receptor - the best-supported partner in the absence set by independent-publication count, and the reason a menin inhibitor is in prostate cancer trials | Gene | 9 | 4/5 |
| Are the fusions temporary? No: the KMT2A fusion is the one thing that does not change between diagnosis and relapse | Mechanism | 3 | 4/5 |
| Are the menin partners outliers, or did we pick them? (run) | Analysis | 1 | 3/5 |
| Arginine methylation gates KMT2-complex access to chromatin at two residues, in both directions, independently of the menin tether AND of the WIN motif - a parallel control point, not a rival to menin dependence | Mechanism | 10 | 3/5 |
| ARID1A (BAF250A) - required in the MLL-AF9 screen, present at the Myc enhancers, and flat in every selectivity measure | Protein | 12 | 3/5 |
| ARID1B (BAF250b) - the cBAF paralogue whose deletion PROMOTES MLL-AF9 leukaemogenesis, which makes it the one gene in this beat whose published KMT2A-fusion result points the wrong way for a drug target | Gene | 10 | 4/5 |
| ARID1B is not dispensable - it is paralogue-buffered. In ARID1A-mutant lines its CRISPR dependency goes from -0.0724 to -0.3709 (p=0.0002) while ARID1A's own falls away (+0.1925, p=0.044) and ARID2/SMARCA4 stay flat. Cycle 80's 'dispensable everywhere' framing was wrong and the caveat that entry carried was right | Analysis | 1 | 3/5 |
| ARID1B's buffering effect survives leave-one-out in 11 of 11 - even dropping the line whose own effect is -1.2269 leaves -0.2129 at p = 0.00465. But the lineage-concentration test says there was LITTLE confound to remove, cycle 84's headline confirms an absence rather than defeating a threat, and my own pre-registered TVD threshold fired on a measure that is large by construction at n=11 | Analysis | 1 | 3/5 |
| ARID2 (BAF200) - the PBAF subunit whose loss ACCELERATES MLL-AF9 leukaemia, and which is nonetheless required to maintain it | Protein | 6 | 3/5 |
| ARID4B / SAP180 (Q4LE39) - the Sin3A-complex subunit that shares SIN3A's HDAC1-binding region, is in the MLL-fusion interactome, and is the second of only two epigenetic vulnerabilities a CRISPR screen found in KMT2A-rearranged ALL | Gene | 4 | 3/5 |
| ASB7 (Q9H672) - the brake on H3K9me3's own positive feedback loop, released by CDK1 in mitosis, and it reached this graph as the flattest dependency in the read queue | Gene | 3 | 3/5 |
| ASF1A - the compensating paralogue: the only gene in this beat that is not required in a single one of 1,208 cell lines, and it still has a leukaemia phenotype | Gene | 6 | 3/5 |
| ASF1B - the paralogue that actually does the work in blood: it occupies >70% of H3.3 nucleosomes in fetal liver while HIRA is dispensable there | Gene | 5 | 4/5 |
| ASH2L — the WRAD subunit that has DPY30's essentiality profile and none of its co-dependency signal | Protein | 13 | 3/5 |
| ASH2L and RBBP5 rank 17,248 and 14,622 of 17,728 for KMT2A-selectivity, which is what this graph's own SET-domain-is-dispensable thread predicts - the audit found agreement where it looked for contradiction | Analysis | 2 | 3/5 |
| ASH2L is studied in leukaemia and has never been placed in a cell state there — and the KMT2A-rearranged arm needs it LESS than average | Analysis | 3 | 4/5 |
| ASH2L SPRY and RBBP5 347-356: a phospho-reader contact gated by RbBP5 Ser350, and the only WRAD interface with a measured fold-change | Interface | 3 | 4/5 |
| ASH2L: the only WRAD subunit ever perturbed in a KMT2A::AFF1 cell, once, weakly | Explainer | 9 | 4/5 |
| Ask whether the childhood AML in the KDM3B-haploinsufficiency syndrome cohort carried a KMT2A rearrangement - the one human test this mechanism has, and it is a records request | Experiment | 3 | 3/5 |
| Asked for the first time whether a KMT2A fusion GAINS chromatin sites under a menin inhibitor: all three pre-registered criteria fire, and the set they fire on is 52 low-amplitude bins reaching 6x the genome median, 16 of them with no gene within 20 kb and 1 of 52 on a CpG island where 66% of the fusion's real sites are | Analysis | 4 | 4/5 |
| Asking IntAct for its own fusion constructs found a sixth, exposed a duplicate record that would have inflated the count by three, and failed its own control 4 of 5 - so the floor is lower, not closed | Analysis | 2 | 3/5 |
| ASNS - the resistance gene for a backbone drug, never measured in this disease | Gene | 3 | 3/5 |
| Assay telomere maintenance across the thirteen B-lineage ALL DepMap lines, and see whether it predicts the DAXX dependency split | Experiment | 3 | 1/5 |
| At gene resolution the menin inhibitor is the stronger single agent, and only the combination approaches the degron | Analysis | 3 | 3/5 |
| At gene-body scale the AFF1-exclusive recurrent class is 6 against an exact institution-stratified null of 0.86 - but the singleton class is 63 against 74, so recurrence carries the signal and exclusivity alone does not | Analysis | 2 | 4/5 |
| At low drug doses the leukaemia dies through FLT3, not through HOXA9 - a second H3K79me2 pathway the dose-response hides | Mechanism | 3 | 4/5 |
| At promoter resolution the published N/C oncoprotein criterion calls 1043 promoters in fusion-negative CD34+ HSPCs - above the median across 27 KMT2A-rearranged patients - while the same-reagent controls in that sample call 66 and 11 | Analysis | 2 | 4/5 |
| At the 2 kb bins a menin inhibitor strips the most fusion from, both repressive marks GAIN and the active mark is LOST, monotonically in eviction depth (Spearman +1.000, +1.000 and -1.000) against a baseline-matched null that is flat to within 0.007 - the silencing clause of hyp-q117's prediction 5, measured for the first time | Analysis | 3 | 3/5 |
| At the 692 RS4;11 bins where an MLL1 N-terminus and menin co-occupy, VTP-50469 takes menin to 0.20 and DOT1L to 0.20, drops H3K79me2 to 0.66, and leaves MLL1-N-reactive material at 0.83 - four factors, one drug, one chromatin, and a clean ordering | Analysis | 1 | 4/5 |
| At the DNA level almost every KMT2A-rearranged patient has a reciprocal allele - 94% across partners, and 5% have nothing else | Epidemiology | 5 | 4/5 |
| At the Hox cluster, menin is required for most of the H3K4 methylation and MLL1 is required for only a subset - the cofactor has a bigger chromatin footprint than the enzyme | Mechanism | 1 | 4/5 |
| At the KMT2A anchor itself, KDM3B loss does not raise H3K9me1 AND H3K9me2 - it raises me1 3.9-fold while me2 FALLS to 0.44x, an inversion of the mono-to-di ratio that the paper's abstract describes as a joint increase | Mechanism | 2 | 3/5 |
| At the MLL1-N HELD SET, floor-normalised, the MLL1-N channel is inert to three decimals in both human lines (1.036 and 1.0359) - AND THAT IS A STATEMENT ABOUT THAT POPULATION, NOT ABOUT THE CHANNEL: at MLL1's own top sites in mouse the same channel reads 0.3012 under a DOT1L inhibitor and 0.3298 under a menin inhibitor | Analysis | 1 | 4/5 |
| At the same bins in the same cells, menin's share ratio is 0.20-0.26 and the MLL1 N-terminus antibody's is 0.80-0.91 - so a shared-epitope MLL1-N ChIP under-reports the menin inhibitor's occupancy effect by 3.5 to 4.0-fold, and the number is now measured rather than asserted | Analysis | 2 | 4/5 |
| ATF3 (P18847) - the one cascade member the DOT1L inhibitor hits HARDER than the menin inhibitor, and a transcriptional REPRESSOR being counted as a stress output | Gene | 5 | 3/5 |
| ATF4 / CREB2 (P18848) - the hub this graph inferred from its targets and never wrote, and its own transcript does not move under either menin inhibitor | Gene | 9 | 4/5 |
| ATF4's own transcript does NOT move under either menin inhibitor - and the whole ISR arm is reproduced by a DOT1L inhibitor, so it is not a menin-interface readout | Analysis | 3 | 4/5 |
| ATF5 / ATFX (Q9Y2D1) - the most reproducible repression in the earlier dataset, and the three probe values the graph quotes are SEM, not RS4;11 | Gene | 4 | 4/5 |
| Atlas confidence class tracks the prey:bait ratio, not abundance - so the proposed copy-number triage of the atlas-only partners does not exist | Analysis | 3 | 4/5 |
| Atlas-only interactome partners are predicted by how abundant the prey is, not by which bait was pulled - and if so this graph's interactome denominator is inflated | Hypothesis | 4 | 1/5 |
| ATM - the DNA-damage kinase that phosphorylates three of the four KMT2A 3' partners | Gene | 6 | 5/5 |
| ATM phosphorylates ELL at T551, S561 and S589 - inside the OCEL domain this graph already calls essential for MLL-ELL immortalisation | Mechanism | 3 | 3/5 |
| ATM phosphorylates ENL at conserved SQ sites and flips it from elongation to Polycomb repression - on sequence every KMT2A::MLLT1 fusion keeps | Mechanism | 4 | 3/5 |
| ATR - the replication-stress kinase with the best preclinical case in this disease and the best published reason not to inhibit it | Gene | 13 | 4/5 |
| ATR phosphorylates KMT2A at S516 to break the SCF(Skp2) contact - a phospho-gated degradation switch sitting inside the retained fragment | Mechanism | 3 | 3/5 |
| ATRX - DAXX's partner and the other arm of H3.3 deposition; in this disease its only signal is in the four lymphoid cell lines | Gene | 6 | 2/5 |
| Attribution audit 1 of 5 - who co-purifies with KMT2A::AFF1: the inventory does not survive, the individual partner blots mostly do | Analysis | 4 | 3/5 |
| Attribution audit 2 of 5 - post-translational modifications on KMT2A::AFF1: nothing survives at peptide level, and the one strong PTM result is explicitly about the wild-type protein | Analysis | 4 | 4/5 |
| Attribution audit 3 of 5 - where KMT2A::AFF1 sits in the nucleus: the endogenous image does not survive, the overexpression images do and say something different | Analysis | 5 | 3/5 |
| Attribution audit 4 of 5 - the half-life and turnover of KMT2A::AFF1: this class SURVIVES, and it is the only endogenous fusion-attributable protein measurement this beat found | Analysis | 4 | 4/5 |
| Attribution audit 5 of 5 - where KMT2A::AFF1 sits on chromatin: the field's standard attribution heuristic is invalidated by the paper that founded it, but two real survivors exist | Analysis | 7 | 3/5 |
| Attribution is asymmetric: q151's IRX2 negative survives a window that is 89.2% someone else's gene, and a positive in the same window would not have | Analysis | 4 | 4/5 |
| ATXN7L3 — the shared adaptor that actually sets H2Bub levels, and a KMT2A-selectivity hit nobody in this field has looked at | Protein | 7 | 3/5 |
| Audit of the infant presenting-feature evidence: what exists, what does not, what was rejected, what could not be read | Analysis | 4 | 4/5 |
| Audit, CORRECTED: the PHD add-back result was replicated in 2008 by a second group in a different fusion, and this graph already cited it | Analysis | 3 | 4/5 |
| Auditing all 2,476 committed entries for single-convention H2AK119ub: 122 mention the mark, 10 carry both conventions, 2 name the one they use, and 2 quoted a paired-convention number without saying so. Both are amended - and the more useful result is that the two conventions disagree PER STATISTIC rather than globally, so declaring the mark unusable would have been wrong | Analysis | 1 | 3/5 |
| Auditing the graph against the PI's brief, not against its own ledger (run) | Analysis | 1 | 5/5 |
| Auditing the seven strikes before applying them: nine of ten decisions stand, four for different reasons than were given, and one clinical argument fails | Analysis | 17 | 4/5 |
| AUGMENT-101 (NCT04065399) — the registration trial, and what 22.8% actually means | Trial | 2 | 4/5 |
| AUGMENT-101: the partner composition of the trial that approved a menin inhibitor, with KMT2A::AFF1 at n=2 evaluable | Epidemiology | 3 | 4/5 |
| Azacitidine - the one hypomethylating agent actually given to infants with KMT2A-rearranged ALL: safe, demonstrably demethylating, and it did not change survival | Drug | 8 | 4/5 |
| B2M (beta-2 microglobulin) - the invariant light chain every MHC class I molecule needs, the classic class I escape route, and a gene this disease's literature has never once named | Gene | 6 | 3/5 |
| BAF does not work where the fusion works: most direct MLL-AF9 targets do not respond to Brg1 loss, and the SWI/SNF address is a distal MYC enhancer cluster 1.7 Mb away | Mechanism | 4 | 4/5 |
| BAF inhibition against the menin axis: on the evidence it is a complement, not an alternative - and the case rests on one laboratory | Explainer | 6 | 3/5 |
| BAG6 / BAT3 - a DOT1L partner that is about H3K79me2 itself, reciprocally co-immunoprecipitated, and not a spoke | Gene | 5 | 3/5 |
| BAHCC1 - a BAH-domain H3K27me3 reader that an MLL fusion binds and upregulates in mouse, and the locus carrying the two largest MLL1-N-reactive rises under a menin inhibitor in human RS4;11 | Gene | 9 | 3/5 |
| BARD1 (Q99728, 777 aa) - BRCA1's obligate partner, and the member of the cascade that actually touches the chromatin: its PxVxL motif at 569-573 binds HP1, and CTCF binds BARD1 rather than BRCA1 in an undamaged cell | Gene | 5 | 3/5 |
| BARD1 and EXO1 are the only two proteins in the resection layer with ZERO chromatin-occupancy datasets anywhere - ENCODE, ChIP-Atlas, ReMap and a hand-checked GEO title list all return nothing - and BARD1's silence is the loud one, because its obligate partner BRCA1 has thirty-one | Analysis | 3 | 4/5 |
| Basket and umbrella designs: pooling rare fusions into one trial | Explainer | 3 | 4/5 |
| Bayesian borrowing: how many infants a prior is worth, and when it lies | Explainer | 3 | 3/5 |
| BCAT1 in core-binding-factor AML - the closest analogue in another fusion family, where TWO different fusions converge on one metabolic enzyme by rewiring the chromatin at its locus | Analogy | 2 | 3/5 |
| BCL11A — the sickle-cell target whose binding sites lose methylation in this disease | Gene | 3 | 0/5 |
| BCL2 — the one co-dependency in this beat that already has an approved drug pointed at it | Protein | 7 | 4/5 |
| BCOR — the other side of the CBX8 conflict, and a target you would be inhibiting in the direction of disease | Protein | 8 | 3/5 |
| BCOR, not CBX8, is the AHD contact MLL-AF9 cannot lose - and the same two partners bind ENL far more tightly than AF9 | Mechanism | 5 | 4/5 |
| BCORL1 — the BCOR paralogue that is in the only crystal structure of the PRC1.1 core, and is the one PRC1.1 subunit nobody has tested in KMT2A-rearranged leukaemia | Protein | 8 | 3/5 |
| BCR — domain architecture and residue coordinates | Protein | 6 | 4/5 |
| BCR::ABL1 (Philadelphia chromosome), t(9;22)(q34;q11) | Fusion | 11 | 5/5 |
| Before quoting anything, this beat re-derived six figures that two earlier beats had stored - three human, three mouse - from the deposited files end to end, and all six came back identical, which is the control that licenses every cross-beat comparison in the entry above it | Analysis | 1 | 4/5 |
| BENC - the MYC blood enhancer cluster 1.7 Mb downstream, required for MLL-AF9 leukaemia maintenance, and named in zero entries of this graph until now | Non-coding | 5 | 4/5 |
| BET bromodomain inhibition in KMT2A-rearranged leukemia — spectacular preclinically, stalled clinically | Target | 4 | 3/5 |
| Between-patient variation in oncoprotein occupancy is not a fusion-partner effect: across six partners the within-partner range of the amplitude statistic is as wide as the between-partner range of its medians | Analysis | 2 | 3/5 |
| BICRA (GLTSCR1) - the ncBAF scaffold, zero PubMed records in KMT2A leukaemia, and a lineage-independent dependency in KMT2A-rearranged lines | Protein | 8 | 3/5 |
| Big liver, big spleen: the organomegaly numbers measured in infants, not pooled from children | Explainer | 5 | 3/5 |
| Bin the deposited H2AK119ub NTvKO 2 x 3 design: twelve files, three replicate conventions, public since 2025-11-23 and never analysed - it is the only route to the silencing clause of hyp-q117's prediction 5, it is the internal validation of the PCGF1 knockout this project's null depends on, and it carries a spread the H3K79me2 arm cannot | Experiment | 1 | 4/5 |
| Biomea Fusion — icovamenib (BMF-219): the covalent menin inhibitor that left oncology for diabetes | Group | 4 | 4/5 |
| Bite-back: a DOT1L inhibitor in CALM-AF10 deepens a genome-wide H3K79 deficit that already causes chromosome breaks | Risk | 4 | 3/5 |
| Bite-back: a target nominated from an imported mechanism inherits a fusion the index disease does not have | Risk | 4 | 3/5 |
| Bivalent and primed chromatin at fusion target loci — and why the H3K4/H3K27 story is weaker than usually told | Mechanism | 5 | 3/5 |
| Bleximenib (JNJ-75276617) — menin inhibitor with a cleaner cardiac profile, and the only one with a 2-year-old floor | Drug | 7 | 2/5 |
| BLIN-3 (CVCL_QW47) — a three-month-old's KMT2A::AFF1 line used to show the pro-B to pre-B block can be pushed | Explainer | 2 | 3/5 |
| Blinatumomab in infant KMT2A-rearranged ALL — the largest single outcome gain in thirty years | Drug | 4 | 3/5 |
| BLNK (SLP-65) - the B-cell receptor adapter, in the Q152 AFF1-only core and a known lineage-infidelity marker in myeloid leukaemia | Gene | 3 | 2/5 |
| Blocking IKK/NF-kB in an infant is removing the switch every immune cell runs on — and the class has already failed clinically on exactly that | Risk | 4 | 4/5 |
| Blocking where DOT1L binds instead of what it does - the modality that removes the mark only at fusion targets | Mechanism | 5 | 3/5 |
| Blot all three PBX proteins in KMT2A::AFF1 B-lineage cells, then delete them singly and in combination - the family has never been tested together in any human leukaemia line | Experiment | 3 | 3/5 |
| BMI1 - the self-renewal gene that KMT2A fusions can do without, because HOXA9 covers for it at the same locus | Gene | 11 | 4/5 |
| BMI1, CDKN2A and CDK6 are one circuit, not three genes - and in KMT2A-rearranged disease it has a loop nobody has measured | Mechanism | 5 | 3/5 |
| BMP2K (BIKe) - a nuclear serine/threonine kinase, and the ZNF384 fusion partner that is not a chromatin protein | Gene | 3 | 3/5 |
| BMP2K::ZNF384 - a PROTEIN KINASE as the 5' partner, with its catalytic domain retained: the counterexample to 'the partner is always a chromatin coactivator' | Fusion | 3 | 3/5 |
| BOD1L (BOD1L1) — the top SETD1A co-dependency, and the only candidate in this cycle tested by CRISPR tiling in a KMT2A::AFF1 line | Protein | 8 | 3/5 |
| Boltz co-folding plan: six complexes worth folding, three that must not be, and the positive controls that decide whether to believe any of it | Analysis | 3 | 3/5 |
| Bone marrow haematopoietic stem cell — the postnatal comparator, and why the same fusion behaves differently here | Cell type | 6 | 4/5 |
| Bone-marrow adipocyte — the fat cell that suppresses normal blood formation and feeds leukaemia a chemoresistance signal | Cell type | 2 | 3/5 |
| Bone-marrow sinusoidal endothelial cell — the vessel wall that keeps stem cells alive, and posts vesicles that accelerate MLL-AF9 leukaemia | Cell type | 3 | 3/5 |
| Born with it: congenital KMT2A::MLLT1-type AML, a subdural haemorrhage that began before birth, and death on day four | Patient story | 1 | 3/5 |
| Bortezomib is called an NF-kB inhibitor, and in MLL leukaemia it does two different things in two lineages — neither of which is reliably NF-kB in the lymphoid one | Mechanism | 3 | 4/5 |
| Both approved menin inhibitors cause multi-organ hyperplasia in animals, and one of them in the pancreas irreversibly | Risk | 6 | 3/5 |
| Both arrows on KDM3B depletion are broad: H3K9me1 rises genome-wide AND CTCF falls at 84.6% of 12,443 anchors - the KMT2A anchor's 0.40x is the 3.6th percentile among strength-matched anchors, not a unique event | Mechanism | 2 | 2/5 |
| Both datasets this beat used carry an exposure mismatch that could have produced its results, and both were measured rather than argued away: MOLM13's MENIN pair is 4 days against everything else's 3, and GSE260742's VTP arms are 48 h against 72 h DMSO controls - the first moves a criterion by 0.024 and the second is matched between the two arms being compared | Analysis | 2 | 4/5 |
| Both MBTD1 fusions end at H3K27me3-poor chromatin, one by excluding PRC2 and one by poisoning it - so the shared endpoint is the phenotype and MBTD1 is the coincidence | Hypothesis | 6 | 1/5 |
| Bounded absence: every chromatin measurement under a menin inhibitor is in an adult-derived line, and none is in an infant KMT2A::AFF1 model | Analysis | 6 | 3/5 |
| Bounded absence: in GSE159608's SEM line, VTP-50469 was profiled for H3K4me3 only - no menin, no H3K27ac, no H3K79me2, no RNAP2 and no IgG under the drug - and no library in the series carries a spike-in normalisation, so an absolute change in any mark is unmeasurable here | Analysis | 3 | 5/5 |
| Bounded absence: no menin-inhibitor trial reports response rate by 3-prime fusion partner in the primary literature | Analysis | 4 | 4/5 |
| Bounded absence: no published CRISPR or dependency screen in any infant-derived KMT2A::AFF1 model | Explainer | 2 | 4/5 |
| Bounded absence: no published study has tested whether a KMT2A fusion GAINS chromatin sites under a menin inhibitor - and the same pipelines found gains for two other proteins when they looked | Analysis | 5 | 3/5 |
| Bounded absence: not one menin-inhibitor study, trial or preclinical paper has ever recorded reciprocal fusion status | Explainer | 6 | 3/5 |
| Bounded failure with a near-miss worth recording: a GEO series matching the topic exactly belongs to a different paper | Analysis | 3 | 5/5 |
| Bounded failure: 'menin inhibitor-resistant cells' is a drug entry's central claim and neither the paper nor any repository defines it | Analysis | 3 | 5/5 |
| Bounded failure: a PMCID that exists and a body that does not - the MLL amino-terminus transformation paper is unreadable by both PMC routes | Analysis | 3 | 5/5 |
| Bounded failure: the CDK4/6 cell lines behind two therapeutic entries are unrecoverable although the article is marked free access | Analysis | 3 | 5/5 |
| Bounded failure: the founding menin-cofactor paper names no fusion, has no PMC record and deposited nothing - and three entries depend on it | Analysis | 4 | 5/5 |
| Bounded failure: the one unresolved source that is actually about the index fusion | Analysis | 3 | 5/5 |
| Bounded unreachable: the Blood supplemental table that three entries read their NLRC5 and CIITA group assignments from cannot be retrieved by ANY programmatic route - PMC serves a landing page and the publisher 403s this client - so those claims are re-readable but not re-verifiable without a human's institutional access | Analysis | 2 | 4/5 |
| Bounded unreadable: the only affinity purification of a SET-retaining KMT2A-derived fusion complex fails all four routes, and the molecule is the reciprocal product | Analysis | 4 | 4/5 |
| Bounded with every archive and every route named: after both public SUV39H1 deposits were read this cycle, there is still NO SUV39H1 occupancy measurement in any haematopoietic cell, any KMT2A-rearranged cell, or any damage state - in ENCODE (three routes, zero), ChIP-Atlas (one deposit, MCF-7 only) or GEO (two deposits, glioma and breast) | Analysis | 2 | 4/5 |
| Bounded, with every archive named: H3K9me1 and H3K9me2 in a CD34+ progenitor are absent from BLUEPRINT, EGA, Roadmap/Human Epigenome Atlas, the IHEC Data Portal and ENCODE - 49,663 IHEC datasets carry 178 assay labels and H3K9me2 is not one of them - and the absence is a consortium artefact, because GEO has had the CD34+ H3K9me2 data since 2017 | Analysis | 4 | 5/5 |
| Bounding an absence the graph already asserts: the H3K79me2 decay half-life, counted, dated and controlled - and why three of the six hits are about the drug's half-life | Analysis | 5 | 4/5 |
| BRCA1 (P38398, 1,863 aa) - named in 19 entries of this graph and never written: the HR mediator that CTCF and the H3K9 machinery are now reported to license at a break, and the only cascade member with a human therapy-related-leukaemia signal after topoisomerase II therapy | Gene | 7 | 3/5 |
| BRCA1 at the KMT2A exon-11 CTCF anchor is real, cell-type-restricted, and survives the summit-matched null Q35 asked for: 93.7th and 92.3rd percentile of same-cell CTCF anchors in HeLa-S3 and H1, rising to 95.2 and 95.7 under width-and-TSS matching - and 34.0 and 45.1 in the only two blood lines, where ENCODE's 300,000-peak pre-IDR lists are also empty | Non-coding | 2 | 3/5 |
| BRCA2 (P51587, 3,418 aa) - the RAD51 loader that receives the resected end BRCA1 licensed, named in 10 entries and never written; DepMap mean -0.519, and its 12-record KMT2A intersection is entirely germline-panel and pan-cancer sequencing with no mechanism | Gene | 2 | 3/5 |
| BRD2 - a bounded absence: zero KMT2A papers name it, it is inhibited by every BET compound used in this disease, and it is the paralogue most likely to carry the toxicity | Gene | 4 | 3/5 |
| BRD3 - named in the founding BET paper's own mechanism and in one title since, and not once separated from BRD4 by any experiment in this disease | Gene | 9 | 3/5 |
| BRD4 — the best-drugged protein in this beat, and the one whose clinical result is already in and disappointing | Protein | 9 | 4/5 |
| BRD9 — dispensable in the average cell, rank 39 of 17,728 in KMT2A-rearranged lines, and with an on-target proof most epigenetic targets never get | Protein | 4 | 3/5 |
| BRD9 survives the null; CEBPA sits at the median of random genes | Analysis | 1 | 3/5 |
| BRD9::NUTM1, t(5;15)(p15.33;q14) - one fusion is enough to make infant B-ALL in a mouse, and it is the one that behaves best in a child | Fusion | 7 | 3/5 |
| Break formation, break persistence and break fate are three quantities, and every assay in this dispute reports the middle one - which is why the triad's third premise is ambiguous rather than weak | Explainer | 2 | 3/5 |
| Breakpoint anatomy, and an audit of the prognosis claim | Mechanism | 9 | 3/5 |
| Breakthrough therapy and accelerated approval: the menin field took the fast review and declined the shortcut | Explainer | 12 | 4/5 |
| Bringing down a white count of half a million in a four-kilogram baby | Explainer | 4 | 3/5 |
| BRINP1 (DBC1/DBCCR1/FAM5A) - the last bait-supported partner of the six core proteins without an entry, a neural-specific BMP/retinoic-acid-inducible protein pulled down with DOT1L as bait in one quantitative AP-MS experiment and nowhere else | Gene | 2 | 2/5 |
| BRIP1 — downstream effector; rank 22 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 9 | 3/5 |
| Bruising and petechiae: the bleeding signs of thrombocytopenia at presentation | Explainer | 3 | 3/5 |
| BUD13 - a RES-complex splicing factor 1.66 Mb from KMT2A on 11q23.3, whose one chromatin paper puts it in the soluble fraction | Protein | 6 | 3/5 |
| Building the instrument that asks whether this corpus has already measured something: it fails, 85% of comparable pairs flag as disagreements and the one real conflict never surfaces - because measurements live in prose, so the fix is a typed reporting field and it is now in the standing brief rather than in an open question | Analysis | 1 | 2/5 |
| Busulfan - the alkylating agent that replaces radiation in infant conditioning, and whose labelled paediatric target range is below the range the modern trial data support | Drug | 6 | 4/5 |
| Buying an already-impaired asset — what diligence would you do, and what is the biological equivalent? | Analogy | 4 | 1/5 |
| C2CD3 - the centriole-elongation regulator fused to KMT2A exon 8 in an MPNST, predicted OUT OF FRAME, and the partner whose RefSeq transcript is 390 residues shorter than UniProt's canonical | Gene | 11 | 3/5 |
| C4orf36 - a protein-coding gene with three current TSSs spanning 43,782 bp, two of them inside or beside AFF1's promoter window, and the project's table has room for one | Gene | 5 | 3/5 |
| CABIN1 - a 2,220-residue calcineurin inhibitor that is also a full member of the H3.3 chaperone complex, and nobody has asked which job matters in blood | Gene | 3 | 3/5 |
| CALM-AF10 is predominantly cytoplasmic in transfected non-haematopoietic cells - and NUCLEAR in leukaemia cells (title corrected 2026-09-21; the five systems are five instances of one design) | Mechanism | 6 | 3/5 |
| CALM-AF10 needs BMI1 - and so does MLL-AF9, so this is a shared polycomb dependency and not a point of difference (title corrected 2026-09-21) | Mechanism | 3 | 4/5 |
| CALM-AF10 reaches DOT1L through exactly the same OM-LZ interface as KMT2A::MLLT10 - the recruitment transfers, the addressing does not | Mechanism | 8 | 4/5 |
| CALM-AF10 strips H3K79 methylation from the rest of the genome while adding it at HOXA - one fusion, two opposite effects on the same mark | Mechanism | 3 | 4/5 |
| CALM-AF10 was meant to separate the menin axis from the HOXA programme - and the indirect evidence has now turned against separability, because KMT2A-free HOXA lesions keep proving menin-DEPENDENT | Hypothesis | 9 | 1/5 |
| Canela 2017 deposited NO cohesin-depletion experiment - and it did deposit human END-seq in a B-cell-precursor leukaemia line, which nobody here had looked for | Analysis | 3 | 5/5 |
| Canela 2019's full text never names MLL or KMT2A, and its HCT116 cohesin arm is lovastatin-arrested in G1 - so the only directional cohesin experiment was run in a cell where transcription-coupled fragility should be lowest | Analysis | 2 | 4/5 |
| Canela 2019's RAD21-degron END-seq IS deposited and IS readable today - one sample per arm, no replicates, no minus-auxin control, hg19, bigWig coverage only | Analysis | 2 | 5/5 |
| Canonical versus non-canonical NF-kB in KMT2A-rearranged leukaemia — the two arms have opposite signs, and the two papers usually read as contradicting each other actually agree | Mechanism | 4 | 4/5 |
| CAR cell (CXCL12-abundant reticular) / LEPR+ perivascular stromal cell — the cell that makes the signal holding blood stem cells in the marrow | Cell type | 4 | 4/5 |
| Cardiac troponin release on MCL-1 inhibition - reported for two structurally distinct compounds and described by one developer as a likely CLASS effect, which makes it an essential-function ceiling rather than a chemistry problem | Risk | 3 | 3/5 |
| Cardiomyocyte - the non-haematopoietic cell that two of this graph's drug targets are required in, which makes it the graph's clearest bystander-organ liability | Cell type | 3 | 4/5 |
| CARM1 / PRMT4 (Q86X55) - the H3R17me2a writer, and the enzyme whose product is read by the KMT2A C-terminus that every fusion deletes | Gene | 5 | 3/5 |
| Catalytic-dead UCH test: does KMT2A::USP2 need its deubiquitinase activity to transform? | Experiment | 3 | 3/5 |
| Catalytic-dead versus degrader: a four-arm test that resolves the HDAC7 direction conflict and supplies the pharmacodynamic marker this drug class has never had | Experiment | 3 | 3/5 |
| CBFA2T3 (ETO2 / MTG16) domain architecture | Protein | 1 | 4/5 |
| CBFA2T3::GLIS2 supplies its own CAR-T antigen - FOLR1 came out of a list of fusion-specific genes in an isogenic human model. KMT2A-rearranged leukaemia is treated with a LINEAGE antigen it can abandon, or with one a drug has to create; nobody has built the fusion-specific surface list for KMT2A::AFF1. | Analogy | 2 | 3/5 |
| CBFA2T3::GLIS2, inv(16)(p13.3q24.3) | Fusion | 7 | 4/5 |
| CBFB — domain architecture and residue coordinates | Protein | 9 | 4/5 |
| CBFB::MYH11 (CBFbeta-SMMHC), inv(16)(p13;q22) | Fusion | 7 | 5/5 |
| CBS (P35520) - the largest fall in the whole panel (-4.07), a token that collides with Cajal bodies AND CTCF binding sites, and a germline phenotype whose hallmark is thrombosis | Gene | 4 | 3/5 |
| CBX1 / HP1-beta (P83916, 185 aa) - the HP1 paralogue with the fitness cost and no role in this graph's cascade: DepMap mean -0.349 with 16.6% of 1,257 lines below -0.5, four times deeper than HP1-gamma or HP1-alpha, and zero papers place it anywhere near KMT2A | Gene | 5 | 3/5 |
| CBX3 / HP1-gamma (Q13185, 183 aa) - the EUCHROMATIC HP1 paralogue, and the one CTCF actually prefers: the reader that carries BRCA1/BARD1 onto H3K9-methylated break chromatin, flat in DepMap, and a fusion partner in one KMT2A::AFDN AML patient | Gene | 6 | 3/5 |
| CBX5 / HP1-alpha (P45973, 191 aa) - the H3K9me3 reader that recruits the writer, the writer's destroyer and the second writer; and the one member of that circuit with a published pro-leukaemic role, as part of an MLL leukaemia stem-cell programme that immortalises myeloid progenitors WITHOUT Hoxa or Meis | Gene | 6 | 3/5 |
| CBX8 — the one place in this interactome where two good papers flatly disagree, and DepMap takes a side | Protein | 9 | 3/5 |
| CCDC32::CBX3, a previously unreported second fusion found alongside KMT2A::AFDN in a relapsing AML - and the only record in PubMed that pairs CBX3 with KMT2A at all | Fusion | 2 | 2/5 |
| CCG 1953 (n=115 infants): the first trial to genotype every infant found the partner does not predict outcome | Epidemiology | 2 | 3/5 |
| CCND3 (cyclin D3) — the scan's rank-4 hit, and the only one of the four with a drug class already in children | Protein | 12 | 3/5 |
| CCNT1 / cyclin T1 — the regulatory half of P-TEFb, and the one part of the elongation core with any dependency variance | Protein | 8 | 3/5 |
| CCNT1 and CCNT2 have no histone substrate and reach chromatin on someone else's back: Brd4 recruits cyclin T1 and Cdk9 to acetylated chromatin and drives Pol II Ser2 phosphorylation - a borrowed address, which is a third annotation state the corpus has no word for | Mechanism | 1 | 3/5 |
| CCNT2 / cyclin T2 - expressed in every KMT2A-rearranged line and needed by none of them, so the cyclin T split is real rather than an expression artefact | Protein | 4 | 4/5 |
| CD15 (Lewis-x, SSEA-1, 3-fucosyl-N-acetyllactosamine) - a sugar, not a protein: the most-named antigen in this graph that no gene encodes | Target | 9 | 4/5 |
| CD19 - the molecule this disease is treated by, named in 114 entries and written in none of them until now | Gene | 7 | 0/5 |
| CD19 CAR-T in infants with KMT2A-rearranged ALL — it works, it is manufacturable, and it does not hold | Target | 4 | 4/5 |
| CD19 looks lower in KMT2A-rearranged patients in the RNA-seq arm of TARGET and identical in the microarray arm of the same study - so this graph should not record a CD19 deficit | Analysis | 3 | 2/5 |
| CD22 (SIGLEC2) - the antigen that comes on BEFORE CD19, which makes it both the backup target and the pre-loaded escape route | Gene | 5 | 4/5 |
| CD22-directed therapy (inotuzumab ozogamicin) — the second B-lineage antigen, with high response and poor durability | Target | 1 | 4/5 |
| CD274 (PD-L1) - named in zero entries of this graph until now, a direct MLL1-H3K4me3 target gene in another tissue, and a cell-intrinsic dependency of MLL-AF9 leukaemia-initiating cells | Gene | 4 | 3/5 |
| CD33 (SIGLEC3) - the aberrant myeloid antigen on a B-lineage blast, and the one antibody-drug-conjugate target with a positive randomised result in KMT2A-rearranged disease | Gene | 9 | 4/5 |
| CD34 - named in 132 entries of this graph and written in none, and it does not mean what the graph has been using it to mean | Gene | 10 | 4/5 |
| CD38 - the one marker that is BRIGHTER in KMT2A-rearranged B-ALL, an antigen-targeted therapy that has already produced lineage switch, and an enzyme rather than a receptor | Gene | 4 | 3/5 |
| CD65 - a neutral glycolipid epitope (V3FucnLc8Cer), no gene, and the CD number that was split in two because its antibodies did not agree | Target | 5 | 3/5 |
| CD65s (VIM-2, sialylated ceramide dodecasaccharide) - the myeloid antigen that, with CD15, makes NG2 a perfect predictor of KMT2A rearrangement | Target | 6 | 4/5 |
| CD65s has no known synthesising enzyme, and the three fucosyltransferases nearest to it are explicitly excluded | Mechanism | 2 | 3/5 |
| CD7 - the T/NK antigen on a B blast that flags KMT2A rearrangement and worse event-free survival, and the fourth antigen on the lineage-switch list | Gene | 5 | 3/5 |
| CDC73 / parafibromin — the PAF1C subunit that was genetically tested, and a second tumour suppressor required by the fusion | Protein | 11 | 4/5 |
| CDK12 - a different kinase with a different cyclin, and in KMT2A-rearranged lines it is an anti-dependency | Protein | 4 | 4/5 |
| CDK13 - rank 171 of 17,728, equally deep in both lineage halves, and essentially unstudied in leukaemia | Protein | 9 | 3/5 |
| CDK4 - the other half of the class name, and it is NOT the gene this disease needs | Gene | 8 | 4/5 |
| CDK4/6 inhibition in KMT2A-rearranged leukemia — the class was already tried, and the trial never reported | Target | 9 | 3/5 |
| CDK6 - the kinase the KMT2A-r rationale actually rests on, and the pan-essentiality flag and the selectivity are both true | Gene | 11 | 4/5 |
| CDK9 - the kinase the whole SEC story runs through, which this graph held only as half of a two-protein summary entry | Protein | 12 | 4/5 |
| CDK9 inhibition in KMT2A-rearranged infant leukemia — the most direct hit on the hijacked machinery, and the narrowest window | Target | 5 | 3/5 |
| CDK9 peak widths more than double after fusion degradation, firing the pre-registered re-score trigger | Analysis | 3 | 3/5 |
| CDKN2A - one gene, two reviewed UniProt records with the same primary symbol, and a deletion that is three times rarer here than in the infant leukaemias next door | Gene | 12 | 3/5 |
| CEBPA — ranks 25th on the KMT2A scan and sits at the median of random genes | Protein | 5 | 3/5 |
| Cell identities considered and not written: what the search actually returned for basophils, mast cells, eosinophils, NK cells and the rest | Analysis | 4 | 3/5 |
| Cell state in KMT2A-rearranged leukaemia is organised by lineage, not by the fusion — five independent axes split the same way, and every one of them splits AML from ALL rather than partner from partner | Hypothesis | 5 | 1/5 |
| Cell type or the fusion? MV4-11 LOOSENS the confound the graph's own lineage split was built on - but its founding paper calls it biphenotypic | Analysis | 2 | 4/5 |
| Cell-state enumeration: 23 queries, what was written, what was rejected and why — including an empirical confirmation that PubMed reads SEM as two journal names | Analysis | 2 | 4/5 |
| Cell-surface capture proteomics on an isogenic human KMT2A::AFF1 model against its matched normal progenitor - the experiment an mRNA screen cannot replace | Experiment | 4 | 3/5 |
| Census of every published chromatin-occupancy measurement made under a menin inhibitor: eight datasets, every one TSS-anchored, every one tabulating losses only | Analysis | 8 | 4/5 |
| Central nervous system involvement at diagnosis in KMT2A-rearranged infant leukaemia | Explainer | 4 | 4/5 |
| CEP112 is a 955-residue centrosomal coiled-coil protein on 7 spectra with zero leukaemia literature — its only nuclear annotation is a single 2024 citation, and a long coiled-coil is the classic non-specific AP-MS passenger — declined | Interface | 3 | 2/5 |
| CHAC1 / BOTCH (Q9BUX1) - the largest single effect in the whole menin-inhibitor response (-5.11 log2) and a glutathione-degrading pro-apoptotic enzyme, named nowhere in this graph until now | Gene | 5 | 4/5 |
| CHAF1A (CAF-1 p150) - the subunit that reads PCNA and makes histone deposition replication-coupled, and the half of CAF-1 that leukaemia has not looked at | Gene | 5 | 3/5 |
| CHAF1B (CAF-1 p60) - the one histone chaperone in this beat with a real leukaemia literature, and a mouse experiment that contradicts DepMap's verdict on its druggability | Gene | 7 | 4/5 |
| CHD4 (Q14839) - the NuRD ATPase, a pan-MLL-fusion co-purifier, and the gene whose disruption drives lineage switching in KMT2A::AFF1 relapse | Gene | 5 | 3/5 |
| check-pi-dimensions.py selected fusion entries by id prefix and swept in an analogy node, reporting 50/51 where the truth is 49/50 - identical to one decimal, which is why it survived - and the one genuinely unlinked fusion has no analogue in this corpus, so no edge was written | Analysis | 1 | 5/5 |
| CHEK1 (CHK1) - the node where this graph's chidamide synergy actually lands, and the reason that synergy is an HR-impairment argument | Gene | 11 | 3/5 |
| CHEK2 (CHK2) - named in every combination mechanism here and measured on its own in none of them | Gene | 9 | 3/5 |
| Chidamide (tucidinostat) - the HDAC inhibitor in both of this graph's menin-inhibitor combination papers, and the only one paired with a menin inhibitor in the lymphoid index disease | Drug | 3 | 3/5 |
| Childhood leukaemia worldwide, ages 0-14 | Epidemiology | 2 | 4/5 |
| Children with NPM1::ALK lymphoma immunise themselves against their own fusion protein, and the antibody titre predicts relapse - while no autoantibody against any KMT2A fusion has ever been reported. The difference is not the junction; it is that ALK is an ectopic self-antigen and KMT2A and AFF1 are not. | Analogy | 3 | 3/5 |
| Children's Cancer Hospital Egypt (n=150 KMT2A-r): EFS 50% to 17% across four partner groups in a single-centre cohort | Epidemiology | 2 | 3/5 |
| Children's Oncology Group — the trial network, the AALL protocol series and the biobank that no single lab can substitute | Group | 6 | 4/5 |
| Chromatin accessibility is named in the PI's own dimension and the detector has no token for it - nor for enhancer, nucleosome, Polycomb or remodelling - so 121 of the 195 entries scored as having nothing do name a chromatin concept | Analysis | 2 | 3/5 |
| Chromatin loop anchors are DNA-break hotspots - and the two papers that established it disagree about why | Mechanism | 4 | 3/5 |
| Chromatin-bound XPO1 as a shared, druggable address for HOXA-driven leukaemia - and the objection that it may be a general chromatin cofactor rather than an address at all | Hypothesis | 5 | 1/5 |
| Chromocentres and pericentromeric satellite heterochromatin — no KMT2A evidence, but the AT-hook argument says there should be | Mechanism | 3 | 2/5 |
| CHUK (IKK-alpha) — the only kinase that sits in BOTH NF-kB arms, which makes it the one subunit whose inhibition has an ambiguous sign in this disease | Protein | 7 | 3/5 |
| CIBMTR post-transplant AML (n=426 KMT2A-r, curated cytogenetics): no outcome difference by fusion partner | Epidemiology | 2 | 3/5 |
| CIITA - the class II transactivator, a gene menin sits on, and the only antigen-presentation gene in this disease with a knockout that proves the drug acts through it | Gene | 6 | 3/5 |
| CK2 phosphorylates KMT2A at T2724/S2726 to license taspase1 cleavage - and that site is in the half the fusion throws away | Mechanism | 2 | 4/5 |
| CK2 phosphorylation of KMT2A S136/S142 tunes the LEDGF grip - a second, non-menin, phospho-gated handle on the fragment every fusion keeps | Interface | 3 | 3/5 |
| Cks1 and Cks2 hold both halves of KMT2A and set its level through the cell cycle | Interface | 2 | 2/5 |
| Class switch recombination: a B cell deliberately mutates and cuts its own antibody locus, and the same enzyme causes MYC-IgH translocations | Mechanism | 8 | 5/5 |
| CLEC12A (CD371, CLL-1, MICL) - the leukaemic-stem-cell antigen whose therapeutic rationale rests on an absence, and which menin inhibition appears to induce | Gene | 16 | 4/5 |
| Clec12a is REQUIRED for NUP98::NSD1 AML pathogenesis - a marker turning out to be a dependency, in a different fusion family, and untested in KMT2A-r | Mechanism | 3 | 3/5 |
| CNS disease at diagnosis in infants: a real excess, measured by a procedure that partly creates it | Explainer | 5 | 4/5 |
| Co-dependency scan: what else does a menin-dependent cell need? (run, not planned) | Analysis | 2 | 3/5 |
| COG AALL0631 — lestaurtinib in infant KMT2A-rearranged ALL: negative overall, positive where the drug actually hit | Trial | 3 | 4/5 |
| COG AALL15P1 — azacitidine epigenetic priming in infant KMT2A-rearranged ALL: on-target, well tolerated, no survival effect | Trial | 3 | 4/5 |
| COG AAML0531/1031 (n=2,080): MLLT10 fusions are adverse, and the 5-prime partner barely changes it | Epidemiology | 2 | 4/5 |
| COG AINV18P1 (NCT03792256) — palbociclib is deliverable in children with relapsed ALL, at 50 mg/m² for 21 days | Trial | 2 | 4/5 |
| Cohesin as an architectural co-lesion class — mutated in AML, associated with NPM1 rather than KMT2A, and leukemogenic on partial loss | Pathway | 2 | 3/5 |
| Collaborate or compete: an honest matrix, including where the lab would be duplicating a better-resourced effort | Group | 6 | 3/5 |
| Combine an IKK inhibitor with a clinical menin inhibitor in a KMT2A::AFF1 B-ALL line, and read out fusion OCCUPANCY rather than viability | Experiment | 3 | 3/5 |
| Common lymphoid progenitor (CLP) — the CD10-positive lymphoid route that infant KMT2A leukaemia appears NOT to take | Cell type | 3 | 3/5 |
| Common myeloid progenitor (CMP) — the fork at which KMT2A leukaemia almost always turns one way | Cell type | 4 | 3/5 |
| Comparing every citation's stored author list against the paper its DOI resolves to - 15,219 comparable blocks, 99.6% agreeing, and all 60 disagreements are placeholder strings, one Crossref metadata error and one Scandinavian letter - which closes the year check's known blind spot and finds no wrong-paper citation on either axis | Analysis | 1 | 4/5 |
| Comparing every citation's stored year and journal against the record its DOI actually points at - 16,420 comparable blocks, 92.0% exact, and all 22 that disagree by two years or more resolve on reading to six DOIs with online-versus-print date conventions, so the wrong-paper failure mode is bounded from above for the first time | Analysis | 1 | 4/5 |
| Competing model 1: the reciprocal product starts the leukaemia and then leaves | Mechanism | 5 | 3/5 |
| Competing model 2: the reciprocal allele is lost as the leukaemia evolves, and losing it selects for something worse | Mechanism | 5 | 2/5 |
| Competing model 3: reciprocal status is a proxy for where the break fell, and the thing that changed is the DIRECT product | Hypothesis | 5 | 1/5 |
| Competing model 4: t(4;11) cells are addicted to the direct fusion and completely indifferent to the reciprocal one | Explainer | 4 | 4/5 |
| Competitive release and adaptive therapy — what ecology says happens when you remove the dominant species | Analogy | 6 | 1/5 |
| Complex I inhibition triggers the mitochondrial integrated stress response through DELE1 and HRI, and that is what creates the MCL-1 dependency - a metabolic drug manufacturing an apoptotic vulnerability | Mechanism | 3 | 3/5 |
| Compute: which backend for which piece of phase-2 work, and the one constraint that matters for each | Explainer | 3 | 4/5 |
| Condensates in KMT2A-fusion leukemia — an honest verdict: not established for AFF1/AFF4/AF9, load-bearing only in ENL-mutant and NUP98 fusions | Mechanism | 9 | 3/5 |
| Confidence in this graph carries no information about whether anyone read the paper | Analysis | 4 | 0/5 |
| Conventional (myeloid-related) dendritic cell - the DC lineage RELB actually builds, and the thymic part of that phenotype is architecture rather than a cell-intrinsic requirement | Cell type | 4 | 4/5 |
| Cord blood does transform — when the translocation is engineered rather than expressed | Explainer | 2 | 0/5 |
| CORRECTED SAME CYCLE: the replication test was UNINFORMATIVE, not negative. Eleven of the twelve proximity panels do not sample the nucleus - they are centrosome, RTK, kinase, ion-channel, CFTR and mitochondrial baits - so KMT2A's 0th percentile in three of them measures panel composition, not promiscuity. In the one transcription-factor panel KMT2A is at the 71.7th and menin is absent, which is DIRECTIONALLY CONSISTENT with the K562 result at n=1 | Analysis | 1 | 5/5 |
| CORRECTED: the AF4-specific interactome gap is ZERO, not one - RPA2 was declined on purpose in cycle 159 and my no-match read was the tool warning I ignored | Analysis | 3 | 3/5 |
| CORRECTED: two of eleven CXXC readers HAVE been measured alongside a KMT2A fusion, and the result supports the menin-interface hypothesis | Analysis | 9 | 3/5 |
| Correcting the fusion with genome editing: verdict NOT FEASIBLE for infant leukaemia, though intron-targeted disruption is a real published strategy | Target | 3 | 4/5 |
| Corrections owed to other beats: nine entries whose stated provenance is now resolvable, and one unflagged import | Analysis | 3 | 4/5 |
| CORRECTS A DISPATCH PREMISE: GSE149183's menin-versus-DOT1L-inhibitor head-to-head exists in MOLM13 (KMT2A::MLLT3) ONLY. RS4;11 - the index fusion - is in the series but carries H3K79me2 alone, with no VTP-50469 arm, no MEN1 ChIP and no DOT1L ChIP, and the two arms are on different genome builds | Analysis | 2 | 5/5 |
| Counted absence: AFF1/AF4 - the partner in the commonest infant fusion - has no phase-separation literature under any alias, and the two hits that look like it are token collisions | Analysis | 4 | 3/5 |
| Counted absence: no menin-inhibitor trial has ever reported a response RATE in NUP98-rearranged patients | Trial | 6 | 4/5 |
| Counted absences keyed on a complex subunit miss the papers that name only the complex - demonstrated on our own SSRP1 entry, which declared no KMT2A paper about FACT while this graph cites one about the index fusion in four other entries | Analysis | 3 | 0/5 |
| Counter-argument reuse across 8,080 notes is 1.04x and only 1.6% are class-level objections that ignore their own claim: the ledger's standing quality worry was measured on 53 notes and does not generalise | Analysis | 2 | 3/5 |
| Counting laboratories instead of papers demoted nothing, because BioPlex 2.0 and 3.0 have different last authors - and the 3' partners' own neighbourhoods are the emptiest part of the graph | Analysis | 4 | 0/5 |
| Covalent or reversible is the axis on which ‘the menin inhibitor class’ most plausibly breaks | Explainer | 3 | 0/5 |
| CPT1A - the outer-mitochondrial-membrane fatty-acid gatekeeper that is also a lysine succinyltransferase, fused to KMT2A exon 3 in the one case that is tether WITHOUT address | Gene | 13 | 3/5 |
| CREBBP (CBP) — binds the KMT2A transactivation domain, which no fusion keeps | Protein | 6 | 4/5 |
| CRISPR-engineered t(4;11) in human fetal liver — the only model that reproduces infant-specific biology | Explainer | 2 | 4/5 |
| CSNK2A1 (casein kinase 2 alpha) - the one kinase that turns up three separate times in KMT2A biology | Gene | 10 | 3/5 |
| CSNK2A2 - CK2's other catalytic subunit, expressed in every KMT2A-rearranged line and, if anything, slightly favourable to lose | Protein | 10 | 3/5 |
| CSNK2B / CK2beta (P67870) - the regulatory subunit of casein kinase 2, in the pan-MLL-fusion core, with no CSNK2B-and-KMT2A literature at all | Gene | 3 | 2/5 |
| CSPG4 / NG2 - the flow-cytometry surrogate for a broken KMT2A, and a direct target gene of the fusion that makes it | Gene | 13 | 4/5 |
| CSPG4/NG2 is 0.0 nTPM in normal bone marrow, so the ratio metric is undefined for it - and that zero is the favourable half of its profile, which a ratio-ranked table hides entirely | Analysis | 1 | 3/5 |
| CTCF - named in the id of an existing entry in this graph and having no entry of its own, and the protein whose binding sites break preferentially in KMT2A-rearranged patients | Gene | 10 | 3/5 |
| CTCF keeps CALM-AF10 leukaemia undifferentiated through TGM2 - an architectural dependency, not a menin one | Mechanism | 2 | 3/5 |
| CTCF loss on KDM3B depletion is a graded property of anchor strength, not a set of targeted events: decile medians fall monotonically 0.78 to 0.62 across 12,443 RPE anchors, and if that gradient is biological then every strong anchor in the genome is a candidate instability site | Hypothesis | 2 | 1/5 |
| CTCF/cohesin boundaries and the HOXA topological domain — the 3D scaffold the fusion program runs on | Mechanism | 5 | 3/5 |
| CTCF/cohesin occupancy at the KMT2A exon-11 anchor is both the cause of the break and the chaperone of its correct repair - so losing it gives FEWER breaks and MORE rearrangements | Hypothesis | 6 | 1/5 |
| ctDNA MRD under a menin inhibitor: blood flow diverges from blood DNA, because the disease is in the spleen and marrow | Explainer | 4 | 2/5 |
| CTH (P32929) - gene_exact returns TWO reviewed records and the second is VSIG2, a third instance of rule 62 on the same symbol the Ensembl resolver already got wrong | Gene | 4 | 2/5 |
| CTNNB1 (beta-catenin) — the Wnt link inside DotCom, and the one piece of KMT2A biology that is not chromatin | Protein | 5 | 3/5 |
| CTR9 — a PAF1C subunit the field assumes is a fusion partner, with no paper that tested it | Protein | 14 | 3/5 |
| CURATED from committed-but-unread results: murine MLL-AF9 (MLLT3) retains H3K79me2 like human MOLM13 (MLLT3) and unlike RS4;11 (AFF1) - four confirmations fire, two refutations do not, the cross-partner delta is 3.2-3.6x the between-culture spread, and the flatness survives an amplitude stratification in 8 of 8 measurements | Analysis | 1 | 3/5 |
| CURATED: Q120 called the MLL1-N channel 'inert to three decimals'. At MLL1's OWN top sites in mouse it falls to 0.3012 under a DOT1L inhibitor and 0.3298 under a menin inhibitor - so 'inert' was population-specific, and a drug that does not touch menin moves the MLL1 channel as much as one that does | Analysis | 1 | 3/5 |
| CXCL12 (SDF-1) - the marrow retention chemokine this graph already had a mechanism entry for and no entry for the protein | Gene | 7 | 4/5 |
| CXCL12-CXCR4 retention — the axis everyone calls the niche dependency, and the CRISPR screen that says the ligand is not required | Mechanism | 4 | 4/5 |
| CXCR4 - named in eighteen entries of this graph with no entry of its own, and the one niche molecule with a drug, a paediatric trial and a direct KMT2A-r experiment | Gene | 11 | 4/5 |
| CXCR4 function in KMT2A-rearranged blasts is an output of the fusion's own HOXA/MEIS1 program, so a menin inhibitor should switch off the niche axis without a CXCR4 antagonist | Hypothesis | 5 | 1/5 |
| CXXC to unmethylated CpG DNA: nine mapped contact residues, and an affinity that spans 44 uM to 33 nM depending on the construct, the DNA and the salt | Interface | 5 | 5/5 |
| CXXC-DNA interface of the KMT2A fusion: a validated but hard target | Target | 5 | 3/5 |
| CXXC1 (CFP1) - a CpG-reading COMPASS subunit that binds MLL1 and recruits it to HoxA7, and whose CXXC domain cannot substitute for KMT2A's in a fusion | Protein | 7 | 3/5 |
| CXXC4 (IDAX) - TET2's CXXC domain, sitting on a separate gene after an evolutionary inversion, and annotated cytoplasmic only by similarity | Protein | 8 | 3/5 |
| CXXC5 (RINF) - the one CXXC reader measurably down-regulated in KMT2A-rearranged AML, which is the only direction-of-change any family member has in this disease | Protein | 8 | 3/5 |
| Cycle 102 declared before it ran that an input pair 'bounds library and coverage variation but NOT ChIP efficiency' and is therefore a LOWER BOUND - the size of that underestimate is now measured in human KMT2A::AFF1 MV4;11 and it is sixteen-fold at the peaks: 0.6% for an input pair against 9.4% for a menin ChIP pair over the same bins, in the same cells, on the same day | Analysis | 3 | 4/5 |
| Cycle 104's M1 - 'no scoreable mark moves at D1, so the menin inhibitor's chromatin effect is proportionally a peak phenomenon' - DOES NOT SURVIVE. The same-condition floor at D1 is 2.4%, not the 10% borrowed from the top stratum, and all three scoreable marks exceed it (H3K4me3 9.8%, H3K79me2 7.8%, H3K27me3 4.8%). Two of the three exceed even GSE260742's OWN stratum-matched input floor, which was on disk the whole time. Cycle 104's alternative M2 fires instead | Analysis | 4 | 4/5 |
| Cycle 104's open question - 'why do two marks break the floor at D10 and not at D1?' - has a false premise. Against the measured same-condition floor of 2.3% at D10, THREE marks break it there (H3K79me2 16.2%, H3K4me3 12.6%, H3K27me3 6.3%), and the same three break it at D1 too. There is no D1-versus-D10 contrast to explain; there is a continuous bulk gradient that a single borrowed 10% figure had chopped in two | Analysis | 2 | 4/5 |
| Cycle 107's headline same-condition floor of 3.03% at D1 is a median over a MIXED population of two genotypes. Restricted to the non-targeting control genotype it is 10.49%, so the borrowed 10% floor cycle 107 declared 'too generous by 3.3x' was in fact about right there - cycle 107's own F2, not its F1. | Analysis | 1 | 3/5 |
| Cycle 110's 'D10 GAINED 66%' rescored on the absolute scale: D10 lost 76.5% of its H3K79me2, no stratum gained anything, and on the genuine RS4;11 rows the gradient spans 41-fold against the contaminated table's 30-fold | Analysis | 2 | 4/5 |
| Cycle 76 warned that count thresholds in falsifiers may not transfer across set sizes. Sweeping all 2,301 entries found 5 scored criteria with a count threshold and exactly ONE that is both fragile and live - hyp-q117's uncashed PEAK ARM, now amended before it runs | Analysis | 1 | 5/5 |
| Cycle 77 published epigenetics as this graph's weakest PI dimension at 35.9% by dedicated field. Reading the entries that have no field shows 10 of 10 carry genuine, specific, cited epigenetic annotation in prose - so the dimension is 56.2% (at least 50.4% on a Wilson bound) and about 20 points of the 'gap' was a formatting artefact | Analysis | 1 | 4/5 |
| Cycle 81 named lineage as the single biggest hole in the ARID1B paralogue-buffering result. Permuting ARID1A status only WITHIN lineage strata moves the estimate from -0.2985 to -0.2961 - a change of 0.0024 - with p = 0.00140, the instrument check surviving, both specificity controls flat and zero mutant lines dropped. Lineage explains none of it | Analysis | 1 | 3/5 |
| Cycle 81's pre-registered PRIMARY stratum was underpowered at n=4 for five cycles. A different source gives n=124: ARID1B buffering is -0.2475 (p=5e-05) in truncating-ARID1A lines and +0.0117 (p=0.66) in missense-only ones - a complete dose-response. My own specificity control failed, and it failed because I chose it from inside the complex I was studying | Analysis | 1 | 4/5 |
| Cyclophosphamide - where the KMT2A literature reports two different activated oxazaphosphorines and only one of them is this drug's metabolite | Drug | 4 | 3/5 |
| Cytarabine - the one conventional drug KMT2A-rearranged infant ALL is MORE sensitive to, and the only case in this beat where a mechanism changed a protocol | Drug | 9 | 4/5 |
| Cytoplasmic localisation in KMT2A fusions: the SEPTIN case has an image, the GPHN case has none, and neither partner wins the compartment | Mechanism | 6 | 3/5 |
| Dataset: cBioPortal - open, easy, and containing exactly two KMT2A::AFF1 fusion records | Analysis | 1 | 4/5 |
| Dataset: ChEMBL chemical matter - open, quantitative, and easy to misread as a druggability score | Analysis | 1 | 4/5 |
| Dataset: DepMap CRISPR essentiality - the bulk download is now behind a captcha, and this changes how phase 2 must be built | Analysis | 3 | 4/5 |
| Dataset: gnomAD constraint - an open, instant tolerability prior that cannot discriminate between our candidates | Analysis | 1 | 4/5 |
| Dataset: GTEx normal-tissue expression - fully open, and the version-string trap that silently returns nothing | Analysis | 2 | 4/5 |
| Dataset: Human Protein Atlas - the protein-level and single-cell check that GTEx cannot give | Analysis | 1 | 4/5 |
| Dataset: PDB and AlphaFold - the structural census, including the two absences that shape every plan | Analysis | 2 | 4/5 |
| Dataset: St. Jude Cloud - the right cohort for this disease, behind a Data Access Agreement we have not applied for | Analysis | 2 | 4/5 |
| Dataset: TARGET via the GDC - open expression and mutations, but the fusion calls themselves are controlled | Analysis | 1 | 4/5 |
| Daunorubicin - the anthracycline an infant gets before her first birthday, with a measured null in vitro and sixty years of heart downstream | Drug | 7 | 4/5 |
| DAXX - the strongest of five selective dependencies among 254 unwritten interactors but it FAILS Bonferroni correction (p=0.0128, rank 4 of 254), and not one paper connects it to this disease | Gene | 10 | 3/5 |
| DAXX and ATRX are absent from the only MLL-fusion AP-MS interactome - and PML is in it against all seven baits, alone, without a single one of its other body components | Analysis | 3 | 4/5 |
| DAXX and ATRX as drug targets: six ChEMBL rows and zero of them an affinity, against menin's 1,776 - but three crystal structures of the interface that would have to be blocked | Target | 4 | 3/5 |
| Day 3 of a DOT1L inhibitor has already removed 85-90% of H3K79me2 absolutely, and the collapse becomes progressively LESS uniform: the p10-p90 spread of per-gene retention widens from 2.4-fold at d3 to 8-44-fold at d9 in all four arms | Analysis | 2 | 4/5 |
| DDIT3 / CHOP (P35638) - the cascade's middle node, and the symbol whose two reviewed human records and 16,893-record alias are the worst identifier trap in this beat | Gene | 7 | 4/5 |
| DDX10 domain architecture (UniProt Q13206) | Protein | 1 | 5/5 |
| DDX55 - a large-subunit rRNA helicase that is nucleolar by imaging and nucleoplasmic by its own founding paper, and the narrowest RBP bait to reach KMT2A after DDX52 | Gene | 6 | 2/5 |
| DDX6 - the only protein ever proposed to do for a cell what Tat does for the virus, on the strength of one 2016 paper | Protein | 8 | 2/5 |
| Decitabine - degrades DNMT1, and in ALL cells it degrades KMT2A too: the hypomethylating agent with two mechanisms and a menin-inhibitor combination already in the clinic | Drug | 8 | 3/5 |
| Decitabine degrades DNMT1 - and in ALL cells the same treatment lowers KMT2A protein, with the shared CXXC-family DNA-binding module offered as the reason | Mechanism | 4 | 3/5 |
| Decitabine's target is a pan-essential gene, and KMT2A-rearranged lines depend on it LESS than other leukaemia lines - rank 16,949 of 17,728 | Risk | 4 | 3/5 |
| Decompose the CBX1 DepMap screen to single guides before anyone quotes -0.349 as biology: a no-wet-work, one-afternoon check that would either kill the HP1 paralogue asymmetry or make it the only HP1 question in this graph with a phenotype | Experiment | 2 | 3/5 |
| Defect report: analyses/does-this-deposit-agree-with-itself/run.py keys each GEO record on !Sample_geo_accession, which in a SOFT record comes AFTER !Sample_title - one line, and it inverted the finding | Risk | 2 | 5/5 |
| Degrade DOT1L, inhibit DOT1L, or leave a dead enzyme in place - run all three against the same cells and the same marrow | Experiment | 5 | 3/5 |
| Degrade one CXXC reader, ChIP the fusion: the one experiment that settles whether the address is contested | Experiment | 5 | 3/5 |
| DEK - a chromatin architectural protein that gatekeeps H3.3 and boosts HP1alpha, is a fusion partner in its own right, and is the substrate behind this graph's third CK2 route | Protein | 6 | 3/5 |
| DEK::NUP214 is the sixth lesion on the XPO1 address - and the only one where the drug response was measured in primary patient cells | Mechanism | 3 | 4/5 |
| DepMap across the whole CTCF-BRCA1 licensing cascade in one call: CTCF is a near-total pan-essential at -1.83, BARD1 is deeper than BRCA1, the HP1 paralogue that matters is flat while the one that does not is four times deeper - and DNA2's row has 80 screens where everything else has 1,258 | Analysis | 2 | 4/5 |
| DepMap agrees with the mouse genetics: ARID1B is not a FUSION-SELECTIVE dependency (+0.0145, p=0.80) and reads -0.08 in both groups - but CYCLE 81 SHOWED THAT FLATNESS IS PARALOGUE BUFFERING, not dispensability. ARID1A and ARID2 ARE dependencies and are equally so in both groups - so no BAF subunit tested is fusion-selective. And MEN1 (-1.26) is a harder and more selective dependency than KMT2A itself (-0.81) | Analysis | 1 | 4/5 |
| DepMap cannot answer whether MEN1 is selectively required in NUP98-rearranged lines, because it contains none — and it takes only ~3 to answer it | Analysis | 3 | 4/5 |
| DepMap co-dependency cannot rank the 97 unwritten interactome partners either, pan-cancer OR restricted to leukaemia lines: mean r 0.008 rising to 0.023 under restriction while the leukaemia-matched null rises with it, giving 1.08x the chance-expected count. Recomputing the null on the restricted lines is the only thing that stopped this being reported as a discovery, and my first pass criterion called a below-chance result a PASS | Analysis | 1 | 5/5 |
| Depth matching changes this pair's call counts by under one percent, so library depth is not what separated the two beats - a candidate explanation cleared | Analysis | 2 | 4/5 |
| Dexamethasone - the steroid an infant is actually on for most of the protocol, and the one with a high-certainty neurodevelopmental signal in babies | Drug | 7 | 4/5 |
| DHX16 / hPRP2 (O60231) - the spliceosomal catalytic-activation helicase, pan-MLL-fusion, and one of only two in the 42 whose index-fusion p-value exceeds 0.05 | Gene | 3 | 2/5 |
| DHX9 / RNA helicase A (Q08211) - the other TDRD3 effector, and it is itself the 3' partner of a leukaemia fusion | Gene | 4 | 3/5 |
| Diagnosis versus relapse in the same child: relapse comes from a subclone that was already there and already quiescent, shown twice, seven years apart, by two unrelated methods | Cell state | 3 | 4/5 |
| Differentiation syndrome is the one human pharmacodynamic readout KMT2A-rearranged leukaemia already shares with APL - and in APL it is a complication of a cure, while here it is a complication of a 30% response rate | Analogy | 2 | 4/5 |
| Diffing the core scaffold's curated interactome against the graph: 46 of 217 partners are things here, CDK9 is not one of them, and the filter I built to rank the rest was counting one platform twice | Analysis | 6 | 0/5 |
| Directed extraction of P-TEFb from the reservoir: HIV-1 Tat is the worked example, and the only cellular candidate rests on one unreplicated paper | Mechanism | 5 | 4/5 |
| DNA damage raises menin levels through ATM/ATR phosphorylation, and the residue has never been mapped | Mechanism | 2 | 2/5 |
| DNA-PKcs phosphorylates AF9 at S395 and releases it from the super elongation complex - the only AF9 regulatory element the fusion keeps | Mechanism | 3 | 3/5 |
| DNA2 (P51530, 1,060 aa) - EXO1's redundant partner in long-range resection, dual mitochondrial and nuclear, and the gene whose DepMap row is measured in 80 screens where every other cascade member has 1,258 | Gene | 5 | 3/5 |
| DNMT1 - the antagonist: its CXXC domain reads unmethylated CpG in order to STOP methylation, and it is the only heterologous CXXC that runs an MLL-AF9 leukaemia | Protein | 6 | 4/5 |
| DNMT3A - an independent adverse factor in adult KMT2A-rearranged AML and conspicuously absent from paediatric disease, which is the whole finding | Gene | 8 | 3/5 |
| DNTT (TdT) - a real gene the graph calls by its enzyme nickname, and TdT-negativity is 100% KMT2A-rearranged in the largest paediatric series | Gene | 7 | 4/5 |
| Do different breaks give different biology? A verdict on partner identity vs breakpoint position | Mechanism | 5 | 3/5 |
| Do NUP98's seven fusions resemble each other more than they resemble their partners' other fusions? The test cannot be run for six of them, and the seventh resembles neither side | Analysis | 3 | 3/5 |
| Do the other WRAD subunits behave like DPY30? (run, not planned) | Analysis | 2 | 3/5 |
| DOCK10 (Zizimin-3) - the Cdc42/Rac1 exchange factor fused to KMT2A exon 8 in an undifferentiated pleomorphic sarcoma, and the only one of the seven this graph already held as an H3K79me2-marked gene | Gene | 9 | 3/5 |
| Docking onto pre-bound XPO1 is a general route to leukaemic chromatin, used by at least seven different lesions - not three coincidences | Mechanism | 7 | 4/5 |
| Does a menin inhibitor break homologous recombination? Test the menin - SETD2 - LEDGF - CtIP chain in a blast, before the next genotoxic combination is designed | Experiment | 2 | 1/5 |
| Does a menin inhibitor create a BMI1 dependency? A two-arm knockout-under-drug experiment in KMT2A::AFF1 cells, with the CDKN2A readout that decides the mechanism | Experiment | 3 | 1/5 |
| Does KMT2A::AFF1 bind the histone chaperone SET/TAF-I beta, and does that contact overlap the menin-binding motifs? A co-IP and a peptide competition | Experiment | 3 | 1/5 |
| Does KMT2A::AFF1 change histone turnover at its target genes, or does it read a chromatin state it did not make? | Hypothesis | 3 | 1/5 |
| Does KMT2A::AFF1 deliver DOT1L to the AHD or displace it? A competition experiment in t(4;11) cells | Experiment | 4 | 3/5 |
| Does menin hold FANCD2 in a KMT2A-rearranged cell, and does revumenib let go? Nobody has asked — zero records over every menin-inhibitor name | Experiment | 4 | 3/5 |
| Does menin inhibition have any MHC class II headroom to work with in B-precursor infant ALL? A flow cytometry experiment on samples that already exist | Experiment | 2 | 1/5 |
| Does revumenib displace JunD, and at what concentration relative to KMT2A? (The yes/no half is already answered) | Experiment | 3 | 4/5 |
| Does the diagnostic marker survive the drug? Surface NG2, CD133, CD10 and CD33 under menin and DOT1L inhibition, with the rearrangement held fixed | Experiment | 4 | 1/5 |
| Does the fusion 'lose restraint'? The pattern of KMT2A-side loss, and why the tidy reading does not survive contact with the ledger | Mechanism | 7 | 3/5 |
| Does the fusion carry an H2B ubiquitin ligase? A co-IP and an H2BK34ub CUT&RUN in KMT2A::AFF1 cells | Experiment | 2 | 3/5 |
| Does the fusion need the PWWP arm? An artificial CXXC + H3K36me2-reader + AF4-interaction protein substitutes for a whole MLL fusion - but LEDGF itself is not required for the fusion to reach chromatin | Mechanism | 5 | 3/5 |
| Does the fusion's programme fall apart in the same order in KMT2A::AFF1 as in MLL::AF9? The chain's only ordering measurement, repeated on the index fusion | Experiment | 5 | 3/5 |
| Does the menin co-dependency survive lineage adjustment? (run) | Analysis | 2 | 3/5 |
| Does the sarcoma fusion bind menin? One co-immunoprecipitation with the right control settles six years of the question | Experiment | 2 | 3/5 |
| Does WDR5 move between complexes? An acute KANSL1 degron with WDR5 co-IP, WDR5 CUT&RUN and H4K5/K8/K16ac readout in a KMT2A-rearranged line | Experiment | 2 | 1/5 |
| DOT1L — the target where excellent chemistry met an indirect interaction | Protein | 7 | 4/5 |
| DOT1L and H3K79 in KMT2A::MLLT1: a direct partner contact, mutually exclusive with the elongation complex, and the only fusion with a DOT1L-inhibitor complete remission | Mechanism | 4 | 3/5 |
| DOT1L and H3K79 in KMT2A::MLLT3: recruitment is a graded dial that sets methylation and transformation - and the fusion it was discovered in produced no remission in the DOT1L trial | Mechanism | 3 | 4/5 |
| DOT1L carries 52 in-gene genome-wide-significant SNPs at the 97.8th length-matched percentile, led by height, pulse pressure and blood-pressure traits - a speculative cardiovascular lead for DOT1L-directed drugs | Analysis | 1 | 1/5 |
| DOT1L does things that have nothing to do with methylation - which is why blocking its active site was never going to remove all of it | Mechanism | 6 | 4/5 |
| DOT1L is widely framed as a transcription-elongation factor, but the one direct test found in erythroleukaemic cells reported a role in initiation - in a non-KMT2A-rearranged line, so it is a counter-lead for the elongation model, not a refutation | Explainer | 1 | 2/5 |
| DOT1L leaves chromatin before menin does when the fusion is degraded, and the ordering survives a change of instrument that destroys the magnitudes - ChIP-qPCR at selected loci, target-restricted read counts and genome-wide peak presence all rank DOT1L ahead of menin while disagreeing about every number | Mechanism | 4 | 3/5 |
| DOT1L methylates H3K79 non-processively - so the three states are one distribution, not three signals | Mechanism | 4 | 4/5 |
| DOT1L sits in a B-lineage proximity map, and we nearly did not look | Analysis | 2 | 0/5 |
| DOT1L was not refuted - the wrong thing was blocked, at a dose nobody finished escalating | Hypothesis | 5 | 1/5 |
| DOT1L's localization record is a mouse kidney paper wearing a human label - and the one image of it in a leukaemia cell is a supporting figure a title search cannot see | Mechanism | 7 | 3/5 |
| DOT1L808 - a 5 nM DOT1L degrader that cleared an orthotopic leukaemia and still works after menin inhibitors fail | Drug | 3 | 3/5 |
| Download and bin GSE127507's nine RS4;11 tracks (1.99 GB), rebuild a human binner, and score the eviction gradient in the index fusion KMT2A::AFF1 - the one measurement that would move this finding from KMT2A::MLLT3 to the disease this graph is about | Experiment | 2 | 4/5 |
| Doxorubicin - named in twenty entries of this graph, cuts the KMT2A breakpoint where etoposide does, and appears nowhere in Interfant-06 | Drug | 5 | 4/5 |
| DPF2 (BAF45D) - a cBAF-specific reader required in MLL-AF9 cells, with one PubMed record in this disease and no selectivity signal | Protein | 7 | 3/5 |
| DPY30 — the smallest COMPASS subunit, and the only one that behaves like a selective dependency | Protein | 14 | 3/5 |
| DPY30 aims the H3K4 machinery while ASH2L powers it, which is why only DPY30 tracks menin | Hypothesis | 4 | 1/5 |
| DPY30 D/D domain and the ASH2L SDI helix: four hydrophobic pockets, one load-bearing leucine - and a 94-residue numbering offset that relocates the whole motif | Interface | 3 | 4/5 |
| DPY30 has a second job at the trans-Golgi network, and the authors who found it could not put ASH2L or RBBP5 there | Mechanism | 3 | 3/5 |
| DPY30: the founding negative does not cover it, and it has no KMT2A contact to lose | Explainer | 8 | 4/5 |
| Drug exposure and clonal replacement are completely confounded across this pair - the relapse sample is a different clone in a different lineage, and the paper's own reading is that the drug killed the cells the diagnostic sample was made of | Analysis | 3 | 4/5 |
| Duration and reinvestment risk — a 4.6-month response is a short-duration instrument, and short duration changes everything about how you value it | Analogy | 5 | 1/5 |
| DUX4 (double homeobox 4) domain architecture | Protein | 1 | 4/5 |
| DUX4::IGH (IGH-DUX4), t(4;14)/ins(14;4) — D4Z4 repeat insertion into the IGH locus | Fusion | 8 | 4/5 |
| Dying in induction: the place where infant protocols actually differ | Explainer | 5 | 4/5 |
| Dynamic BH3 profiling before and after menin inhibition — a one-week assay on primary cells that would choose the BH3-mimetic partner, and has never been run in lymphoid disease | Experiment | 3 | 1/5 |
| Each partner prefers a different KMT2A exon: partner-specific break position in 3,401 patients | Breakpoint | 8 | 3/5 |
| EAF1 — the interactor with an actual subnuclear phenotype: an MLL fusion evicts it from Cajal bodies, and the bodies themselves fall apart | Protein | 7 | 3/5 |
| EAF2 (U19) — the EAF paralogue whose ELL-binding domain is a mapped tumour-suppressor module, described entirely in prostate cancer | Protein | 5 | 3/5 |
| Early T-cell precursor (ETP) — the thymocyte that has not yet given up being myeloid, and where KMT2A-rearranged T-ALL sits | Cell type | 4 | 4/5 |
| EBF3 — a single large-scale MS hit against menin, in a B-lineage transcription factor family, which is the only reason it is worth recording | Protein | 4 | 2/5 |
| EBNA1BP2 (EBP2) - the DOT1L spoke with the HIGHEST stoichiometry and the WEAKEST evidence, and the case that shows why abundance is the third dimension | Gene | 6 | 2/5 |
| Ebselen: the only small molecule reported to bind LEDGF itself - and it does it by making selenium-sulphur bonds with whatever thiols it meets | Drug | 3 | 2/5 |
| EED - the PRC2 subunit this disease actually needs, with drugs in the clinic and zero leukaemia studies | Gene | 11 | 4/5 |
| EHMT2 / G9a - the H3K9me1/2 writer that sets whether the KMT2A LOCUS ITSELF rearranges, and whose loss delays MLL-AF9 AML in a supplementary figure nobody can find | Protein | 6 | 3/5 |
| EIF2AK3 / PERK (Q9NZJ5) - the kinase whose transcript is flat under both inhibitors, whose arm IS functionally required in MLL-AF9 leukaemia stem cells, and whose common name collides with phospho-ERK | Gene | 4 | 4/5 |
| EIF2AK4 / GCN2 (Q9P2K8) - the amino-acid-sensing eIF2alpha kinase: transcript flat, and NOTHING has ever been published about it in any KMT2A-rearranged system under either name | Gene | 4 | 4/5 |
| EIF4G1 (Q04637) - a translation-initiation scaffold in the pan-MLL-fusion core, alone, with no other eIF4F subunit anywhere in the 960 | Gene | 2 | 2/5 |
| Eight claims this corpus carries from PMID 23995757, checked one at a time against the full text: five confirmed, one scope-limited, one materially different, one not in the paper at all | Analysis | 2 | 5/5 |
| Eight of 27 GSE252378 samples fail a pre-registered depth or readability gate, and two of them are the only HOXA-negative non-AFF1 candidates | Analysis | 1 | 5/5 |
| Eighteen libraries, no replicate: what the only absolute-scale chromatin dataset in this project is structurally unable to say, and why this project's own floors may not be borrowed to fill the gap | Explainer | 2 | 5/5 |
| Eleven abstract-level bounded absences re-tested with the instrument that overturned the HDAC6 one - ten survive, one is not checkable this way, none overturned | Analysis | 5 | 4/5 |
| Eleven hand-picked intervals are not a null: the CTCF loss on KDM3B depletion scales monotonically with baseline anchor strength (decile medians 0.78 to 0.62), so a strong anchor compared against gene bodies looks unique and compared against its own strength class is the 58th of 1,625 | Explainer | 2 | 4/5 |
| Eleven immortalised lines passaged for decades: the competing explanation this beat could not close | Risk | 7 | 3/5 |
| ELF1 - a direct transcriptional target of MLL fusion proteins and HOXA9 that is ALSO a BioID neighbour of KMT2A, and that is focally deleted in paediatric AML without a KMT2A rearrangement | Gene | 10 | 3/5 |
| ELF2 / NERF - an ETS factor that works with RUNX1 on a B-cell kinase promoter, and one of eleven TF baits recovering KMT2A | Gene | 3 | 2/5 |
| ELL — rank 7 on selectivity and the deepest common-essential in the top ten, with one NMR fragment to its name | Protein | 7 | 4/5 |
| ELL has never been placed in a cell state — its entire leukaemia state literature is its own fusion transcript used as a residual-disease marker | Analysis | 3 | 4/5 |
| ELL is in Cajal bodies - or nuclear speckles, depending which paper you read - and the MLL-ELL fusion empties them | Mechanism | 5 | 3/5 |
| ELL S309 is the most frequently observed phosphosite across public datasets - and it is a proline-directed site with no kinase, not an ATM site | Analysis | 3 | 3/5 |
| ELL-EAF1: a phosphorylation-gated interface reported to drive phase separation - and the assays used cannot distinguish that from clustered binding | Interface | 5 | 2/5 |
| ELL: the discarded N-terminal EAF-binding site, and a second subtraction the graph had not recorded — the fusion delocalises endogenous EAF1 | Mechanism | 3 | 3/5 |
| ELL2 — a SEC subunit that almost no cell needs, next to a paralogue almost every cell needs | Protein | 13 | 3/5 |
| ELL2 — domain architecture and residue coordinates | Protein | 7 | 4/5 |
| ELL3 — the third ELL paralogue, which marks enhancers and recruits SEC rather than sitting inside it | Protein | 2 | 3/5 |
| ELOA / TCEB3, Elongin A (Q14241) - a Pol II elongation factor in the pan-MLL-fusion core, ALONE, with none of its own complex and a non-zero negative control | Gene | 4 | 2/5 |
| ELOVL1 - the fatty-acid elongase that infant MLL-AF4 ALL retains from its fetal origin, and the lipid enzyme on the opposite side of the divide from ACSL4 | Protein | 6 | 3/5 |
| ELP1 (IKBKAP/IKAP) - the Elongator scaffold that was first named for the IKK complex, is a paediatric-cancer predisposition gene, and has an RNA Pol II contact in IntAct | Gene | 14 | 3/5 |
| ELP2 (STATIP1/StIP1) - the double beta-propeller of the Elongator core, whose informal name collides with a different human gene and whose STAT3 function is a by-similarity annotation | Gene | 14 | 3/5 |
| ELP3 - the catalytic subunit, the only Elongator protein with a real acetyltransferase domain, and the one whose loss in mouse blood causes marrow failure and then p53-mutant leukaemia | Gene | 19 | 3/5 |
| ELP4 (PAXNEB) - a required subunit of Elongator, the one partner of the seven with a genuine histone-acetyltransferase connection, and the one whose fusion supplies only its last 43 residues | Gene | 11 | 3/5 |
| ELP5 (DERP6) - the bridge that joins ELP3 to ELP4, the most essential Elongator subunit in DepMap, and a gene whose cytoplasmic call rests on an overexpression experiment | Gene | 12 | 3/5 |
| ELP6 (TMEM103/C3orf75) - an Elongator subunit named after a membrane protein it is not, whose entire localisation record comes from a Drosophila paper its own symbol cannot retrieve | Gene | 12 | 3/5 |
| Eltanexor (KPT-8602) - the second-generation SINE whose whole point is that you can give it more often | Drug | 4 | 3/5 |
| Enasidenib - an approved mutant-IDH2 inhibitor sitting next to the one methylome co-mutation that IS enriched in KMT2A-rearranged AML, and never tested there | Drug | 4 | 3/5 |
| ENCODE spells zero as HTTP 404, ReMap spells it as HTTP 401, and GEO spells it as a well-formed count of zero under a retired symbol - three archives, three spellings, and two of them are indistinguishable from a broken connection | Explainer | 3 | 5/5 |
| Endogenous aldehydes and silenced ALDH2 — the rival explanation for an FA dependency in acute leukaemia, and the only one with an experiment behind it | Mechanism | 3 | 3/5 |
| Enhancer usage in KMT2A-rearranged leukemia — occupancy and amplification, not hijacking, and not super-enhancers | Mechanism | 5 | 4/5 |
| Enhancer-promoter contacts at KMT2A-fusion target loci — what the fusion uses, what it does not, and what survives the drug | Mechanism | 4 | 3/5 |
| ENL is the highest-expressed target in cerebellum and nobody has studied it there | Explainer | 4 | 0/5 |
| ENL is the only elongation cofactor that separates fusion-occupied promoters from wild-type KMT2A promoters by more than the H3K4me3 negative control does, in primary infant KMT2A::AFF1 | Analysis | 2 | 4/5 |
| ENL redistributes rather than persists: it is the only channel that holds more of its signal at the myeloid-program peaks than at the B-lineage ones, by 2.06x in my instrument and 1.26x in the authors' own - and in absolute terms it falls further than menin does | Analysis | 3 | 3/5 |
| ENL stays after the fusion leaves — an epigenetic lesion that outlives the protein that made it | Resistance | 3 | 2/5 |
| ENL's disordered region and condensates, restricted to what actually bears on KMT2A::MLLT1 - which is one figure panel | Explainer | 6 | 2/5 |
| ENL's nuclear annotation has no citation at all, and every picture of ENL in a nucleus is of a mutant or a fusion, never the wild-type protein | Mechanism | 5 | 3/5 |
| Enumerating every H2AK119ub number in 168 analysis result files instead of hand-picking fourteen: the two conventions flip sign on 35 of 68 comparable ratios but MATERIALLY on only 2, the exhaustive list finds exactly one real single-convention quotation against two arithmetic coincidences, and the statistic cycle 105 cited as proof they agree is one of the two places they materially disagree | Analysis | 1 | 3/5 |
| Enumerating the WRAD-versus-KMT2A-fusion literature: what was searched, found, rejected and could not be read | Analysis | 5 | 4/5 |
| Enumeration for the index-fusion model beat: what was searched, found, rejected and could not be read | Analysis | 3 | 4/5 |
| Enumeration for the partner-outcome beat: what was searched, what was used, what was rejected, what could not be read | Analysis | 4 | 3/5 |
| Enumeration for the subnuclear beat: every compartment queried, every count, and the papers that looked on-topic and were not used | Analysis | 3 | 3/5 |
| Enumeration for the USP2 / MAML2 / second-BCR beat: what was searched, what was counted, what was rejected | Analysis | 2 | 4/5 |
| Enumeration of candidate cooperating lesions in KMT2A-rearranged leukaemia - what was written, what was recorded as a gap, and what was read and rejected | Analysis | 4 | 4/5 |
| Enumeration of the reciprocal KMT2A fusion literature: what was searched, found, rejected and could not be read | Analysis | 4 | 4/5 |
| Enumeration: every phosphorylation-dependent and kinase-regulated contact on KMT2A and its fusions that this beat could find | Analysis | 3 | 4/5 |
| Enzomenib (DSP-5336) — menin inhibitor with the highest reported KMT2A-r response rate and little differentiation syndrome | Drug | 5 | 2/5 |
| EP300 — the acetyltransferase whose paralogue split is the finding: p300 is the 108th most KMT2A-selective gene, CBP is the 16,950th | Protein | 5 | 3/5 |
| EP300::ZNF384 - the commonest ZNF384 fusion, and it throws away the acetyltransferase | Fusion | 6 | 4/5 |
| EP400 - the ATPase that swaps H2A.Z in; its complex is required by MLL leukaemia stem cells, and in DepMap it is one of the three genes LEAST required in KMT2A-rearranged lines | Gene | 8 | 3/5 |
| EPB41L3 / DAL-1 - a membrane-skeleton tumour suppressor that binds and modulates two arginine methyltransferases, and whose own promoter methylation is a clinical test | Protein | 6 | 3/5 |
| EPC1 - the NuA4/TIP60 subunit whose C-terminal fragment grips MBTD1, making it the contact a leukaemic fusion cannot do without and the mildest dependency in that whole complex | Gene | 7 | 4/5 |
| EPHA7 - ephrin type-A receptor 7, a published direct promoter target of the ALL1/AF4 (KMT2A::AFF1) fusion protein | Gene | 4 | 3/5 |
| EPHA7 is the one core member with a published KMT2A::AFF1 promoter ChIP - and this beat's own data put it second on separation while denying it to the AF9 samples | Analysis | 3 | 3/5 |
| Epigenetics reads 39.2% and looks like the thinnest PI dimension. Roughly half of the shortfall is a missing FIELD NAME over content that is already there, a third is proteins with no chromatin context to record, and the real content gap is about a ninth of the corpus | Analysis | 3 | 3/5 |
| EPS15 (AF1p): the EH domains may or may not be discarded, and either way nobody has shown it matters | Mechanism | 4 | 3/5 |
| EPS15 / AF1p — domain architecture, and the one coordinate nobody has published | Protein | 6 | 3/5 |
| Erasing H2Bub: three deubiquitinases share two adaptors, and removing the enzyme the field names lowers the mark instead of raising it | Mechanism | 4 | 4/5 |
| ERG - a heptad stem-cell transcription factor whose 15 mentions in this graph are mostly about OTHER diseases, and whose best-established role in B-ALL is loss of function, not cooperation | Gene | 7 | 3/5 |
| Erythroid progenitor - the committed red-cell precursor, distinct from the bipotent MEP that two entries had to borrow, and the compartment that pays for any haem-pathway or fetal-globin intervention | Cell type | 4 | 3/5 |
| ESR1 / estrogen receptor alpha - menin's best-documented non-leukaemic partner, and the only one a menin inhibitor is being given to patients to disrupt on purpose | Gene | 7 | 0/5 |
| Estradiol does not redistribute SUV39H1 - because the replicates do not agree well enough to see it: over 56,171 CTCF anchors the ACROSS-condition Spearman (0.358) is HIGHER than the within-condition replicate correlations (0.326 for -E2, 0.207 for +E2), and the same 147 bp anchor reads 51.8, 69.1, 90.8 and 96.3 in the four samples | Analysis | 2 | 3/5 |
| ETO2::GLIS2 rewires chromatin in stages and hijacks the osteogenic homeobox factor DLX3 as its first required step — a genome-edited human iPSC model that resolves leukaemia initiation into an ordered sequence | Mechanism | 2 | 4/5 |
| Etoposide (VP-16) - the drug that makes this disease and cures several others, and the only entry in this graph whose main finding is that you must not stop using it | Drug | 6 | 4/5 |
| ETV6 — domain architecture and residue coordinates | Protein | 7 | 4/5 |
| ETV6::NTRK3 (ETV6-TRKC), t(12;15)(p13;q25) | Fusion | 6 | 5/5 |
| ETV6::RUNX1 (TEL-AML1), t(12;21)(p13;q22) | Fusion | 12 | 5/5 |
| Every age-restricted target nominated by the model is pan-essential or invisible | Analysis | 2 | 0/5 |
| Every chromatin readout of a menin inhibitor measured in this corpus is graded by how much fusion the drug removed from a site, so a within-sample average over the fusion's occupancy set is the wrong statistic and will report near-null in a responding cell - the signal is the SLOPE against eviction depth, not the level | Hypothesis | 2 | 1/5 |
| Every DOT1L dependency number this project has computed, in one place, lineage-split and in raw Chronos units | Analysis | 5 | 4/5 |
| Every gene in the H2B ubiquitination axis, ranked against the whole genome for KMT2A selectivity — and the writers are not selective | Analysis | 1 | 4/5 |
| Every human t(11;19) KMT2A::MLLT1 cell line, with accessions fetched and read back - and not one of them is known to be reciprocal-negative | Analysis | 5 | 4/5 |
| Every human t(9;11) cell line, with every accession fetched and read back: eleven lines, ten patients, and two of them are B-ALL | Analysis | 6 | 4/5 |
| Every IntAct number in this project is drawn through a query that misses half the record - and what it misses is the taspase1 fragments | Analysis | 3 | 4/5 |
| Every MS-evidenced KMT2A modification site, flagged retained or lost against the breakpoint - and the retained portion is NOT enriched for acetylation once you use the right null | Analysis | 4 | 4/5 |
| Every multi-entry dangling reference in this graph has exactly one author: demand counts entries, and entries are not independent | Analysis | 2 | 4/5 |
| Every niche-disrupting drug strips the patient's own stem cells of the same shelter — the bite-back that applies to the whole beat | Risk | 4 | 4/5 |
| Every noise floor in this thread is computed from within-sample shares, which sum to one. A purely local change therefore leaks into every other stratum by arithmetic, so no floor measured this way can distinguish 'the bulk moved' from 'the peaks moved and the shares renormalised'. A tighter floor is not thereby a cleaner one. | Explainer | 1 | 5/5 |
| Every partner this project imports from the only MLL-fusion AP-MS interactome was pulled from a Strep-HA transgene in Jurkat T-ALL cells — so the host's own lineage factors are in the prey pool, and one of them is LEF1 | Analysis | 3 | 5/5 |
| Every peak file of all 13 ENCODE BRCA1, CBX3 and CBX1 experiments opened at the exon-11 element, not just the two Q37 reached: BRCA1 is there in BOTH pre-IDR replicates of THREE experiments - HeLa-S3, H1 and HepG2, global IDR 0.059, 0.577 and 0.482 - and it is a clean zero in both K562 experiments and in GM12878 against 300,000-peak pre-IDR lists | Analysis | 2 | 4/5 |
| Every per-sample normalisation is a constant multiplier: it never changes the shape, it only moves the line between 'gained' and 'lost' - which is why 'share', 'raw' and 'absolute' give the same ranking and three different answers to 'did this go up?' | Explainer | 2 | 5/5 |
| Every PI-dimension coverage line in this project is two-valued, and a third of what it counts as missing is a state the metric has no way to express - so the epigenetics figure will not improve by filling fields, and should not be made to | Hypothesis | 2 | 3/5 |
| Every published KMT2A partner in sarcoma, counted - plus the papers this beat read and did not use, so the next beat does not repeat the search without the decisions | Analysis | 6 | 4/5 |
| Every published MLL-fusion degron tags an overexpressed construct, not the endogenous allele - and that distinction decides what the washout kinetics mean | Explainer | 3 | 4/5 |
| Every upstream NF-kB component this beat enumerated, with its query, its count, and why it did or did not get an entry | Analysis | 4 | 4/5 |
| Every WRAD subunit, DOT1L, ENL, AF9 and LEDGF carries a cited histone-mark finding and none carries an epigenetics field - 12 of the 32 index-fusion core proteins are pure notation gaps, 9 are covered, and the 11 with nothing are all on the negative-regulatory side of elongation | Analysis | 1 | 4/5 |
| Evicting the fusion is not enough: PRC1.1 has to arrive, and losing it causes menin-inhibitor resistance in vivo | Resistance | 4 | 3/5 |
| Eviction is a claim about menin. The field, and this graph, transfer it to the fusion without a measurement that supports the transfer | Explainer | 3 | 4/5 |
| EWS::FLI1 builds its own enhancers at GGAA microsatellites, and a single inherited base change that lengthens one repeat raises the fusion's binding and the patient's risk. KMT2A fusions occupy pre-existing, invariant CpG islands - which is why this disease has no germline modifier of its target set, and why its mouse models work at all. | Analogy | 3 | 3/5 |
| EWSR1 — domain architecture and residue coordinates | Protein | 7 | 4/5 |
| EWSR1::FLI1 — the comparator that shows condensate formation has an optimum, and that forcing a fusion into the nucleolus switches it off | Mechanism | 3 | 4/5 |
| EWSR1::FLI1 (EWS-FLI1), t(11;22)(q24;q12) | Fusion | 6 | 5/5 |
| EWSR1::FLI1 has no residue-resolved, fusion-demonstrated PTM in its retained portion - every mapped site falls past the breakpoint, and the one site shown on the fusion has no residue | Analysis | 3 | 3/5 |
| EWSR1::ZNF384 - the same EWSR1 exon 7 fragment that drives Ewing sarcoma, fused instead to a zinc-finger protein, in B-ALL | Fusion | 5 | 3/5 |
| EWSR1::ZNF384 versus EWSR1::FLI1 - the same EWSR1 exon-7 module on two different DNA-binding proteins, and nobody has compared them | Experiment | 4 | 1/5 |
| Exactly one gene in 8,248 beats menin, and it is FLT3 | Analysis | 1 | 3/5 |
| Excluding spleen, lymph node and thymus moves 9 of 29 normal-tissue safety ratios and not one of the worst cases - the artefact is real, concentrated and confined to the middle of the table, and it takes the ACTB reference down with it | Analysis | 1 | 4/5 |
| EXO1 (Q9UQ84, 846 aa) - the long-range resection nuclease at the bottom of the CTCF cascade, and the point where this graph's two independent 2026 HR papers meet: CtIP starts the resection, EXO1/DNA2 finish it | Gene | 6 | 3/5 |
| Experiment — is a KMT2A-septin fusion menin-dependent? The one-plate version | Experiment | 4 | 3/5 |
| Experiment (proposed) — cross-family interface point-mutant panel: is the obligate interface real in each fusion? | Experiment | 7 | 3/5 |
| Experiment: a 6 / 24 / 72 hour / 7 day VTP-50469 time course in SEM reading menin occupancy and H3K4me3 together, to decide whether the 23% is a partial effect or a slow one | Experiment | 3 | 4/5 |
| Experiment: a topology-controlled binding survey of the MLL AT-hook region, plus a triple AT-hook alanine mutant in an endogenously tagged fusion | Experiment | 4 | 3/5 |
| Experiment: apply all three pressures and ask whether the survivors are the same cell | Experiment | 4 | 3/5 |
| Experiment: bait the KMT2A breakpoint cluster region and sequence everything it joins to, in a fetal-like human progenitor | Experiment | 5 | 3/5 |
| Experiment: block the beta-2 adrenergic receptor in a KMT2A-rearranged model — the leukaemogenic nerve signal runs through a receptor an old, cheap, infant-licensed drug already hits | Experiment | 2 | 1/5 |
| Experiment: blot menin in a SET-NUP214 immunoprecipitate, then run a menin inhibitor and selinexor alone and combined in LOUCY and MEGAL | Experiment | 3 | 3/5 |
| Experiment: build the missing KMT2A::AFF1 degron and titrate it — what fractional occupancy does the program actually need? | Experiment | 5 | 3/5 |
| Experiment: combinatorial dose-titration of the HOXA9/MEIS1 program to find its minimal cut set | Experiment | 4 | 3/5 |
| Experiment: CRISPR knockout of CLEC12A in KMT2A-rearranged models, with and without a cooperating RAS lesion | Experiment | 2 | 1/5 |
| Experiment: degrade TOP2A and TOP2B separately in a fetal-like human progenitor and map DNA breaks at the KMT2A locus without a poison | Experiment | 4 | 1/5 |
| Experiment: does a MEN1 resistance mutant pay a price when the drug is not there? The competition assay nobody has run | Experiment | 4 | 3/5 |
| Experiment: does AF1q self-associate, and does KMT2A::MLLT11 transform? The two measurements nobody has made on the 10th most common KMT2A fusion | Experiment | 6 | 3/5 |
| Experiment: does chemotherapy itself install menin-inhibitor resistance? The two-arm controlled test, plus the serial-sample ladder | Experiment | 3 | 3/5 |
| Experiment: does KMT2A::AFF1 form condensates at endogenous levels, and does it need them? The separation-of-function and IDR-swap test | Experiment | 4 | 3/5 |
| Experiment: does marrow stroma protect KMT2A-rearranged cells from a menin inhibitor? Nobody has run the week-long experiment that would say | Experiment | 2 | 3/5 |
| Experiment: does MLL-AF4 transform a staged fetal progenitor when it cannot transform cord blood? | Experiment | 2 | 3/5 |
| Experiment: endogenously tagged KMT2A::AFF1 imaged through a menin-inhibitor time course, with a five-compartment segmentation and a half-life arm | Experiment | 4 | 3/5 |
| Experiment: five-fraction subcellular blot of a t(4;11) line, with a menin-inhibitor arm - converting thirty years of unattributable images into attributable numbers using only existing antibodies | Experiment | 5 | 4/5 |
| Experiment: give an antioxidant with the CXCR4 antagonist — if the drug stops working, the niche is a redox buffer and not a hiding place | Experiment | 2 | 3/5 |
| Experiment: go back to the diagnostic sample and look for the myeloid clone before it existed | Experiment | 4 | 3/5 |
| Experiment: induce CyP33 in a KMT2A-rearranged cell and ask, allele by allele, whether the brake still works at HOXA9 | Experiment | 4 | 3/5 |
| Experiment: is the primed state in KMT2A::AFF1 actually bivalent? Multi-mark CUT&Tag on primary infant blasts | Experiment | 5 | 3/5 |
| Experiment: long-hold degron depletion of endogenous KMT2A::AFF1, to ask whether the leukaemic program recovers without the fusion | Experiment | 2 | 3/5 |
| Experiment: map what stays on chromatin when the menin inhibitor has done everything it can do | Experiment | 3 | 3/5 |
| Experiment: measure KMT2A-AFF1 spatial proximity in the human fetal progenitor, in the cell and at the time the translocation actually happens | Experiment | 6 | 3/5 |
| Experiment: measure the two missing time constants — how fast the KMT2A::AFF1 program collapses on drug, and how fast it comes back off drug | Experiment | 3 | 3/5 |
| Experiment: put four residues back - the minimal add-back control the PHD3 result has never had | Experiment | 6 | 3/5 |
| Experiment: put the resistant and the sensitive fusion side by side - if a MEN1 interface mutant keeps the fusion in place while the wild type moves it, relocation is real and menin is what chooses the address | Experiment | 3 | 1/5 |
| Experiment: read the endocrine limb and the marrow limb of menin-MLL in the SAME animals at the SAME exposure | Experiment | 2 | 3/5 |
| Experiment: spike-in-calibrated, fusion-attributable occupancy of KMT2A::AFF1 in the first 24 hours of menin inhibition, scored for gains as well as losses | Experiment | 4 | 1/5 |
| Experiment: spike-in-normalised H3K4me3, menin and IgG CUT&Tag in SEM under VTP-50469 and EPZ-5676 - the one missing experiment that turns every ratio in this beat into an absolute number | Experiment | 3 | 4/5 |
| Experiment: time-to-resistance, not synergy index, as the readout for menin-inhibitor combinations | Experiment | 2 | 1/5 |
| Experiment: titrate wild-type KMT2A up and down in one leukemia cell and watch what happens to the fusion's grip on chromatin | Experiment | 3 | 3/5 |
| Experiment: where do KMT2A::AFF1 blasts go when a menin inhibitor releases the block? Single-cell lineage destination under drug | Experiment | 3 | 3/5 |
| Export or docking? A locus-resolved H3K79me2 ChIP under an XPO1 inhibitor separates the two CALM-AF10 models, and it has never been run | Experiment | 3 | 1/5 |
| Express a partner-free ZNF384 C-terminal truncation in HSPCs alongside TCF3::ZNF384 - the one experiment that decides whether the fusion partner is necessary | Experiment | 4 | 1/5 |
| Expressed, required, maintains — three different claims about where a gene matters, and the graph must label which one it has | Explainer | 4 | 4/5 |
| External and historical controls: the design infant leukemia actually uses | Explainer | 3 | 4/5 |
| Eytan Stein (MSKCC), Ghayas Issa (MD Anderson) and the clinical menin-inhibitor investigator network | Group | 4 | 3/5 |
| EZH1 - the paralogue that makes the approved EZH2 drug the wrong drug for this disease | Gene | 11 | 4/5 |
| EZH2 - the Polycomb enzyme that collaborates with the fusion instead of opposing it, and that no single-agent inhibitor can switch off | Gene | 11 | 4/5 |
| EZHIP (CXorf67, CATACOMB) - a protein that jams PRC2 by pretending to be an H3K27M oncohistone, and the 3' payload of MBTD1's other fusion | Gene | 9 | 4/5 |
| FAAP100 — FA core complex; rank 36 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 11 | 3/5 |
| FACT (SPT16-SSRP1) - the chromatin arm of transcription elongation, and a clean negative result for the KMT2A::AFF1 interactome | Protein | 7 | 3/5 |
| FAERS shows no endocrine signal for either menin inhibitor - and proves it could not have | Analysis | 2 | 3/5 |
| FANCA — FA core complex; rank 20 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 9 | 3/5 |
| FANCD2 — the FA effector menin binds, and the weakest FA gene in this graph's own selectivity scan | Protein | 11 | 4/5 |
| FANCF — FA core complex; rank 11 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 9 | 3/5 |
| FANCG — FA core complex; rank 27 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 12 | 3/5 |
| FANCI — ID2 module; rank 15 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 9 | 3/5 |
| FANCL — FA core complex; rank 26 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 11 | 3/5 |
| Fault trees, minimal cut sets and common-cause failure — reliability engineering on a buffered oncogenic program | Analogy | 5 | 1/5 |
| FBXL19 - a CpG-island reader that delivers CDK-Mediator and RNF20 to developmental promoters, and whose experimental localisation is mostly cytoplasm | Protein | 5 | 3/5 |
| FDA already required this study: PMR 4730-1 names endocrine-related disorders due to chronic menin inhibition | Explainer | 2 | 5/5 |
| Fetal CD19+CD34+CD10-negative PreProB progenitor — a cell that exists before birth and almost not at all after | Cell type | 4 | 4/5 |
| Fetal liver haematopoietic stem and progenitor cell — the leading candidate cell of origin for t(4;11) infant ALL | Cell type | 7 | 4/5 |
| Fetal-restricted permissive factors across fusion families - the class has exactly ONE fully worked member, and for ETV6::RUNX1 the fetal advantage is real but no factor is named | Explainer | 5 | 3/5 |
| Fever and fatigue: two of the five headline signs cannot be elicited from a baby | Explainer | 4 | 3/5 |
| Fever and headache thirty-two months after transplant: KMT2A::AFDN AML relapsing into the CNS, and a menin inhibitor that cleared the spinal fluid | Patient story | 1 | 3/5 |
| Fever and infection: the reason most of these babies see a doctor, and the reason some of them die | Explainer | 4 | 4/5 |
| FHD-286 - the dual BRG1/BRM inhibitor that carries every SWI/SNF therapeutic claim in this disease, with a minimum enrolment age of 16 | Drug | 6 | 3/5 |
| Fiduciary conflict of interest — law does not remove a conflicted agent, it separates the mandates | Analogy | 5 | 1/5 |
| Fifth explanation for the Fanconi signal: it runs through menin binding FANCD2, not crosslink repair — tested, refuted, prior 0.07 | Hypothesis | 7 | 2/5 |
| Fifty-three 2 kb bins gain MLL1-N-reactive signal under VTP-50469 in RS4;11, and the same 53 coordinates gain 1.77-fold in MOLM13 against a class-matched null of 1.01 with the MOLM13 input flat at 1.01 - so there IS a small, reproducible, input-controlled redistribution, and it carries no CpG-island signature | Analysis | 2 | 3/5 |
| First deposit to put both drug classes on the MEN1 channel in one experiment: VTP-50469 leaves ZERO of the 19 DMSO menin peaks at 15 canonical menin-MLL target loci, while EPZ5676 keeps 14, compound 10 keeps 14 and compound 11 keeps 8 - strength-matched permutation p = 0.0003, and the zero is unchanged at every flank from 0 to 100 kb | Analysis | 5 | 4/5 |
| First systematic enumeration of the KMT2A fusion interactome, and the diff against this graph | Analysis | 3 | 4/5 |
| Five KMT2A-free NUP98 fusions bind MLL1 and the NSL complex — and one unbiased mass-spectrometry study failed to reproduce it | Mechanism | 4 | 3/5 |
| Five new arginine-axis entries in one day, and not one of their genes is a selective dependency - in an instrument that recovers MEN1 at p=5e-05 and TDRD3 is not a dependency at all | Analysis | 3 | 3/5 |
| FLI1 — domain architecture and residue coordinates | Protein | 6 | 4/5 |
| Flow-cytometric MRD: the fastest readout, and the one a lineage switch walks straight out of | Explainer | 9 | 4/5 |
| FLT3 / CD135 — the strongest non-tether co-dependency, and a target the field may have written off on a badly executed trial | Protein | 13 | 3/5 |
| FLT3 in KMT2A-r leukemia — near-universal overexpression, but activating mutation in only ~3% of infants | Gene | 9 | 4/5 |
| FLT3 in ZNF384-rearranged leukaemia - the fusion builds its own enhancer 25 kb upstream, and gilteritinib works in xenografts | Target | 4 | 4/5 |
| FLT3 is the second largest KMT2A-selective dependency and it is HEAVIER in B-lineage than in myeloid cells | Mechanism | 6 | 4/5 |
| FLT3-ITD signals from inside the cell, not from the surface - and whether it is the ER or the Golgi decides which pathway fires | Mechanism | 5 | 4/5 |
| Fludarabine - the immunosuppressive half of modern conditioning, given as a phosphate prodrug, cleared by the kidney, and dosed by a body-surface-area rule that measurably fails in children | Drug | 5 | 4/5 |
| For AFF1 in primary infant material, which antibody you use moves the answer more than which patient, which lineage, or cell line versus patient - a pre-registered falsifier that fired | Analysis | 2 | 4/5 |
| Forty-five percent of t(4;11) patients express a KMT2A fusion transcript that keeps the whole WRAD interface | Explainer | 7 | 3/5 |
| Forty-one SEM libraries in GSE159608 sort themselves by antibody from the signal alone, across two protocols, two operators and ten months - so the deposit's own labels are confirmed by an instrument that does not share the labels' failure mode | Analysis | 3 | 4/5 |
| Four beats in a row were picked by noticing the same shape by hand; this is the instrument that finds it - 171 gene symbols named in six or more entries with no entry of their own | Analysis | 3 | 0/5 |
| Four counted absences re-run against a second index, and all four hold | Analysis | 2 | 3/5 |
| Four days after the fusion is destroyed, menin signal at non-fusion promoters is 27% higher than control | Analysis | 3 | 2/5 |
| Four different ways to lose menin, and the graph has been treating them as one | Explainer | 5 | 4/5 |
| Four hours of MS67 in MV4;11, two KMT2A antibodies: the cheapest test of whether WRAD reaches the fusion or only wild-type KMT2A | Experiment | 2 | 3/5 |
| Four matched input tracks, used for the two things an input is actually for: no chromosome-scale copy-number difference between the CRISPR clone and its control (max 1.0988, min 0.9470 in both processing states), and the knockout's H2AK119ub depletion from CpG islands is REAL because its own genomic DNA is enriched there, not depleted | Analysis | 2 | 3/5 |
| Four regulatory elements on AF9, and the fusion keeps exactly one - the phospho-switch that controls SEC binding | Analysis | 3 | 3/5 |
| Four sources give ZNF384 three different zinc-finger counts - 8, 6 and 'five to eight' - and the paralogue's feature table explains where the 6 comes from | Analysis | 6 | 3/5 |
| Four ways a WDR5 result can be true and have nothing to do with KMT2A | Explainer | 8 | 4/5 |
| Four YEATS antagonists exist, four public transcriptome datasets of YEATS inhibition exist, and not one paper or dataset has ever asked what happens to the AFF2- or AFF3-scaffolded complexes — and the analysis needs no wet work | Analysis | 4 | 4/5 |
| FOXC1 - a mesenchymal forkhead factor derepressed in HOXA-high AML that blocks monocytic differentiation, with a real mechanism and zero published connection to KMT2A rearrangement | Gene | 6 | 3/5 |
| FOXM1 - a one-panel MEN1 co-IP from a 4,119-row atlas, attached to a protein that is independently a validated MLL-rearranged leukaemia stem-cell dependency | Gene | 4 | 3/5 |
| FOXP1 - the forkhead repressor that licenses the pro-B to pre-B transition and blocks apoptosis with NF-kB, sitting at a 105x MLL1-N bin in a leukaemia whose defining lesion is a pro-B arrest | Gene | 9 | 3/5 |
| Fractional occupancy needs a free concentration as well as a Kd, and nobody has measured either for a KMT2A fusion | Analysis | 3 | 3/5 |
| FTO — highly expressed in MLL-rearranged AML, and the single flattest dependency row in this beat: 0.2% of 1,208 lines | Gene | 4 | 3/5 |
| FTSJ3 (Q8IY81) - the pre-rRNA 2'-O-methyltransferase at the weakest edge of the MLL-fusion nucleolar block: two baits of seven, not the index fusion, and never screened | Gene | 5 | 2/5 |
| Fusion partner predicts the molecular subgroup almost perfectly, and survival not at all | Epidemiology | 2 | 0/5 |
| Fusion-driven surface antigens are NOT more exposed in normal tissue than expression-matched controls - ratio 0.91, permutation p = 0.79 - so the screen's empty intersection is the base rate and not a property of the fusion | Analysis | 2 | 3/5 |
| Fusion-positive clones that never become leukaemia: persistence in remission, spontaneous clearance, and silent rearrangements in healthy people | Mechanism | 3 | 3/5 |
| FUT4 - the myeloid alpha-1,3-fucosyltransferase, a hub gene of the KMT2A-rearranged expression module, and the gene HGNC once officially called CD15 | Gene | 6 | 3/5 |
| FUT9 - the dedicated Lewis-x synthase, structurally solved, and untouched by the KMT2A literature | Gene | 8 | 3/5 |
| FYRN/FYRC: the clip that holds the cut reciprocal protein together, and the only fusion-adjacent interface anyone has tried to break with a decoy | Interface | 2 | 3/5 |
| GAS7 — growth-arrest-specific F-BAR protein, the second pillar of the forced-oligomerisation model | Protein | 11 | 4/5 |
| GATA2 - the least KMT2A-selective gene on this beat, ranking 17,591 of 17,728, and a factor whose leukaemia biology is about stemness and chemoresistance rather than about the fusion | Gene | 6 | 3/5 |
| GATA2 outlier activation in KMT2A::USP2 B-ALL - the only transcriptional output ever measured for this fusion | Mechanism | 2 | 2/5 |
| GATA3 - one of only two transcription-factor baits in a 109-bait BioID screen that recover DOT1L | Gene | 3 | 2/5 |
| GATAD2A / p66-alpha (Q86YP4) - the subunit that bridges NuRD's two modules, the best-ranked NuRD gene in this project's KMT2A-selectivity scan, and present in the pan-fusion interactome under MLL-AF9 but NOT the index fusion | Gene | 6 | 3/5 |
| GATAD2B / p66-beta (Q8WXI9) - the NuRD scaffold with the broadest presence in the pan-MLL-fusion interactome, five of seven baits and still not the index fusion, and a haploinsufficiency syndrome that caps any therapeutic idea | Gene | 6 | 3/5 |
| GEO labels both aliquots of the lineage-switching patient 'treated with the Menin inhibitor', but the paper says 148752 is the B-ALL at diagnosis and only 152985 arose during treatment - the deposit's drug flag is a case label wearing an aliquot label's clothes | Analysis | 2 | 4/5 |
| GFI1 — the repressor that LSD1 inhibitors actually work through, and the scan hit whose literature points the opposite way | Protein | 9 | 3/5 |
| Giving a G9a/GLP inhibitor alongside etoposide or doxorubicin removes a DNA-repair licence at the moment TOP2 breaks are being made - and the sibling compound UNC-0638 is measured to block BRCA1/BARD1 arrival at a break, in children on curative therapy | Risk | 5 | 3/5 |
| Giving a translocation-promoting epigenetic drug in a translocation-defined B-lineage leukaemia, to infants | Risk | 5 | 3/5 |
| Giving the reopening conditions an owner, and the first run changes two decisions (run) | Analysis | 3 | 4/5 |
| GLIS2 (GLI-similar 2) domain architecture | Protein | 1 | 4/5 |
| GLUD1 is a hexameric mitochondrial matrix dehydrogenase recovered on 11 spectra with non-zero control signal from a nuclear pulldown — and this corpus has already declined one KMT2A partner whose sole source was a cryo-EM structure of GLUD1 — declined | Interface | 5 | 2/5 |
| GMP-like state — the destination of therapy-driven lineage switch and, separately, the state most sensitive to menin inhibition | Cell state | 4 | 3/5 |
| GNL2 / Ngp-1 (Q13823) - a nucleostemin-family nucleolar GTPase in the MLL-fusion nucleolar block, in the index fusion's column at p = 0.0492, and the one member with a published granular-component assignment | Gene | 4 | 2/5 |
| GOLGA2 (GM130) - a Golgi matrix protein with 249 partners in the one yeast screen that reported it binding AFF4, which had five | Protein | 4 | 1/5 |
| Gothe 2019's deposit is all-human, has base-resolution break lists, includes primary CD34+ marrow and a transcription-inhibition arm - and contains no CTCF or cohesin perturbation of any kind | Analysis | 2 | 4/5 |
| Gothe 2019's full text IS reachable - not through PMC, which has no deposit, but through an author search that surfaces the bioRxiv preprint; fourteen routes, and the two Europe PMC id links that look like a PMC record are both traps | Analysis | 2 | 5/5 |
| GPATCH4 (Q5T3I0) - a nucleolar and Cajal-body helicase cofactor in the pan-MLL-fusion core, with no DHX15 and no G-patch relative beside it | Gene | 4 | 3/5 |
| GPHN (gephyrin) — synaptic scaffold and molybdenum-cofactor enzyme, KMT2A fusion partner in t(11;14)(q23;q24) | Protein | 8 | 4/5 |
| GPKOW - a G-patch spliceosomal protein whose BioID neighbourhood contains AFF4, ELL, ENL, CDK9, KMT2A and DOT1L | Gene | 3 | 2/5 |
| GPT2 (Q8TD30) - the EARLIEST-moving and third-most menin-selective gene in the serine arm, and the one REH cannot control because it is below the array floor there | Gene | 4 | 3/5 |
| Graft-versus-host disease in a transplanted infant - the only antileukaemic benefit and the main cause of death are the same process at different grades | Risk | 5 | 3/5 |
| Graft-versus-leukaemia in KMT2A-rearranged infant leukaemia - the mechanism the whole transplant rests on, demonstrated in ALL generally, assumed in this disease, and with a published mechanistic reason to doubt it | Explainer | 5 | 3/5 |
| Granulocyte-monocyte progenitor (GMP) — the committed cell an MLL fusion can turn back into a stem cell | Cell type | 4 | 4/5 |
| Gray 2023's own 'exon 11 CTCF site' in RPE cells, measured: centroid GRCh38 chr11:118,488,662-118,488,761, inside canonical exon 11 and 34 bp from the independently measured summit - the graph's CTCF adjudication is confirmed, not overturned | Non-coding | 2 | 4/5 |
| Growth and endocrine consequences of being treated for leukemia as a baby | Explainer | 5 | 3/5 |
| GSE127507 deposits a matched input for BOTH conditions in MOLM13 only - RS4;11 and ML-2 have a DMSO input and no VTP-50469 input - so no input-corrected cross-condition occupancy statement is possible in the human index-fusion line from this series, and none exists anywhere | Analysis | 1 | 5/5 |
| GSE127507 ran a Drosophila spike-in, measured it, and deliberately did not use it - so the VTP-50469 founding dataset carries no recoverable scale factor either, and the depositors say so in the sample record | Analysis | 2 | 5/5 |
| GSE139196: SUV39H1 ChIP-Seq in MCF-7 with and without 40 minutes of estradiol - a ligand-inducible SUV39H1 occupancy experiment, filed under the retired symbol KMT1A in its own sample titles | Experiment | 3 | 5/5 |
| GSE159608 — 419 automated CUT&Tag libraries across 7 KMT2A-rearranged primary patient samples, 5 lines and a normal CD34+ donor, including KMT2A fusion occupancy, a menin-inhibitor arm in SEM, and three single-cell CUT&Tag libraries | Analysis | 3 | 5/5 |
| GSE173599 deposits menin ChIP at three hours and nowhere else - no 24 h, no 4 d - so the central question this beat raises, whether menin's persistence is fusion-independence or merely a slow off-rate, cannot be answered from the only degron deposit that exists, and the GEO record advertises four-day menin ChIP that was never deposited | Analysis | 2 | 4/5 |
| GSE210480 carries FOUR CTCF bigWigs under EIGHT sample accessions, byte-identical, under different filenames - so counting GEO sample records doubled the replicate count and would have halved every standard error | Explainer | 1 | 5/5 |
| GSE225028: SUV39H1 and H3K9me3 CUT&RUN in SU-DIPG13 and SU-DIPG36 - the only published human SUV39H1 occupancy map deposited as a readable hg38 bigWig, and the enzyme and its own mark were profiled in the same cells | Experiment | 2 | 5/5 |
| GSE252378 carries an institution-level batch effect: unrelated pairs from the same hospital overlap more than cross-hospital pairs, and a cohort-median comparator absorbs that into the same-patient claim | Analysis | 2 | 3/5 |
| GSE252378 contains menin CUT&RUN in exactly one patient - a KMT2A::ENL lineage-switching pair under a menin inhibitor - and none in any of its eight KMT2A::AFF1 patients | Analysis | 2 | 5/5 |
| GSE252378 contains no megakaryoblastic sample, so the 0-of-18 non-AFF1 IRX1 occupancy bound does not cover the one subgroup where IRX1 is actually expressed | Analysis | 2 | 4/5 |
| GSE252378 deposits no transcriptional readout: all 171 samples are library_strategy OTHER and the metadata never says RNA, so every programme claim from this deposit is occupancy and none is expression | Explainer | 2 | 5/5 |
| GSE252378 fragment BEDs: a complete KMT2A N-terminal / C-terminal antibody set in 27 patient samples across six fusion partners, deposited and until now unopened by this corpus | Analysis | 3 | 5/5 |
| GSE252378 holds eight KMT2A::AFF1 oncoprotein panels from two centres, not the three this corpus had used | Analysis | 2 | 5/5 |
| GSE252378 holds the only AFF1 CUT&RUN in primary KMT2A::AFF1 patient material - four libraries across two patients, three disease states and the SEM cell line, all hg38 | Analysis | 2 | 5/5 |
| GSE252378 labels one of its two SEM AFF1 libraries KMT2A-AFF2, a fusion that does not exist in the deposit and does not exist in SEM - a filter on that field silently halves the SEM data | Analysis | 2 | 5/5 |
| GSE252378's 27 KMT2A-fusion samples are 24 independent patients: three pairs are one patient sampled twice | Analysis | 2 | 5/5 |
| GSE260742 declares an H3K27me3 second channel in its MLLAF9 Control arm, and no floor can be computed from it: all three rep1/rep2 pairs agree about only 86.31-88.90% of the shallower track's covered bins, so 11-14% of the SHALLOWER track's coverage falls where the DEEPER one has none. Depth cannot explain that. | Analysis | 1 | 3/5 |
| GSE260742's murine H3K79me2 samples come from FOUR distinct cultures - F3, F3_NT, NT and the PCGF1-KO clone C1 - and the titles name only two of the distinctions; 'Timecourse Control' is the F3 line, and 'NTvKO Control' covers two different filename families that are not the same material | Analysis | 1 | 4/5 |
| GSE260742's PCGF1-knockout samples carry no deposited measurement of PCGF1 - no protein, no transcript, no sequencing of the edited locus - and the knockout rests on one guide and one clone with no rescue, so every null result from that arm is a null in an unverified genotype | Analysis | 1 | 4/5 |
| GSE260742's VTP-50469 kinetic series carries no SGC0946 sample at any timepoint, so the denominator of F cannot be measured inside that batch and the fraction cannot be recomputed at any time - the only SGC0946 arms in the series are in different experiments at a single 72-hour or 7-day exposure | Analysis | 1 | 4/5 |
| GSE299100 supplies the vehicle-versus-vehicle pair that neither GSE260742 nor GSE127507 could - two independent control hairpins, both DMSO, same date, uniformly processed to hg38_rmdup.tdf, for MEN1, MLL1 and input - in MV4-11, which Cellosaurus confirms carries KMT2A::AFF1 though it presents as monocytic rather than the infant B-ALL this project studies. It also holds MEN1 and MLL1 ChIP under five different menin inhibitors in that line, and the six control files total 1.87 GB | Analysis | 1 | 3/5 |
| GSE68720 - 97 infant ALL patients from COG P9407 with the KMT2A partner named per sample (mll_par) and a GPL570 expression matrix, 74 partner-named KMT2A-r cases and 17 germline controls | Analysis | 1 | 4/5 |
| GSK3 is required by KMT2A-rearranged leukaemia and nobody has shown it touches KMT2A | Mechanism | 2 | 3/5 |
| GSM8006584 names its antibody KMT2A-C1 in its title, its characteristics field and its own filename, and KMT2A-C2 in its description - so keying the antibody off the free-text description gives patient TB-92-0488 two C2 libraries and no C1 | Analysis | 1 | 4/5 |
| GSM8123377 and GSM8123403 carry the same supplementary filename but for the `.filt.bam` marker, yet GEO titles one 'MLLAF9 Control - DMSO H2AK119ub rep2' and the other 'NTvKO Control - DMSO H2AK119ub paired'. Scored directly, they are DIFFERENT libraries (Spearman 0.83), so the collision is a naming accident and both arm titles stand. | Analysis | 1 | 3/5 |
| GSM8123386/387/388 carry the GEO title 'MLLAF9 Control - ... H3K79me2 rep2' and the supplementary filename 'ChIP_K79_F3_NT_*'. Two committed analyses treat them as a separate culture and one asserts 'FOUR INDEPENDENT MURINE CULTURES'. If the titles are right there are three, one of them replicated. REPORTED AS A DISPUTE, NOT APPLIED. | Analysis | 2 | 3/5 |
| GSM8123405 is mm10 DATA in an hg38-DECLARED TDF - the exact mirror of Q122's mm10-declared / hg38-coordinate defect, in the same series - and the container silently clipped 72.8 Mb (2.76%) of chr13-chr19 and chrX at deposition; the declared extents name the container and max_end names the data | Analysis | 2 | 4/5 |
| Guanine nucleotide supply sustains the LEDGF/menin/MLL-fusion complex - the one place in this graph where metabolism sits UPSTREAM of the menin interface | Mechanism | 4 | 3/5 |
| H2A.Z - two genes of identical length, one KMT2A paper, and the measured quantity is a ratio nobody has repeated | Mechanism | 5 | 3/5 |
| H2AK119ub - the mark every PRC1.1 claim in this graph rests on, named in fifteen entries and written in none until now | Mechanism | 6 | 4/5 |
| H2AX - filed as a gene and not as a mark, and the reason that decision changes what the graph can say | Gene | 7 | 3/5 |
| H2AZ1 - the one histone variant with a direct KMT2A-fusion paper: MLL-AF10 and MLL-ENL recruit Tip60 to Hoxa9 to acetylate H2A.Z | Gene | 7 | 3/5 |
| H2B ubiquitination is upstream of the fusion's defining mark and is still not a target, because the fusion uses a general mechanism rather than a special one | Hypothesis | 2 | 3/5 |
| H2BK120ub (H2Bub1) — the ubiquitin tag on histone H2B that licenses H3K79 methylation, and the mark this graph was missing | Mechanism | 5 | 5/5 |
| H2BK34ub — a second ubiquitination site on H2B that also stimulates DOT1L, written by MSL1/MSL2, and important at HOXA9 and MEIS1 | Mechanism | 4 | 4/5 |
| H3.3 - the graph's most-named epigenetic object with no entry, 325 mentions, and not one measurement in a KMT2A-rearranged cell | Mechanism | 6 | 4/5 |
| H3C1 stays rejected, and now with the two numbers the registry row lacked: its accession carries TEN gene names, and removing every substrate and ribosome symbol moves interactome coverage 43.8% -> 46.1% | Analysis | 4 | 4/5 |
| H3K27ac - named in 40 entries with no entry of its own, and the strongest KMT2A::AFF1 measurement of it is invisible to every abstract search | Mechanism | 7 | 4/5 |
| H3K27me3 - the repressive mark this graph argued about for seventy-seven cycles without ever writing an entry for it | Mechanism | 9 | 4/5 |
| H3K36me2/3 - the mark that physically switches PRC2 off, that LEDGF reads to reach chromatin, and that a comparator fusion uses to keep EZH2 off HOXA | Mechanism | 5 | 3/5 |
| H3K4me2 - the LSD1 substrate, and the only histone mark ever compared head-to-head between two KMT2A fusion partners in human cells | Mechanism | 6 | 3/5 |
| H3K4me3 - the mark KMT2A's own SET domain writes, that the fusion cannot write, that an interface in this graph already binds, and that switches PRC2 off | Mechanism | 6 | 3/5 |
| H3K4me3 and wild-type MLL1 are the negative controls for the partition, and both come out flat | Analysis | 3 | 3/5 |
| H3K4me3 is by far the most reproducible track in primary infant leukaemia CUT&Tag - replicate rho 0.97-0.98 - which makes it both the assay's proof of competence and the benchmark that every fusion-site enrichment should be quoted against | Analysis | 2 | 4/5 |
| H3K4me3 is the one mark in GSE260742 with no declared second channel at all - six samples, no replicate suffix anywhere - so no same-condition pairing exists and its noise floor remains a transfer from another mark whatever else is measured. | Analysis | 1 | 4/5 |
| H3K4me3 oscillates around the clock and MLL1 is what lets it - a cell state of KMT2A biology this project has never once mentioned | Cell state | 1 | 3/5 |
| H3K79 methylation is what keeps Polycomb off - and that, not gene silencing, is what a DOT1L inhibitor actually undoes | Mechanism | 4 | 3/5 |
| H3K79me1 - the first methyl group, the one H2B ubiquitination is not needed for, and the state HOX loci fall back to as blood cells mature | Mechanism | 6 | 3/5 |
| H3K79me2 - the di-methyl state the leukaemia actually runs on, and the one menin turns out to govern only half of | Mechanism | 6 | 4/5 |
| H3K79me2 builds up as B cells mature - so in B-ALL the drug's target is what the rescued compartment runs on | Mechanism | 2 | 4/5 |
| H3K79me2 reports only the DOT1L arm of a menin inhibitor's action and is blind to its PRC1.1 arm - so the mark's response is unchanged in a PCGF1 knockout even though PCGF1 loss is a published resistance mechanism, and a cell resistant through PRC1.1 loss would look fully drug-engaged by this readout | Hypothesis | 2 | 1/5 |
| H3K79me3 - the third methyl group, the one that needs the most enzyme flux and the one human DOT1L makes least of | Mechanism | 4 | 3/5 |
| H3K9ac - the mark KMT2A fusions pile up on their own targets, the one the AF9 reader actually binds, and the one a DOT1L inhibitor strips off first | Mechanism | 4 | 4/5 |
| H3K9me1 - the only H3K9 state whose level at the KMT2A breakpoint cluster region has ever been measured, and it is LOW there until KDM3B is removed | Mechanism | 8 | 3/5 |
| H3K9me1 depletion over the KMT2A breakpoint cluster replicates in a leukaemia line - as a broad-domain property of the 7.5 kb BCR, not of the 1 kb CTCF element, where the two tracks disagree in sign | Analysis | 2 | 3/5 |
| H3K9me2 - named sixty times in this graph with no entry of its own, the mark that defines the lamina-associated domains the fusion's targets sit beside, and the only H3K9 methylation state ever measured at a KMT2A fusion's own binding sites | Mechanism | 8 | 3/5 |
| H3K9me3 - measured in KMT2A::AFF1 cells, in a supplementary figure, and it rises GENERALLY where H3K27ac falls SPECIFICALLY in the same experiment | Mechanism | 6 | 4/5 |
| H3R2me2a - the asymmetric arginine mark two residues from H3K4 that LOCKS the WRAD module off the histone tail, and the first arginine mark node in this graph | Mechanism | 17 | 3/5 |
| H3R2me2s - the symmetric mark on the SAME residue as H3R2me2a, which permits rather than enhances WRAD access, and whose 'enhancing' half this graph inherited from the paper that was later revised | Mechanism | 9 | 3/5 |
| H4K16ac - the one mark rule 80 actually rescued in this beat: elevated at MLL-AF9 targets in a supplementary figure, and the reason MLL1's own enzyme turns out to be dispensable | Mechanism | 6 | 4/5 |
| H4K20me1 - the transcription- and replication-linked H4 state, whose gene-body level tracks Pol II; it HAS been profiled genome-wide in human haematopoietic stem cells twice, and a query scoped to 'leukemia' cannot see either dataset | Mechanism | 11 | 4/5 |
| H4K20me2 - the abundant repair-linked H4 mark, the 53BP1 docking site, and the first H4K20 state in this graph; never once measured in a KMT2A-rearranged cell | Mechanism | 6 | 4/5 |
| H4R3me2a - the activating arginine mark that a KMT2-family enzyme's OWN tandem PHD module reads, where the Kabuki-syndrome mutations sit, and which no KMT2A-fusion study has ever measured | Mechanism | 12 | 3/5 |
| H4R3me2s - the repressive symmetric arginine mark that recruits DNMT3A, blocks a KMT2 enzyme's own PHD module, and is the ONLY arginine mark ever measured in a KMT2A-fusion system | Mechanism | 11 | 3/5 |
| Haematopoietic stem cell transplant in KMT2A-rearranged infant leukemia — what it is for, and why most children who need it never get it | Explainer | 3 | 4/5 |
| Haemogenic endothelium — the vessel-wall cell that gives birth to blood | Cell type | 11 | 4/5 |
| Half of all KMT2A::MLLT1 patients make no reciprocal product at all - a ready-made control arm of about 240 people | Explainer | 3 | 3/5 |
| Half the 'free' PRC1.1 intersection really was free: Zhou's locus set is a publisher table, Neville's does not exist, and only that half costs 25 GB | Experiment | 2 | 5/5 |
| Half the KDM4C deposition is not a KMT2A fusion at all: MOZ-TIF2 8, MLL-GAS7 6, MLL-AF9 2, and the human xenograft deposited nothing | Analysis | 3 | 4/5 |
| Half the menin at fusion-occupied promoters is held by a tether that is not the fusion | Hypothesis | 4 | 1/5 |
| Half the PRC1.1 intersection was free all along: Zhou's locus set is a publisher supplementary table, and 159 of this graph's gene entries are in it | Analysis | 3 | 4/5 |
| Half this graph's claims are unopposed; these are the ones that matter | Analysis | 2 | 3/5 |
| Has anyone tested an XPO1 inhibitor in a KMT2A-rearranged system? Yes - four preclinical studies and zero clinical ones, counted with the queries and the controls | Analysis | 5 | 4/5 |
| HB11;19 (CVCL_8227) is KMT2A::MLLT1, not KMT2A::AFF1 — and it is the most menin-dependent line in the panel | Explainer | 2 | 5/5 |
| HB11;19 (CVCL_8227) keeps the YEATS domain and expresses both derivative transcripts - so it is the reciprocal-POSITIVE t(11;19) line, and there is no negative one | Explainer | 4 | 3/5 |
| HCFC1 (HCF-1) — a founding member of the wild-type KMT2A complex that the fusion cannot bind | Protein | 5 | 4/5 |
| HCFC2 — menin's other host cell factor, present in the founding paper by gel filtration and never mentioned again | Protein | 7 | 2/5 |
| HDAC1 - a class I eraser that has no dependency claim of its own in this disease, because removing it alone does nothing until HDAC2 goes too | Gene | 4 | 3/5 |
| HDAC1 and HDAC2 belong to at least five different corepressor complexes, so an HDAC1/2 observation names no complex - and this graph carried both enzymes without the scaffolds that would tell them apart | Explainer | 4 | 4/5 |
| HDAC2 - the buffering half of the class I pair, and the one class I enzyme a drug result in acute leukaemia has actually been pinned to, in AML rather than in a KMT2A fusion | Gene | 3 | 3/5 |
| HDAC3 - the only HDAC in this disease whose requirement was established genetically rather than by a drug, and the same experiment shows it is not fusion-specific | Gene | 5 | 4/5 |
| HDAC5 - the eraser in an existing entry's own id, and the one HDAC in this graph that erases a mark on a fusion partner protein rather than on a histone | Gene | 9 | 3/5 |
| HDAC6 - the one HDAC family member this graph refused, whose refusal named a falsifier that has been in the literature since 2020 and fires in the index fusion's own cell line | Gene | 4 | 3/5 |
| HDAC7 - the eraser the index fusion silences, where the proposed therapy is to INDUCE the HDAC, and two 2024-2025 papers point in opposite directions | Gene | 9 | 3/5 |
| HDAC9 - the only HDAC with a KMT2A-rearrangement expression signature across 211 paediatric patients, and it is high, prognostic, and independent of partner and lineage | Gene | 9 | 3/5 |
| HDGF - the third PWWP paralogue, which pulls down LEDGF but has the reader domain WITHOUT the domain that grips MLL | Gene | 6 | 2/5 |
| HDGFL2 / HRP-2 - the second IBD protein, which binds KMT2A at the same site with the same affinity and does NOT need menin to do it | Gene | 10 | 3/5 |
| Hepatosplenomegaly: the swollen abdomen that is often the first thing a parent notices | Explainer | 3 | 3/5 |
| HEXIM1 - the brake pad, the only part of the reservoir anyone has deliberately raised in a KMT2A-rearranged cell, and the result was that the leukaemia grew less | Protein | 17 | 4/5 |
| HEXIM2 - the paralogue that holds the bound P-TEFb pool constant when HEXIM1 is removed, which is why single-gene experiments on this axis read flat | Protein | 7 | 4/5 |
| HEXIM2 quantitatively compensates for HEXIM1 loss to hold the 7SK-bound P-TEFb pool constant - which makes single-gene knockdown of either a buffered experiment, and is the reason a HEXIM1-only measurement cannot be read as the brake's strength | Mechanism | 1 | 4/5 |
| HIRA - the chaperone that puts new H3.3 into transcribed gene bodies, and therefore the machine that runs this graph's clearance clock | Gene | 14 | 3/5 |
| Histone H3.3 - one protein, two genes, and the reason this graph should not file it as gene-h3f3a | Protein | 5 | 4/5 |
| Hitting the same axis at two points was predicted to be sub-additive; the one published test found synergy in all four KMT2A-rearranged lines | Mechanism | 2 | 4/5 |
| HIV-1 integrase on the LEDGF IBD: the same pocket as KMT2A, a thousandfold tighter, and a published competition that displaces the leukaemic complex at IC50 301 nM | Interface | 2 | 4/5 |
| HLA-A - the class I heavy chain a menin inhibitor was actually measured on, and the human orthologue of the MHC class I molecule that protects MLL-AF9 leukaemia stem cells from NK cells | Gene | 6 | 3/5 |
| HLA-B - the class I heavy chain the bivalency screen was actually read out on, and the locus that presents the one KMT2A epitope this graph has a structure for | Gene | 7 | 3/5 |
| HLA-DR - a two-chain MHC class II heterodimer, so no single gene symbol denotes the surface marker a flow report calls HLA-DR | Target | 5 | 3/5 |
| HLA-DRA - the non-polymorphic alpha chain, and the only HLA-DR chain any source on this beat names explicitly | Gene | 2 | 3/5 |
| HLA-DRB1 - the polymorphic beta chain, one of several that can make an HLA-DR dimer, and the reason a chain cannot be inferred from a flow result | Gene | 2 | 3/5 |
| HLF (hepatic leukemia factor) domain architecture | Protein | 1 | 4/5 |
| HMGA1 (P17096) - an AT-hook architectural protein that antagonises histone H1 at scaffold-attachment regions, with a childhood B-ALL relapse correlation that is title-only evidence | Gene | 3 | 3/5 |
| HMGA2 (P52926) - a direct KMT2A::AFF1 target through the let-7b axis, and a recurrent fusion partner whose own fusions work by escaping a microRNA rather than by making a chimeric protein | Gene | 4 | 3/5 |
| HNF4A - a liver and pancreas nuclear receptor acting as the metabolic effector of TIFAB in KMT2A::MLLT3 AML, on a single paper | Protein | 2 | 3/5 |
| HNRNPA2B1 — the panel's strongest KMT2A-selective RNA-layer gene after PTBP1, with ZERO records against MLL or KMT2A | Gene | 4 | 2/5 |
| HNRNPC - the nascent-RNA packaging protein whose BioID neighbourhood contains AFF4, ELL, ENL, CDK9, cyclin T1 and KMT2A | Gene | 3 | 2/5 |
| Holding mark, arm and drug conditions fixed and varying only which confound the replicate pair carries: the floor ranges are DISJOINT at D1 and D10, a processing-confounded pair inflates D1 2.20x while a batch-confounded pair inflates D10 2.21x, and the direction reverses by stratum - so the floor is a property of the pair, not of the mark or the arm, and every floor this project has published came from the pair type that is wrong for D1 | Analysis | 1 | 3/5 |
| HOTAIRM1 lncRNA — the myeloid-differentiation transcript at the 3' end of HOXA, with a KMT2A-r evidence gap | Non-coding | 7 | 2/5 |
| HOTTIP lncRNA — the 5' HOXA switch that holds the leukemic chromatin domain open | Non-coding | 4 | 3/5 |
| How a chromosome translocation actually forms: proximity + breakage + repair | Explainer | 3 | 5/5 |
| How a cytoskeletal partner reaches chromatin at all — the KMT2A N-terminus drags it in, and the traffic runs both ways | Mechanism | 6 | 3/5 |
| How a lift operator became a postal address: the idea behind the XPO1 axis, in plain language | Explainer | 3 | 4/5 |
| How a spliced fusion works: the break lands in front of MLLT1, the gene is never cut, and there is nothing left to make a reciprocal product from | Mechanism | 3 | 4/5 |
| How BAF maintains KMT2A-rearranged leukaemia: it holds the blast undifferentiated, and it does so in other leukaemias too | Mechanism | 4 | 4/5 |
| How common is ZNF384-rearranged leukaemia? Published answers span 1.6% to about 20% and the spread is almost entirely denominator, not biology | Epidemiology | 8 | 4/5 |
| How common PICALM::MLLT10 is, and in which disease - 65% T-ALL, 27% AML, and invisible to karyotype half the time | Epidemiology | 3 | 3/5 |
| How general is subtraction across KMT2A fusions? Common enough to matter, too heterogeneous to be one thing, and mostly invisible to the way this project searches | Mechanism | 5 | 2/5 |
| How HOXA9 binds DNA: a hexapeptide into a PBX pocket, a 1.9 A structure that is mouse HoxA9 plus human Pbx1 homeodomains, and a second route that makes the motif redundant | Mechanism | 3 | 4/5 |
| How long does menin have to be gone? Two months in a mouse islet, a decade or more in a human carrier | Explainer | 9 | 4/5 |
| How many children this affects | Epidemiology | 4 | 4/5 |
| How many infants worldwide, not just in the United States | Epidemiology | 4 | 3/5 |
| How menin holds the beta cell still: JunD recruits it, with HDAC3, onto the Pbk promoter | Mechanism | 1 | 4/5 |
| How menin silences JunD: pocket binding plus uncoupling from MAP kinase signalling | Mechanism | 4 | 4/5 |
| How much HOXA9 and MEIS1 is actually required? Partial dependence, a Hox code, and why this caps what any single target can do | Mechanism | 4 | 4/5 |
| How much of this graph's mechanism is somebody else's fusion? A counted answer: 54% of fusion-bearing evidence, and 0% from a dedicated human KMT2A::AFF1 experiment | Analysis | 6 | 3/5 |
| How much sugar the cell has decides how much DOT1L there is - a metabolic dial on the leukaemia's mark | Mechanism | 3 | 3/5 |
| How P-TEFb gets out of the reservoir: a dephosphorylation, a dissociation, and a reassembly on whichever scaffold is waiting | Mechanism | 10 | 4/5 |
| How the three occupancy archives spell zero: ENCODE 404, ReMap 401, ChIP-Atlas 404 - and ChIP-Atlas spells a one-character URL typo exactly the same way, so a whole sweep can come back cleanly and be entirely false | Analysis | 4 | 5/5 |
| HOXA is occupied as a 107 kb cluster; IRX1 is occupied as one gene, with both IRX clusters cold | Analysis | 2 | 3/5 |
| HOXA occupancy is the partner-invariant: occupied in 17 of 18 non-AFF1 KMT2A-r samples, 2.94x to 29.1x | Analysis | 2 | 3/5 |
| HOXA-AS2 and HOXA-AS3 — mid-cluster antisense transcripts with essentially no KMT2A-r evidence | Non-coding | 6 | 2/5 |
| HOXA-high versus HOXA-low KMT2A-rearranged leukemia — the split that breaks the one-mechanism story | Mechanism | 3 | 3/5 |
| HOXA10 - named in 27 entries as part of the HOXA output and never written; a posterior HOX paralogue that is regulated with HOXA9 and tested far less often | Gene | 9 | 3/5 |
| HOXA7 - the one HOXA paralogue besides HOXA9 with a published loss-of-function requirement for MLL-fusion transformation, and the requirement was shown in vitro only | Gene | 5 | 3/5 |
| HOXA9 — required for survival of established MLL-rearranged leukemia, and dispensable for starting it | Protein | 9 | 4/5 |
| HOXA9 has its own nuclear bodies, and in monocytic AML they move into the eIF4E body - a subnuclear switch measured in patient marrow and never genotyped | Mechanism | 4 | 3/5 |
| HOXA9 is where menin leaves most completely (share ratio 0.14-0.23 over floor) and MLL1-N-reactive material stays most completely (0.74-1.02 over floor), in all three MLL-rearranged lines - so the menin inhibitor decouples menin from the HOXA9 locus without clearing the MLL1 N-terminus from it | Analysis | 1 | 3/5 |
| HOXA9/HOXA10 is unoccupied and unmethylated at H3K4 in two of the three primary infant KMT2A::AFF1 states, while the SEM cell line carries the strongest AFF1 signal over that locus of any sample in the deposit | Analysis | 3 | 4/5 |
| HOXB4, the one direct IRX1 target with ChIP evidence, carries no oncoprotein in any of seven infant patients | Analysis | 2 | 3/5 |
| HOXD13 domain architecture (UniProt P35453) | Protein | 1 | 5/5 |
| HP1-gamma holds a constitutive, sub-threshold foothold on the KMT2A exon-11 CTCF anchor in undamaged cells - the CTCF-primed model's missing resting state - and the reason nobody has seen it is that it sits below the reproducibility filter every public peak set applies | Hypothesis | 2 | 1/5 |
| HPA's per-cell-line RNA file is not dead - it lives under /download/tsv/ while proteinatlas.tsv lives under /download/, and the wrong prefix returns HTTP 200 with a 117,090-byte HTML page | Analysis | 2 | 4/5 |
| HR genes are menin-bound at 1.76x and so is ribosome biogenesis at 1.78x: the pathway-specific reading does not survive its own control | Analysis | 2 | 2/5 |
| HTAN KMT2A-r ALL single-cell multiome — 25 patients (18 infants), scRNA-seq + scATAC-seq + snmC-seq2, with 2 paired pre/post lineage-switch cases and analysis code on GitHub | Analysis | 3 | 4/5 |
| Hunting the one reagent that would unbind every share-based result in this thread: the fly/human ratio is in no supplementary table and the words dm6 and scale factor appear zero times in the full text - and the 181116 batch the processing line names is in NONE of the 78 samples across all four subseries of GSE127508, so no deposited sample is established to carry the spike-in at all | Analysis | 1 | 4/5 |
| hyp-q117's prediction 5 is stored TWICE in one entry, in sections[0].body_md and in data.predictions[4], and the two strings differ - here is the scored outcome and the ALL-CAPS cashed text proposed for both locations, with the clause-by-clause verdict a one-line 'confirmed' would have hidden | Analysis | 2 | 3/5 |
| hyp-q117's prediction 5 says 'in a PCGF1 OR BCOR knockout' and GSE260742's only genetic perturbation is the PCGF1 knockout: across all 158 sample records the strings BCOR, BCORL1, KDM2B, RING1 and RNF2 appear zero times as a perturbation, so a verdict on PCGF1 is not a verdict on the prediction as written | Analysis | 2 | 4/5 |
| Hyperleukocytosis: why a very high white-cell count is a medical emergency | Explainer | 5 | 4/5 |
| Hypothesis — forced-oligomerisation interfaces are the mutation-resistant drug targets the fusion field has been ignoring | Hypothesis | 9 | 1/5 |
| Hypothesis — the elongation hijack is how one partner class satisfies a more general requirement, and the general requirement is what should be drugged | Hypothesis | 5 | 1/5 |
| Hypothesis — the menin lesson generalises: every non-enzymatic fusion has an obligate partner interface that is more druggable than the fusion | Hypothesis | 9 | 3/5 |
| Hypothesis (first clause REFUTED 2026-09-21): the fusion's core dependencies may be cell-type-invariant, but the cell type itself is not fixed | Hypothesis | 2 | 1/5 |
| Hypothesis: a defined subset of fusion binding sites survives saturating menin inhibition on menin-independent tethering, and that residual set is where bypass resistance comes from | Hypothesis | 5 | 1/5 |
| Hypothesis: a menin inhibitor must come BEFORE an antigen-directed immunotherapy, not with it or after it - and every published experiment has already assumed this without anyone testing it | Hypothesis | 5 | 1/5 |
| Hypothesis: a single dormant leukemia stem cell state confers cross-resistance to menin inhibition, venetoclax and T-cell engagement at once — the common-cause failure that orthogonal combination therapy assumes away | Hypothesis | 4 | 2/5 |
| Hypothesis: adaptive scheduling of menin inhibitors will fail, because MEN1 resistance mutations probably cost the cell nothing | Hypothesis | 6 | 1/5 |
| Hypothesis: CLEC12A is a cell-intrinsic dependency in KMT2A-rearranged leukaemia, not only a surface marker - and if so, antigen-negative escape is self-defeating | Hypothesis | 4 | 1/5 |
| Hypothesis: genetic and non-genetic escape from menin inhibition are substitutes, so MEN1 mutations will be rare in infants and the field's resistance biomarker will fail in children | Hypothesis | 5 | 1/5 |
| Hypothesis: H3K79me2 at a KMT2A fusion's own sites survives menin inhibition when the C-terminal partner contacts DOT1L directly (MLLT3/AF9) and decays when it does not (AFF1) - so the mark's response is a property of the partner and not of menin, which predicts the opposite of the direct-contact intuition and is testable in one line | Hypothesis | 1 | 3/5 |
| Hypothesis: IGF2BP2 and IGF2BP3 buffer each other in KMT2A::AFF1 leukaemia, so single-gene CRISPR under-reports both | Hypothesis | 5 | 1/5 |
| Hypothesis: KMT2A and AFF1 break where they do because both breakpoint regions are CTCF/cohesin loop anchors sitting in the same nuclear hub | Hypothesis | 7 | 1/5 |
| Hypothesis: KMT2A-rearranged infant ALL is two populations, not one — a mixture-cure model will fit better than proportional hazards, and combination therapy only needs to be given during the first year | Hypothesis | 4 | 1/5 |
| Hypothesis: KMT2A::AFF1 does not require phase separation — recruitment biochemistry is sufficient, and the condensate model does not transfer from NUP98/ENL | Hypothesis | 5 | 1/5 |
| Hypothesis: KMT2A::AFF1 is continuously required, not a hit-and-run initiator whose job is done once the epigenome is set | Hypothesis | 3 | 4/5 |
| Hypothesis: KMT2A::AFF1 mislocalises to or disrupts nuclear speckles, and paraspeckle biology (NEAT1) is a fusion-repressed differentiation brake | Hypothesis | 2 | 1/5 |
| Hypothesis: KMT2A::AFF1 rewires splicing, because AFF1's own protein family are G-quadruplex RNA-binding splicing modulators and the fusion keeps AFF1 | Hypothesis | 2 | 1/5 |
| Hypothesis: KMT2A's AT-hooks are a DNA-topology reader, not an AT-sequence reader — which would link the fusion's address to the scaffold-attachment architecture that also makes its own gene fragile | Hypothesis | 5 | 1/5 |
| Hypothesis: LEDGF licenses elongation at fusion target genes rather than anchoring the fusion, which predicts that a LEDGF agent is epistatic with BET and CDK9 inhibition and invisible in a fusion-ChIP assay | Hypothesis | 4 | 1/5 |
| Hypothesis: menin inhibition does not clear the fusion from chromatin but redistributes it onto the four fifths of the unmethylated CpG address it normally ignores | Hypothesis | 4 | 1/5 |
| Hypothesis: menin inhibition does not merely displace KMT2A::AFF1 from chromatin, it destabilises it — the evicted fusion is degraded, not parked | Hypothesis | 5 | 1/5 |
| Hypothesis: menin inhibition pushes cells toward the GMP-like state, and the GMP-like state is where menin inhibition works best — so a lineage switch on therapy should predict response, not failure | Hypothesis | 4 | 1/5 |
| Hypothesis: menin inhibitors differ in how much JUND they liberate, and the least JUND-liberating compound will be the most durable | Hypothesis | 4 | 1/5 |
| Hypothesis: menin-inhibitor effect is hysteretic — the program collapses faster than it recovers — so intermittent dosing can hold efficacy at much lower cumulative exposure | Hypothesis | 5 | 1/5 |
| Hypothesis: menin-inhibitor sensitivity falls with cell-cycle exit, so the compartment that causes relapse is the one the drug reaches least — and nobody has sorted by cycle state to check | Hypothesis | 4 | 1/5 |
| Hypothesis: only a mechanistically orthogonal partner pre-empts menin-inhibitor resistance; a second chromatin agent will not | Hypothesis | 4 | 1/5 |
| Hypothesis: prior therapy itself installs menin-inhibitor resistance, and the dose of prior therapy predicts it better than any mutation does | Hypothesis | 4 | 1/5 |
| Hypothesis: releasing the KMT2A::AFF1 differentiation block sends cells toward myeloid, not mature B, in a measurable fraction of infant cases | Hypothesis | 6 | 1/5 |
| Hypothesis: reserving menin inhibitors for relapse in infants is actively harmful, because pretreated disease is already resistant | Hypothesis | 3 | 1/5 |
| Hypothesis: SET::NUP214 activates HOXA partly through recruited wild-type MLL1, which would make a KMT2A-unrearranged leukaemia menin-inhibitor-sensitive | Hypothesis | 3 | 1/5 |
| Hypothesis: t(4;11) infant ALL is a hypermethylated genome whose transposable elements can be reawakened, and that reawakening is an untested immunotherapeutic lever | Hypothesis | 3 | 1/5 |
| Hypothesis: the ceiling on menin-interface disruption is cell-state plasticity, not target mutation | Hypothesis | 5 | 1/5 |
| Hypothesis: the cell-of-origin methylome, not the breakpoint, decides whether a KMT2A::AFF1 leukemia is HOXA-high or HOXA-low | Hypothesis | 5 | 1/5 |
| Hypothesis: the fusion is exempt from KMT2A's regulation, not free of it - the brakes still operate at the same loci, on the other allele | Hypothesis | 5 | 1/5 |
| Hypothesis: the fusion output program fails at a threshold on total cut-set suppression, so three nodes at 40% beat one node at 90% | Hypothesis | 5 | 1/5 |
| Hypothesis: the haem and iron dependency of KMT2A-rearranged lines is monocytic physiology, not fusion biology — and the panel cannot tell us either way | Hypothesis | 4 | 1/5 |
| Hypothesis: the HOXA-negative, IRX1-negative KMT2A-rearranged blast is a low-oncoprotein-dosage state, not a state whose oncoprotein has been redirected to another programme | Hypothesis | 2 | 1/5 |
| Hypothesis: the KMT2A break can be prevented rather than the fusion treated - stated so it can be killed, and it probably should be | Hypothesis | 8 | 1/5 |
| Hypothesis: the KMT2A breakpoint map is shaped by product viability, not only by DNA fragility, and the signature is that breaks respect inter-domain linkers | Hypothesis | 3 | 1/5 |
| Hypothesis: the KMT2A genomic breakpoint carries prognostic information that the field has been sitting on for twenty years | Hypothesis | 5 | 3/5 |
| Hypothesis: the menin inhibitor's effect is inactivation in place, not eviction - the fusion keeps most of its sites and loses its output | Hypothesis | 4 | 1/5 |
| Hypothesis: the menin-MLL complex writes the same mark onto two address lists with opposite cell-state outputs, and which one a tissue reads decides whether blocking menin is a therapy or a lesion | Hypothesis | 6 | 1/5 |
| Hypothesis: the myeloid clone that appears after CD19-directed therapy was already there at diagnosis, and its abundance is a pre-treatment biomarker | Hypothesis | 7 | 3/5 |
| Hypothesis: the paediatric gap is set by the population ratio, not by paediatric biology | Hypothesis | 3 | 1/5 |
| Hypothesis: the PTH rise on menin inhibitors is on-target and exposure-dependent, not renal | Hypothesis | 6 | 1/5 |
| Hypothesis: the R-loop landscape of a KMT2A::AFF1 blast is remodelled by the fusion and is both a vulnerability and a source of ongoing genome instability | Hypothesis | 3 | 1/5 |
| Hypothesis: the reciprocal AFF1::KMT2A product protects only when it is structurally complete, so its prognostic effect is a breakpoint class in disguise | Hypothesis | 3 | 1/5 |
| Hypothesis: the same drug is protective in the islet and harmful in the parathyroid and the growth plate | Hypothesis | 5 | 1/5 |
| Hypothesis: the same-condition floor measured this way is largely a property of where the EXTERNAL stratifier puts its top bins relative to each library's own coverage, not of how well the two replicates agree - which would explain a twentyfold arm span sitting on top of rank concordances that barely differ. | Hypothesis | 1 | 1/5 |
| Hypothesis: the second hit in infant KMT2A-rearranged leukaemia is a fetal developmental window, not a mutation | Hypothesis | 4 | 3/5 |
| Hypothesis: the spread in infant presenting-feature frequencies is mostly measurement, not biology | Hypothesis | 4 | 1/5 |
| Hypothesis: the survival benefit of menin inhibition is governed by the rate at which it delivers patients to a curative consolidation, not by its remission rate — and the field is measuring the wrong thing | Hypothesis | 5 | 1/5 |
| Hypothesis: the three quarters of H3K4me3 that survive menin displacement at fusion target sites are held by a menin-independent complex, and identifying it names the combination partner for a menin inhibitor | Hypothesis | 3 | 1/5 |
| Hypothesis: transfer-RNA and ribosome biology is a genuinely empty cell in KMT2A-rearranged leukemia, and translational capacity may be the unmeasured dependency | Hypothesis | 3 | 1/5 |
| Hypothesis: treatment-remodelled niche, not niche-imposed dormancy, is what residual KMT2A-rearranged disease exploits | Hypothesis | 3 | 1/5 |
| Hypothesis: tubulin/microtubule association is a recurrent, unnamed property of the KMT2A partners whose transforming module has no other assignment | Hypothesis | 6 | 1/5 |
| Hypothesis: what breaks KMT2A in a fetus is TOP2B doing its normal transcription-coupled job in a non-cycling progenitor, with no poison involved and repair capacity as the rate-limiting variable | Hypothesis | 6 | 1/5 |
| Hypothesis: what the KMT2A half loses is control of its own abundance, not control of its activity | Hypothesis | 6 | 1/5 |
| Hypothesis: where a blast goes when the fusion program is released is written in its methylome at diagnosis, not in its transcriptome | Hypothesis | 4 | 1/5 |
| Hypothesis: where a KMT2A fusion sits in the nucleus is set entirely by retained KMT2A modules, and no partner changes the compartment - so every published 'the fusion is here' result is a wild-type KMT2A result | Hypothesis | 5 | 3/5 |
| Hypothesis: YEATS-pocket occupancy disables the reader module of all three SEC-family complexes in proportion to how much of the reader pool each holds — so the drug's footprint is set by an unmeasured partition, not by the fusion | Hypothesis | 3 | 1/5 |
| I audited whether a valid absence token is the RIGHT token, expecting the gene-nbn error to be widespread. It is not: 3 of 4 read were correctly scoped, the scoping is done in prose, and 39 of 40 flagged entries carry no machine-readable scope | Analysis | 1 | 3/5 |
| I withheld these four numbers last cycle to keep an underpowered contrast out of a narrative, and they point the OTHER WAY: the four truncating-ARID1A leukaemia lines mean -0.0401 against a leukaemia wild-type of -0.0923, a naive +0.0523 where pan-cancer gives -0.2475. And NONE of the four carries a KMT2A fusion, so the intersection this whole thread needs is EMPTY, not merely small | Analysis | 1 | 3/5 |
| I-BFM childhood KMT2A-r AML (n=1,130): the 3-prime partner defines two risk groups that differ by 24 EFS points | Epidemiology | 2 | 4/5 |
| I3IN-002 — the first small-molecule IGF2BP3 inhibitor with in vivo activity in an MLL-Af4 model | Drug | 4 | 3/5 |
| iALL-HOXA9 — the HOXA-high state of infant KMT2A::AFF1 ALL, and the one everything is modelled on | Cell state | 2 | 3/5 |
| iALL-IRX1 — the HOXA-negative, IRX1-high state of infant KMT2A::AFF1 ALL | Cell state | 4 | 3/5 |
| IBTK - the only one of the six DOT1L spokes with a reciprocal test, and its own pulldown in the same study does not find DOT1L | Gene | 5 | 2/5 |
| ICE1 — the 2,266-residue scaffold of the little elongation complex, the subunit that acts at initiation, and zero papers connecting it to leukaemia of any kind | Protein | 7 | 3/5 |
| ICE2 — the fourth LEC subunit, the one with no assigned step, no structure, and no leukaemia literature | Protein | 5 | 3/5 |
| ICOSLG on infant t(4;11) blasts converts T cells into regulatory T cells - the one immune-evasion route measured in this exact disease, in this exact age group | Mechanism | 2 | 3/5 |
| Icovamenib (BMF-219) — the covalent menin inhibitor that left oncology for diabetes | Drug | 4 | 2/5 |
| ID1 - the only OTHER named factor whose requirement for a KMT2A fusion depends on cell of origin: needed in fetal-liver-derived MLL-AF9 leukaemia, actively restraining in bone-marrow-derived | Gene | 3 | 3/5 |
| IDH and TET2 mutations are mutually exclusive in AML - so 'IDH2 enriched, TET2 depleted' in one cohort is ONE observation, not two | Mechanism | 2 | 3/5 |
| IDH1 - the same oncometabolite, the same assay, and NO enrichment in KMT2A-rearranged AML (6.7% vs 7.6%, p = 0.53): the control that makes the IDH2 result interpretable | Protein | 7 | 4/5 |
| IDH2 - the hypermethylating co-mutation that IS enriched in KMT2A-rearranged AML (16.0% vs 10.4%), at p = 0.0004 and not the p < 0.0001 the abstract claims | Protein | 8 | 3/5 |
| If HOXA9 substitutes for BMI1 at CDKN2A, then a menin inhibitor should CREATE a BMI1 dependency that does not exist at baseline | Hypothesis | 4 | 1/5 |
| If inhibiting one methyltransferase failed, constraining the methyl donor may not | Hypothesis | 1 | 0/5 |
| If RPA loading at the KMT2A breakpoint cluster region is the licensing step for the etoposide-induced translocation, then the nuclear RPA reserve is a modifier of therapy-related KMT2A-rearranged leukaemia risk - and an ATR inhibitor, which kills by exhausting RPA, would raise that risk rather than lower it | Hypothesis | 3 | 1/5 |
| If the fusion's address requires unmethylated CpG, a hypermethylating co-mutation should be selected AGAINST - and IDH2 is selected FOR, which means the address is not the limiting resource | Hypothesis | 5 | 1/5 |
| If the target promoter set is no more conserved within a patient than between patients, then nothing in the oncoprotein complex remembers the first disease | Mechanism | 2 | 3/5 |
| IFNGR1 - the receptor the whole antigen-presentation mechanism runs through, and the one where low-dose interferon-gamma makes MLL-fusion leukaemia worse | Gene | 6 | 3/5 |
| Ig-based MRD fails specifically in the KMT2A-rearranged patients whose IGH repertoire is proximally biased and still recombining | Hypothesis | 5 | 1/5 |
| IGF2BP1 — the IMP paralogue that belongs to a DIFFERENT fusion, and the cleanest control the family offers | Gene | 6 | 3/5 |
| IGF2BP2 — the paralogue co-over-expressed with IGF2BP3 in MLL/AF4 B-ALL, and the one with an inhibitor in another leukaemia | Gene | 9 | 3/5 |
| IGF2BP3 — an RNA-binding protein required for MLL-Af4 leukaemogenesis in mice that CRISPR barely touches in human lines | Gene | 11 | 0/5 |
| IGF2BP3 marks the fetal programme AND is required for B-ALL survival - the trap is not expression-for-requirement, it is requirement-for-state-maintenance | Explainer | 4 | 3/5 |
| IGF2BP3 works in cytoplasmic RNA granules - the only compartment in this beat where a drug is already pointed, and nobody has looked at it in a leukaemia cell | Mechanism | 5 | 3/5 |
| IgG passes this project's occupancy gate at TWICE the rate of the fusion antibody - because the gate is normalised to each library's own promoter mean and IgG has almost none | Explainer | 2 | 4/5 |
| IKBKB (IKK-beta) — the kinase whose knockdown tracks MLL-leukaemia growth most tightly, and whose inhibitors have failed clinically for a reason | Protein | 4 | 4/5 |
| IKBKG (NEMO) — the scaffold that makes the canonical complex a complex, and a symbol that returns ZERO records in this disease | Protein | 4 | 3/5 |
| IKK inhibition and menin inhibition evict the fusion from chromatin by routes that do not share a node, so they should be additive — and the same reasoning predicts that a menin inhibitor alone partially defeats itself. Prior 0.30 | Hypothesis | 4 | 1/5 |
| IKK/NF-kB retains MLL on chromatin — BOTH the fusion and wild-type MLL, at two promoters, in mouse myeloid AML, and it is occupancy loss rather than protein loss | Mechanism | 3 | 4/5 |
| IKZF1 - the defining co-lesion of every other high-risk B-ALL, and this disease does not use it until after treatment | Gene | 4 | 3/5 |
| IKZF3 / Aiolos (Q9UKT9) - the B-lymphoid transcription factor that goes UP under both inhibitors, regulates BCL2, and is a degradable drug target | Gene | 6 | 3/5 |
| IL-1/IRAK1/4 — the receptor-proximal input the MLL screen actually pointed at, with an Il1r1 knockout in MLL-AF9 mice and an inhibitor that spares normal stem cells | Mechanism | 4 | 3/5 |
| IL3RA / CD123 - not just a myeloid target: the quartile of CD123 expression that carries the KMT2A rearrangements is the quartile that dies | Gene | 5 | 4/5 |
| ILF3 / NF90 - a nucleolar dsRNA-binding coactivator whose chromatin residency was mapped in the same leukaemia line that proximity-labelled KMT2A | Protein | 8 | 3/5 |
| Imatinib: one molecule, three unrelated rare diseases, twenty years of cross-subsidy | Explainer | 4 | 5/5 |
| Immunoprecipitate the KMT2A fusion and map its phosphosites - the experiment this whole field has never done | Experiment | 2 | 3/5 |
| IMPDH2 - the rate-limiting guanine-nucleotide enzyme whose inhibition lowers LEDGF and menin protein and dismantles the MLL-fusion complex itself | Protein | 9 | 4/5 |
| Import class 1: murine MLL-AF9 myeloid transformation, the field's default assay and this graph's largest single import | Explainer | 6 | 4/5 |
| Import class 2: AHD-dependent mechanism, which cannot transfer because KMT2A::AFF1 has no AHD | Explainer | 6 | 4/5 |
| Import class 3: the DOT1L-AF10 coiled-coil axis, an MLLT10 mechanism with no counterpart in the index fusion | Explainer | 6 | 4/5 |
| Import class 4: human myeloid cell lines standing in for infant B-lymphoid disease | Explainer | 4 | 3/5 |
| Import class 5: evidence borrowed from fusions that are not KMT2A fusions at all | Explainer | 5 | 3/5 |
| IMSUTi002-A-2 (CVCL_C9HE) — a doxycycline-inducible KMT2A::AFF1 iPSC line, and the isogenic design nobody in this graph has used | Explainer | 2 | 3/5 |
| In 18 of 27 patient samples, comparing two antibodies raised against the SAME end of KMT2A calls at least as many oncoprotein-target promoters as the real N-over-C comparison does, and swapping the antibody pair moves a sample's own call count by a median of 2.57x | Analysis | 2 | 4/5 |
| In a cell with no fusion, a menin inhibitor is substantially a KMT2B drug | Hypothesis | 4 | 1/5 |
| In a competitive menin-binding scaffold with assumed rates, the drug exposure needed scales with menin relative to the fusion-menin Kd, and whether recovery after a lapse lags collapse is governed by the drug's residence time - a conditional counter-lead to the pulsed-dosing premise, not a prediction | Analysis | 3 | 2/5 |
| In a live mouse, losing menin in bone cells means less bone - and menin overexpression means more | Risk | 2 | 4/5 |
| In a patient, the menin-fusion association is demonstrable before the drug and unmeasurable after it - and the asymmetry is what this pair establishes, not a rate of menin loss | Mechanism | 3 | 3/5 |
| In a PCGF1-knockout clone the menin inhibitor still evicts and the vacated sites are still silenced, but LESS: H2AK119ub at the most-evicted quartile falls from 1.4450 to 1.1325 and from 1.0151 to 0.8842 in two replicate conventions, and H3K27me3 from 2.0007 to 1.0134 - so prediction 5's silencing clause is directionally right and quantitatively overstated | Analysis | 2 | 3/5 |
| In all 24 read-queue rows inspected, the candidate is the BAIT and this project's protein is the prey - nobody has ever tagged KMT2A, AFF4, menin or PSIP1 and found any of them; plus seven bounded rejections | Analysis | 5 | 4/5 |
| In an unsupervised 5 kb correlation of 41 SEM libraries, both KMT2A N-terminal AutoCUT&RUN libraries have menin as their single nearest neighbour - the menin-interface hypothesis appearing as the top-level structure of an analysis that was not looking for it | Analysis | 3 | 3/5 |
| In childhood t(11;19), every lymphoblastic case was MLLT1 and every ELL case was myeloid - the one rule that lets an old cohort be de-contaminated | Epidemiology | 3 | 3/5 |
| In drug-naive primary infant KMT2A::MLLT1 B-ALL, menin is as enriched as the fusion N-terminus at the top fusion promoters (2.73x vs 3.12x over an accessibility reference) while the wild-type C-terminal reporter sits at background (1.10x) | Analysis | 3 | 3/5 |
| In human KMT2A::AFF1 MV4;11 (monocytic, not B-lineage), the vehicle-versus-vehicle noise floor is 9.4% at the top 0.1% of menin/MLL1 sites and 0.1-2.6% in every other stratum - so cycle 102's borrowed 4-10% band is about right AT THE PEAKS and four to five times too generous everywhere else, and it was applied everywhere | Analysis | 4 | 4/5 |
| In human MOLM13, DOT1L's own occupancy under a menin inhibitor runs 0.1364 / 0.3083 / 0.3555 / 0.3913 across MLL1-N eviction-depth quartiles at Spearman -1.000 - the writer is lost in proportion to eviction depth, and its mark follows with a 2.9-fold smaller span | Mechanism | 3 | 3/5 |
| In human RS4;11 (KMT2A::AFF1), menin occupancy at its own top 0.1% of 2 kb bins falls 14.9x to 2.0x over the track median and its share of total coverage falls to 0.200 - reproducing Q117's murine FLAG-MLLAF9 figures (15.9x to 3.0x, ratio 0.179) to within 1.3-fold on all five statistics | Analysis | 3 | 4/5 |
| In infant ALL, IRX1 transcript is enriched in KMT2A::AFF1 (21 of 48) and present but rare outside it (3 of 26) - so the occupancy zero outside AFF1 is not an expression zero | Analysis | 3 | 3/5 |
| In inv(16), disrupting the fusion interface swaps BRG1 for RING1B at three MYC enhancers - the cleanest version anywhere of the experiment nobody has run on menin | Analogy | 5 | 4/5 |
| In KMT2A::AFF1 there is no oncogenic DOT1L unit: all H3K79 methylation is the endogenous MLLT10-directed activity, working on genes the fusion has opened | Hypothesis | 5 | 1/5 |
| In leukaemia KMT2A gives the front of the protein; in sarcoma it gives the back. Every consequence follows from that. | Explainer | 6 | 4/5 |
| In MCF-7 the two signals point in opposite directions over the same 90 kb: H3K9me3 sits at the 15.8th and 10.3rd percentile of 56,171 same-cell CTCF anchors across the KMT2A gene body (0.82x and 0.65x the random-tile mean) while SUV39H1 sits at the 81.7th-86.8th in all four of its tracks - and the 147 bp anchor carries ZERO H3K9me3 in the minus-estradiol track | Analysis | 2 | 3/5 |
| In MOLM13 a menin inhibitor removes three quarters of DOT1L from the fusion's own sites and leaves H3K79me2 there completely intact for three days - the writer and its mark are separable on this timescale, and in RS4;11 they are not | Mechanism | 1 | 3/5 |
| In MOLM13, human KMT2A::MLLT3, from the VTP-50469 founding paper's own series GSE127507, H3K79me2's aggregate response at MLL1-N's top sites is 0.998 - and the same sites split by eviction depth run 0.7746 / 1.0601 / 1.0995 / 1.1421 at Spearman -1.000, with the INPUT stratified identically staying flat | Analysis | 3 | 3/5 |
| In murine MLL-AF9, H3K79me2's response to a menin inhibitor runs 0.586 / 0.819 / 0.928 / 1.187 across the four eviction-depth quartiles of the fusion's own top-0.1% sites - Spearman -1.000, span 0.6005, the largest of any mark measured in these bins except H3K27me3 - while the aggregate over the same 1,228 bins is a single unremarkable 0.8156 | Analysis | 8 | 3/5 |
| In murine MLL-AF9, knocking out PCGF1 changes the menin inhibitor's effect on H3K79me2 by 0.0166 of a share ratio and the DOT1L inhibitor's by 0.0101 - both smaller than the 0.0584 two control cultures of the same line already differ by, so the mark's drug response runs outside PRC1.1 | Analysis | 2 | 3/5 |
| In NUP98-rearranged leukaemia, who responds to a menin inhibitor is decided by the co-mutations, not by the fusion | Hypothesis | 5 | 1/5 |
| In pancreatic neuroendocrine tumours MEN1 and DAXX/ATRX are the two commonest mutations of the same tumour - and both are LOST there while leukaemia needs both intact | Analogy | 4 | 4/5 |
| In patient-derived H3K27M glioma, baseline H3K9me3 over the 7,466 bp KMT2A breakpoint cluster core sits at the 7.8th and 28.5th percentile of 59,821 width-matched CTCF-anchor windows (0.56x and 0.90x the random-tile median) - the methyl-poor-BCR pattern this graph found in epithelium and in a blood line, now in a third lineage and for the trimethyl state | Analysis | 3 | 3/5 |
| In SEM, H3K4me3 responds to menin displacement the way a partially redundant mark should: selectively at menin-bound sites, by about a quarter, and not at all under a DOT1L inhibitor - which bounds how much of a menin inhibitor's lethality H3K4me3 can be carrying | Mechanism | 4 | 3/5 |
| In SEM, the infant-derived KMT2A::AFF1 line, VTP-50469 lowers H3K4me3 at menin-bound sites by 23% relative to H3K4me3-matched menin-free sites (95% CI 13-33%), while the DOT1L inhibitor EPZ-5676 changes it by 1% (CI -4 to +6%) | Analysis | 4 | 3/5 |
| In St. Jude paediatric AML, 2 of the 6 ARID1A-mutant cases are KMT2A-rearranged and BOTH ARID1A mutations are TRUNCATING frameshifts in KMT2A::MLLT10 cases - so the exact combination cycle 86 showed the ARID1B dependency is confined to DOES occur in patients, and cycle 88's empty DepMap intersection is a cell-line sampling artefact rather than a fact about the disease. The paediatric ALL cohort returned zero ARID1A mutations, which is panel coverage and not biology | Analysis | 2 | 3/5 |
| In the deposit paper's own target-gene table, the AFF1-exclusive class is 64 genes against a permutation null of 2.3, and it survives call-rate matching, institution stratification, B-lineage restriction and patient collapse | Analysis | 3 | 4/5 |
| In the HOXA-dead infant states IRX1 carries H3K4me3 and ENL while HOXA9/HOXA10 carry neither | Analysis | 2 | 3/5 |
| In the human index fusion the menin inhibitor subtracts MENIN and leaves MLL1-N-reactive material in place at the same sites - so the drug's chromatin action is decoupling rather than eviction, and what this literature calls fusion eviction is a menin measurement | Hypothesis | 2 | 1/5 |
| In the only cohort that measured it, HOXA genes are ON in exactly the reciprocal-positive patients and OFF in the rest | Explainer | 3 | 3/5 |
| In the only panel that tested both halves of four translocations, 3 of 4 reciprocal fusions transformed and only 1 of 4 direct ones did | Explainer | 3 | 2/5 |
| In the only system where the fusion can be measured separately, a menin inhibitor removes MLL1 from wild-type-dominated sites harder than it removes the tagged fusion from its own sites - 0.1069 against 0.1793 - which is an on-target effect on normal KMT2A-menin complexes and an argument about toxicity nobody in this project has made from occupancy data | Analysis | 1 | 3/5 |
| In the revumenib-exposed relapse sample nothing is enriched above a non-specific reference - not menin, not the fusion N-terminus, not ENL - and the sample's own top-ranked promoters are mitochondrial pseudogenes | Analysis | 3 | 3/5 |
| In the same deposit, the MENIN inhibitor removes DOT1L from all five DMSO DOT1L peaks at canonical target loci (p = 0.0432) while all three DOT1L inhibitors keep 5/5 - and the VTP DOT1L library still calls ACTB, GAPDH and EEF1A1, which is the internal positive control the MEN1 arm lacks | Analysis | 3 | 3/5 |
| In the VTP-50469 timecourse Q124 declared uninterpretable, the eviction-gradient SPAN grows monotonically 0.104 / 0.198 / 0.214 / 0.335 at 4/8/16/24 h with Spearman -1.000 at every timepoint - while the aggregate it was suppressed for is non-monotone and perfectly anti-correlated with library complexity. The span is better behaved, and it is NOT clean. | Analysis | 3 | 2/5 |
| In this fusion family, MHC class I is not silenced - it is elevated and load-bearing, holding NK cells off the leukaemia stem cell | Mechanism | 5 | 3/5 |
| In-silico digest of 81 modelled KMT2A fusion junctions: the peptide that would prove the fusion protein exists | Analysis | 3 | 4/5 |
| In-utero origin, proven: clonotypic KMT2A::AFF1 junctions found in the patient's own newborn blood spot | Mechanism | 3 | 5/5 |
| Independent positive control: of 27 samples, the ONE that calls zero oncoprotein-target promoters is 152985 - the AML that arose during menin-inhibitor treatment, which the paper reports as having oncoprotein and menin reduced to undetectable levels | Analysis | 2 | 4/5 |
| Indexing abstracts for all 4,000 cited papers, the U2 that has bound the citation index since it was built - 98.9% retrieved, and across seven probe topics abstract search reaches 144 papers title search cannot see, including 54 single-cell papers and 25 CRISPR screens | Analysis | 1 | 4/5 |
| Indexing every deposit this corpus cites - 504 accessions, 102 GEO series, all 102 resolving - because the citation index repaired last cycle indexes papers only, and half the known absence failures were refuted by a dataset rather than by a paper | Analysis | 1 | 4/5 |
| Indexing every PMID in every entry - CORRECTED to 4,000 distinct papers across 2,411 entries after the original regex was found to miss 73.7% of them by matching prose but not the schema's own citation field, an undercount that made this entry declare a gap the corpus refuted 14 times over | Analysis | 1 | 3/5 |
| Induction chemotherapy phospho-inactivates KMT2A fusions through PIKK sites the partner retains - and a DNA-PK or ATM inhibitor would block that | Hypothesis | 4 | 1/5 |
| Infant acute lymphoblastic leukaemia (ALL diagnosed under 1 year of age) | Disease | 6 | 5/5 |
| Infant BCP-ALL (n=175): KMT2A::AFF1 2-year EFS 36% versus 37% for every other partner (P=0.9) | Epidemiology | 3 | 3/5 |
| Infants are not small children - four maturing organ systems, three conditioning drugs, and a protocol that treats the first year of life as one category | Explainer | 4 | 3/5 |
| Infants whose leukaemia expresses the reciprocal fusion survive far better - 62.4% versus 11.7% event-free at four years | Epidemiology | 5 | 4/5 |
| ING2 - the PHD finger that reads H3K4me3 and turns it into REPRESSION, and whose founding co-crystal is filed under the MOUSE accession | Protein | 7 | 3/5 |
| Instrument check before any conclusion: reading a browser-track .tdf with a hand-written binner and ranking the result blind returns the Hoxa cluster in five of the top twenty bins, plus Meis1, Jmjd1c, Six1, Arid2, Ncor1 and Tsc22d2 - the canonical MLL-AF9 programme, which is what the track claims to be | Analysis | 3 | 5/5 |
| Instrument check: the top thirty RS4;11 MLL1-N 2 kb bins recovered from a deposited .tdf are JMJD1C (259x the genome median), ZMYND11, BAHCC1, CDK6, MYB, RUNX2, IGF2BP2, FOXP1, SATB1 and ARID1B - canonical KMT2A::AFF1 targets, annotated only against the series' own RefGene windows | Analysis | 1 | 4/5 |
| IntAct curates 47 interactions against engineered MLL fusion proteins, and every accession-keyed query in this project is blind to all of them - while its PSICQUIC mirror stops at 2024 | Analysis | 6 | 4/5 |
| IntAct curates SEVEN MLL fusion proteins as first-class interactors - ENL, AFF4, AF9, GAS7, ELL, AF6 and CALM - and not the index one | Analysis | 4 | 3/5 |
| IntAct holds 51 interaction records whose participant IS a KMT2A fusion across 6 constructs, our coverage instrument dropped every one of them silently, and closing the single gap they contained took the partner list to 21 of 21 | Analysis | 1 | 3/5 |
| Intact PTH rises in 34% of patients on revumenib, and hyperparathyroidism is on the label | Risk | 3 | 3/5 |
| Interactome round 4: what was counted, what was written, what was rejected, and the two alias traps this beat fell into and caught | Analysis | 6 | 3/5 |
| Interactome round 5: 42 queries, 13 entries written, 9 candidates rejected with counts, and four alias failures of four different kinds | Analysis | 8 | 3/5 |
| Interfant-06 — 651 infants, and the definitive answer that myeloid-style consolidation does not help | Trial | 2 | 4/5 |
| Interfant-21 (NCT05327894) — the randomised test of blinatumomab in infant KMT2A-rearranged ALL, open now | Trial | 2 | 4/5 |
| Interfant-99 — the first global infant ALL protocol, and the first negative answer on myeloid intensification | Trial | 2 | 4/5 |
| Interfant-99 and Interfant-06: what they report about partners, and what they do not | Epidemiology | 3 | 3/5 |
| Irreversible femoral growth-plate closure in juvenile rats: the label already tells paediatricians to watch growth | Risk | 1 | 4/5 |
| IRX1 — Iroquois homeobox 1, the gene that names the HOXA-negative half of infant t(4;11) ALL | Gene | 5 | 3/5 |
| IRX1 binds the MLL-AF4 complex non-competitively — menin, LEDGF and DOT1L are all unchanged | Mechanism | 2 | 3/5 |
| IRX1 carries the KMT2A::AFF1 oncoprotein in exactly the patients where HOXA does not — seven patients, GSE252378 | Analysis | 4 | 3/5 |
| IRX1 CUT&RUN in primary t(4;11) blasts — testing Kühn's HEK293T mechanism where it matters | Experiment | 3 | 3/5 |
| IRX1 expression in KMT2A-rearranged paediatric AML is a FAB-M7 megakaryoblastic property, not a fusion property: 13 of 20 M7 versus 2 of 96 M5, and non-KMT2A-r M7 is 54 of 97 | Analysis | 3 | 3/5 |
| IRX1 fusion occupancy is confined to KMT2A::AFF1: 0 of 18 samples across five other partners | Analysis | 4 | 3/5 |
| IRX1 is a second address for the KMT2A::AFF1 oncoprotein, not merely the gene that turns HOXA off | Hypothesis | 2 | 1/5 |
| IRX1 is reported as expressed in AML subsets, so its absence from oncoprotein occupancy outside KMT2A::AFF1 is not an absence of IRX1 | Analysis | 3 | 3/5 |
| IRX1 occupancy is a lineage-switch cell state, and in GSE252378 it is confounded with the AFF1 partner and one institution | Hypothesis | 2 | 2/5 |
| IRX1 occupancy under PARTIAL menin inhibition in KMT2A::AFF1, with a spike-in, because complete eviction destroys the readout | Experiment | 1 | 3/5 |
| IRX1 sits in the 2-of-8 tier - two different patients, not the same one twice - and is not in the recurrent core | Analysis | 2 | 4/5 |
| IRX1 status is set by the cell of origin, and the fusion partner predicts it only because different partners transform different cells - so the partner supplies no IRX1 address | Hypothesis | 3 | 1/5 |
| IRX1's own three-sample pattern is p = 0.022 naively and 0.077-0.176 once patients, institution or lineage are held fixed - the class it belongs to is significant, IRX1 alone is not | Analysis | 3 | 4/5 |
| IRX2 - the IRX-cluster neighbour that is this disease's own prognostic gene, activated only in KMT2A::AFF1, and never written here until now | Gene | 4 | 3/5 |
| IRX2 IS fusion-occupied at gene-body scale in p454 - and q151's promoter-scale zero of 27 turns on one replicate 5% below the threshold, which two other instruments put above it | Analysis | 3 | 3/5 |
| IRX2 is not fusion-occupied at promoter scale in GSE252378: 0 of 27 samples, against a null of 2.73 | Analysis | 3 | 3/5 |
| IRX2 transcript is NOT AFF1-confined: re-deriving GSE68720 finds 1 of 16 KMT2A::MLLT1 infants positive, and that case is IRX2-positive with IRX1 off | Analysis | 2 | 4/5 |
| IRX2-DT (C5orf38) - the divergent partner 215 bp from the IRX2 TSS that makes every 2 kb IRX2 window ambiguous | Gene | 3 | 3/5 |
| Is any histone chaperone selectively required in KMT2A-rearranged leukaemia? Twenty-nine genes, lineage-split - and the answer is no, with one number worth a null and a positive tail nobody expected | Analysis | 3 | 3/5 |
| Is BENC even on in the disease this project is about? A module-resolved accessibility and deletion map in KMT2A::AFF1 B-lineage cells | Experiment | 5 | 1/5 |
| Is fusion intended in biology sometimes? Yes, and the answer has a strategic edge | Explainer | 5 | 5/5 |
| Is IRX1 expressed in normal blood at all? Two of the three papers say no, one says exclusively yes | Analysis | 3 | 2/5 |
| Is KMT2A::AFF1 leukemia epithelial or endothelial? No — it is haematopoietic. But the question is a good one | Explainer | 12 | 4/5 |
| Is menin an SCF-FBXW7 substrate? A one-week immunoblot and a free desk scan that settle Arm A | Experiment | 3 | 1/5 |
| Is MYC the node? Two papers, the same MLL-AF9 model, opposite answers - and the second one failed to rescue | Mechanism | 4 | 3/5 |
| Is reciprocal status or breakpoint position used in MRD design or risk stratification? Once, by necessity, in 16 of 3,401 patients - and nowhere in any risk model | Explainer | 5 | 3/5 |
| Is the CpG address a contested resource? On current evidence, no - and the beat that went looking says so | Hypothesis | 8 | 1/5 |
| Is the drug target always in the retained half? An audit of the project's own framing | Mechanism | 4 | 3/5 |
| Is the menin interface a property of the fusion or of the blood? Test KMT2A::MAML2 thymoma | Experiment | 3 | 3/5 |
| Is the metabolic phenotype a consequence of the fusion programme or an independent dependency? The answer is that BOTH directions are published, and one of them points the other way entirely | Explainer | 7 | 3/5 |
| Is the selectivity just pan-essentiality? No: it explains 0.4% of the variance | Analysis | 1 | 4/5 |
| Is the YEATS asymmetry just intron geometry? Computed from hg38: the direction is explained, the magnitude is not, and both genes fail the same prediction | Analysis | 4 | 3/5 |
| Is TIFAB a direct RelB target? Two papers in the same MLL-AF9 system answer differently | Mechanism | 3 | 3/5 |
| ITGA4 (CD49d, the alpha-4 of VLA-4) - the niche adhesion subunit with an approved antibody and a 2026 KMT2A-r B-ALL xenograft result | Gene | 4 | 4/5 |
| ITGA4 (VLA-4) and NG2 — the niche-adhesion axis of KMT2A-rearranged B-ALL, and the one approved drug that hits it | Mechanism | 3 | 4/5 |
| Ivosidenib - the approved IDH1 inhibitor, recorded here so that nobody reaches for it: IDH1 is the paralogue that is NOT enriched in KMT2A-rearranged AML | Drug | 4 | 4/5 |
| JADE3 / PHF16 (Q92613) - the HBO1-complex scaffold with the strongest pan-fusion evidence in this beat, and an independent published contact with MLL | Gene | 4 | 3/5 |
| JAK1 - recruited and stabilised by AF10 fusions, and the kinase whose downstream STAT1 the class I effect of menin inhibition explicitly does not need | Gene | 8 | 3/5 |
| JAZF1 - a 243-residue zinc-finger protein that turned out to be a NuA4 subunit, and the 5' donor of the commonest endometrial-stromal-sarcoma fusion | Gene | 7 | 3/5 |
| JD-PI95 - a genetically encoded bridging peptide that drags AKAP95 to HSP70 and dissolves its condensates, with in vivo activity in THP-1 | Drug | 2 | 3/5 |
| JDI-12 - published as a JMJD1C inhibitor that preferentially kills KMT2A-rearranged leukaemia and spares cord blood, then used as 'KDM3i' to CREATE KMT2A rearrangements in cord-blood progenitors, by two papers that do not cite each other | Drug | 5 | 3/5 |
| JMJD1C / KDM3C - named in three entries of this graph as one of the only loci that loses fusion occupancy under a menin inhibitor, ranked 23rd of 17,728 for KMT2A-selective dependency in this project's own scan, with the strongest published shRNA effect in SEM - and no entry until now | Gene | 9 | 3/5 |
| JMY - one AP-MS row with AFF4, in HCT116 only, from a paper whose whole argument is that interactomes differ between cell lines | Protein | 4 | 2/5 |
| Johnson & Johnson / Janssen — bleximenib (JNJ-75276617): paediatric from age 2, but not infants, and the dedicated child study was withdrawn | Group | 5 | 4/5 |
| Join the KMT2A breakpoint archive to the Interfant MRD and outcome database, on patient | Analysis | 5 | 3/5 |
| Jolanta Grembecka & Tomasz Cierpicki (University of Michigan) — the chemistry that made the menin interface druggable | Group | 3 | 4/5 |
| JPLSG MLL-10 (n=90 infants): a 38-point EFS split built from age, CNS status and MRD, with the partner never entering the model | Epidemiology | 3 | 3/5 |
| Junction RT-PCR is the one routine assay in this disease that IS fusion-specific - and it is structurally blind to KMT2A* | Explainer | 3 | 4/5 |
| JUND - the AP-1 subunit menin holds down, and the one a menin inhibitor lets go | Gene | 10 | 5/5 |
| JUND liberation — the drug's mechanism of action and one of its mechanisms of resistance are the same event | Resistance | 5 | 4/5 |
| KANSL1 - the NSL scaffold, and the protein through which WDR5 binding to NSL and to MLL/COMPASS is mutually exclusive | Protein | 11 | 3/5 |
| KANSL2 - the second NSL subunit in the WDR5 structure, with one leukaemia record and a dependency profile that is the mirror image of a selective target | Protein | 6 | 2/5 |
| KAT2A / GCN5 - the SAGA catalytic subunit that reaches this disease through its complex rather than through its own symbol, and whose only chemical tool degrades its paralogue too | Gene | 10 | 3/5 |
| KAT2B / PCAF - named in an existing entry's own id and never written, and the only acetyltransferase in this graph whose substrate is a fusion partner protein | Gene | 9 | 3/5 |
| KAT5 / Tip60 - the acetyltransferase in the only direct KMT2A-fusion histone-variant result, and both fusions tested were myeloid | Gene | 7 | 3/5 |
| KAT6A / MOZ — the acetyltransferase that is a fusion oncogene in its own right | Gene | 2 | 0/5 |
| KAT7 / HBO1 — an enzyme, a leukaemia-stem-cell dependency, and an inhibitor already in a crystal | Protein | 6 | 4/5 |
| KAT8 (MOF) — a genuine KMT2A partner that binds the half of KMT2A the fusion discards | Protein | 3 | 4/5 |
| KAT8/MOF is not only a chromatin enzyme: a measured mitochondrial pool binds mtDNA, and the chromatin address depends on which complex it is in | Mechanism | 4 | 4/5 |
| KAT8/MOF sets the quiescence set-point of the blood stem cell - and its catalytic activity is separately required for MLL-AF9 leukaemia, which DepMap also cannot see | Mechanism | 4 | 4/5 |
| Kathrin Bernt (University of Pennsylvania / Children's Hospital of Philadelphia) — DOT1L and H3K79 methylation in KMT2A-rearranged leukemia | Group | 3 | 3/5 |
| KDM1A (LSD1) — acts at the loci the fusion binds, spares normal stem cells, and still has never been shown to touch the fusion protein | Protein | 4 | 4/5 |
| KDM2A - the CXXC reader that antagonises KMT2A leukaemogenesis, and displaces wild-type MLL rather than the fusion | Protein | 6 | 3/5 |
| KDM2B — 513 potent ChEMBL rows that are mostly patent bins, and no structure of the domain they claim to inhibit | Protein | 10 | 3/5 |
| KDM2B, the PRC1.1 CpG-island recruiter, sits at the 99.7th percentile of its own distribution on the fusion's strongest sites in DMSO and does not gain share under either a menin inhibitor or a DOT1L inhibitor - it holds position while comparable bins drift down | Analysis | 3 | 3/5 |
| KDM3B - the H3K9me1/2 demethylase that sits on the KMT2A breakpoint cluster region and keeps it from rearranging, and the only leukaemia gene in this graph whose direction of effect flips between the myeloid and the lymphoid literature | Gene | 11 | 3/5 |
| KDM4B (JMJD2B) - the weakest of the four H3K9me3 demethylases, one of the two erasers knocked down in the only KDM4-perturbation arm in any archive that touches this mark | Gene | 3 | 3/5 |
| KDM4C (JMJD2C/GASC1) — recruited by the retained KMT2A N-terminus, drugged in a KMT2A::AFF1 line, and invisible to CRISPR | Protein | 11 | 3/5 |
| KDM5A (JARID1A / RBP2 H3K4 demethylase) domain architecture | Protein | 1 | 4/5 |
| KDM5A / JARID1A / RBP2 (P29375, 1,690 aa) - already in this graph as the 3' half of NUP98::KDM5A and never written as a gene: the H3K4 demethylase CTCF recruits to a break, the only ERASER in the licensing cascade, and the one cascade member with no blood-lineage ChIP-seq anywhere | Gene | 5 | 3/5 |
| KDM6A / UTX — a commonly asserted KMT2A partner that belongs to a different complex and points the opposite way | Protein | 9 | 4/5 |
| KDM6B (JMJD3) - UTX's paralogue, which this graph has argued about for cycles without writing | Gene | 6 | 3/5 |
| Kerry 2017's 'sufficient but not necessary' is a figure title with no experiment behind the second half - and the paper's own knockdowns run the other way | Analysis | 3 | 4/5 |
| KHDRBS1 (Sam68) — an RNA-binding protein that holds the MLL-AF4 message DOWN, a class no dropout screen can find | Gene | 10 | 3/5 |
| KHDRBS2 (SLM1) — a counted absence: zero leukaemia records over five aliases, in a family that regulates the MLL-AF4 message | Gene | 4 | 2/5 |
| KHDRBS3 (SLM2/T-STAR) — the third STAR paralogue, also zero leukaemia records, also flat in DepMap | Gene | 4 | 2/5 |
| Kinase/PI3K/RAS pathway activation — the only common co-lesion class in KMT2A-r leukemia, and it is mostly subclonal | Pathway | 7 | 4/5 |
| King verification of Q154: the AFF1-exclusive target class survives every stratification and a different seed, and IRX1 individually does not - the partner signal is real at the class level and gone at the gene level | Analysis | 3 | 4/5 |
| King verification of q181: the epigenetics field is NOT hollow (1 of 218 empty), the mark regex has three further blind spots including chromatin accessibility in 25 entries, and my own attempted correction of q181 was wrong | Analysis | 3 | 4/5 |
| KIT / CD117 - the most myeloid-specific antigen in the lineage-assignment panel, and the mutation that is mutually exclusive with KMT2A rearrangement | Gene | 4 | 3/5 |
| KITLG (stem cell factor) - the niche ligand of KIT, zero mentions anywhere in this graph, and its own symbol collides with the SCF ubiquitin ligase this corpus talks about constantly | Gene | 4 | 3/5 |
| KMT2A / MLL1 — the gene that breaks | Protein | 19 | 5/5 |
| KMT2A 747-755 on HLA-B*07:02: a phosphoneoantigen from the half of KMT2A every fusion keeps, with seven crystal structures and a cognate TCR | Interface | 3 | 4/5 |
| KMT2A and several of its fusion partners occupy the same spatial cluster in individual nuclei before any break occurs — single-cell diploid Hi-C, RUNX1-dependent, and 3D architecture does NOT predict which fusion type a cell will make | Mechanism | 2 | 3/5 |
| KMT2A exon 11 / intron 11 breakpoints (BCR subregion C): the infant, HOXA-low, topoisomerase-II-associated break | Breakpoint | 4 | 3/5 |
| KMT2A intron 9 / exon 9 breakpoints (BCR subregion A): the HOXA-high, older-patient break | Breakpoint | 4 | 3/5 |
| KMT2A is a 14-3-3 client by proxy: the contact is on an AFF-family scaffold, not on KMT2A | Hypothesis | 2 | 1/5 |
| KMT2A is called an H3K4 methyltransferase, and it is required for the mark at under 5% of the promoters that carry it | Mechanism | 2 | 4/5 |
| KMT2A K1130 acetylation - the clock-controlled, SIRT1-erased site that every KMT2A fusion retains, 17 residues from the CXXC and 208 from the breakpoint | Mechanism | 4 | 4/5 |
| KMT2A K1130 ubiquitination - the same retained lysine as the clock acetylation site, carrying a chemically exclusive second mark that no KMT2A paper has ever mentioned | Mechanism | 3 | 3/5 |
| KMT2A K1133 acetylation - the better-evidenced half of the pair, and the one that appears in the CBP/p300 acetylome itself | Mechanism | 3 | 4/5 |
| KMT2A K1235 acetylation - inside the SIRT1-interaction region, retained, and the one member of the Choudhary quartet the source paper named and then never assayed | Mechanism | 3 | 3/5 |
| KMT2A K1364 SUMO - the one modification site inside the breakpoint cluster, retained in some patients' fusion proteins and lost in others | Mechanism | 2 | 2/5 |
| KMT2A K2528 SUMO2 - the single best-supported modification site on the whole protein, in the N320 fragment, and LOST in every fusion | Mechanism | 2 | 3/5 |
| KMT2A K636 acetylation - the forgotten member of the Choudhary quartet, retained, and outside the SIRT1-interaction region | Mechanism | 3 | 3/5 |
| KMT2A major breakpoint cluster region (BCR1): intron 7 - exon 13, ~8.3 kb | Breakpoint | 3 | 5/5 |
| KMT2A minor breakpoint cluster region (BCR2): intron 20 - exon 24 | Breakpoint | 5 | 3/5 |
| KMT2A partial tandem duplication: an addition that only works once the normal copy has been switched off — 'recessive gain-of-function' | Mechanism | 4 | 4/5 |
| KMT2A rearrangement creates a requirement for the FA ubiquitin-transfer module — the claim, its prior, and the four results that would kill it | Hypothesis | 6 | 1/5 |
| KMT2A sits in the 14-3-3 proximity neighbourhood, and the YWHAG link reproduces across two independent studies | Analysis | 3 | 3/5 |
| KMT2A-ABT1 is one spoke-expanded BioPlex 3.0 AP-MS row in HEK293T in which ABT1 is the bait and KMT2A the prey, and ABT1's nucleolus is ECO:0000250 only - declined | Interface | 4 | 2/5 |
| KMT2A-AKAP8 (AKAP95): graded 'prey-only' by this project, and it is a direct positive modulator of MLL H3K4 methyltransferase activity from a dedicated MLL paper - ADMITTED | Interface | 4 | 3/5 |
| KMT2A-ANOS1 is one spoke-expanded BioPlex 3.0 AP-MS row with ANOS1 - a secreted, cell-membrane axon-guidance protein - as the bait and KMT2A as the prey in HEK293T - declined | Interface | 4 | 2/5 |
| KMT2A-CLOCK: one paper, six IntAct records, and the bait/prey grade splits it down the middle - CLOCK falls in the discard bin and SIRT1 does not, from the same experiments | Interface | 3 | 2/5 |
| KMT2A-DRC5 - DECLINED. A ciliary dynein-regulatory-complex protein, recovered by BioID in a centrosome-cilium map, and the only one of 135 uncovered partners never mentioned anywhere in this corpus | Interface | 3 | 2/5 |
| KMT2A-EN1 declined: one spoke-expanded BioID row from an ectopic neural homeobox construct in a kidney cell, and the only screen that ever looked found EN1 unexpressed in AML lines | Interface | 5 | 3/5 |
| KMT2A-FGFBP1 is spoke-expanded BioPlex 3.0 AP-MS recovered in BOTH HEK293T and HCT116 - it passes BioPlex's own replication criterion and the partner is a secreted extracellular protein - declined | Interface | 3 | 2/5 |
| KMT2A-HMGN5: recovered by endogenous CRISPR tagging in OpenCell, not by over-expression - a chromatin-decompacting nucleosome binder with a real reason to be near KMT2A | Interface | 3 | 2/5 |
| KMT2A-KLHL22 - DECLINED. The single source is a cryo-EM structure of KLHL22-CUL3 bound to glutamate dehydrogenase, and KMT2A is a HEK293F pull-down passenger with no nuclear rationale | Interface | 3 | 2/5 |
| KMT2A-KRR1 is one spoke-expanded BioPlex 3.0 AP-MS row in HEK293T with KRR1 as bait and KMT2A as prey, sitting in a seven-member ribosomal block at the floor score - declined | Interface | 4 | 2/5 |
| KMT2A-N CUT&RUN in an untreated non-AFF1 lineage-switching blast: the one experiment that separates partner from cell state | Experiment | 1 | 3/5 |
| KMT2A-N/C CUT&RUN on one untreated KMT2A::AFF1 blast from outside Texas Children's, scored at the six AFF1-exclusive gene bodies with a pre-declared margin column | Experiment | 2 | 3/5 |
| KMT2A-OASL is one spoke-expanded BioPlex 3.0 AP-MS row with OASL as bait and KMT2A as prey; OASL is the only partner in the beat natively expressed in blood leukocytes, and its nucleolar annotation is uncoded - declined, with the compartment argument unavailable | Interface | 3 | 2/5 |
| KMT2A-PRKRA is one spoke-expanded BioPlex 3.0 AP-MS row with PRKRA (PACT) as bait and KMT2A as prey; PRKRA's only UniProt compartments are cytoplasm and perinuclear region, both uncoded - declined | Interface | 3 | 2/5 |
| KMT2A-rearranged acute leukemia across all ages: infants are 4% of it | Epidemiology | 5 | 3/5 |
| KMT2A-rearranged acute lymphoblastic leukaemia | Disease | 4 | 4/5 |
| KMT2A-rearranged acute myeloid leukaemia in children and infants | Disease | 4 | 4/5 |
| KMT2A-rearranged AML is two diseases on the phosphorylation layer, and DOT1L phosphorylation is one of the things that separates them | Analysis | 1 | 3/5 |
| KMT2A-rearranged cells need the factors retained through elongation MORE and the factors ejected at pause release LESS — a six-gene asymmetry nobody has reported | Hypothesis | 5 | 1/5 |
| KMT2A-rearranged or NPM1-mutant? Both, in separate arms: WT-MA9 mouse, MOLM13, OCI-AML3, and two patients on AUGMENT-101 | Analysis | 3 | 5/5 |
| KMT2A-rearranged soft tissue sarcoma - the same gene as infant B-ALL, in a young adult's leg, as a solid tumour | Disease | 6 | 4/5 |
| KMT2A-TMCO1 is a single DSSO crosslink in one detergent fraction of isolated U2OS nuclei with no bait on either side; TMCO1 is an ER-membrane calcium channel and the source paper attributes 4% of its links to nucleus-ER contamination - declined | Interface | 4 | 2/5 |
| KMT2A::ABI1 (MLL-ABI1), t(10;11)(p11.2;q23) — the partner that binds an elongation partner | Fusion | 8 | 3/5 |
| KMT2A::AFDN (MLL-AF6), t(6;11)(q27;q23) | Fusion | 6 | 4/5 |
| KMT2A::AFF1 (MLL-AF4), t(4;11)(q21;q23) | Fusion | 8 | 5/5 |
| KMT2A::AFF1 cells run with more free P-TEFb than other leukaemias - and if they do not, this graph's CDK9 story is about recruitment only | Hypothesis | 4 | 1/5 |
| KMT2A::AFF1 has had a published affinity-purification interactome since 2018 — in a paper titled for SETD2, uncurated by IntAct, and cited zero times here | Analysis | 3 | 4/5 |
| KMT2A::AFF1 has no mapped interface to DOT1L: it lacks both structurally defined recruitment modules, and the one complex-level route claimed for it is contested by reconstitution | Mechanism | 12 | 4/5 |
| KMT2A::AFF1 has no measured fusion-specific interactome: the one dataset that appears to supply one is a rank-selected tail in the wrong lineage, and the question is open rather than answered badly | Hypothesis | 2 | 3/5 |
| KMT2A::AFF1 needs a developmental window and a lymphoid-committed cell — the cell type is a condition of transformation, not a consequence of it | Mechanism | 5 | 3/5 |
| KMT2A::AFF1 oligomerises through the retained AFF1 CHD, putting the commonest fusion in the oligomerisation class | Hypothesis | 4 | 1/5 |
| KMT2A::AFF1 retains THD2 by position, so the HBO1 contact can apply to it — but the paper that established that contact tested MLL-ELL, MLL-AF6 and MLL-AF10, never the index fusion | Analysis | 2 | 3/5 |
| KMT2A::AFF1–LEF1 is one AP-MS row (p 0.0261, 10|8 spectra) in a Jurkat T-ALL host, where LEF1 is a resident lineage factor; it is the only one of the six AF4-specific candidates with non-zero negative-control signal, and no Wnt co-factor was co-recovered — declined | Interface | 4 | 2/5 |
| KMT2A::ELL (MLL-ELL), t(11;19)(q23;p13.1) | Fusion | 9 | 4/5 |
| KMT2A::ELL in adult AML: the one partner that separates, in two independent adult cohorts | Epidemiology | 3 | 3/5 |
| KMT2A::EPS15 (MLL-AF1p), t(1;11)(p32;q23) — the infant-ALL cytoplasmic partner | Fusion | 11 | 4/5 |
| KMT2A::GAS7 (MLL-GAS7), t(11;17)(q23;p13) — three patients, and the best mouse model in the partner class | Fusion | 7 | 4/5 |
| KMT2A::GPHN (MLL-gephyrin), t(11;14)(q23;q24) — the 15-residue counterexample | Fusion | 6 | 3/5 |
| KMT2A::MAML2 keeps MAML2's activation domain and loses its Notch-binding domain, and suppresses Notch output | Mechanism | 4 | 2/5 |
| KMT2A::MAML2 type B2/B3 thymoma - the same fusion, a different organ, a different disease | Disease | 5 | 4/5 |
| KMT2A::MAML2, inv(11)(q21q23) - a therapy-related fusion that also causes a solid tumour | Fusion | 10 | 3/5 |
| KMT2A::MAPRE1 (MLL-EB1) - a coiled-coil dimerisation fusion from pro-B ALL with a mouse model, low leukaemogenic potential, and Ets1 as its effector | Fusion | 2 | 3/5 |
| KMT2A::MLLT1 (MLL-ENL), t(11;19)(q23;p13.3) | Fusion | 6 | 4/5 |
| KMT2A::MLLT1 engages P-TEFb through one 66-residue surface: the ENL AHD, residues 494-559, and L550E breaks it | Mechanism | 5 | 4/5 |
| KMT2A::MLLT1 is high-risk in childhood AML and the best-outcome cell in childhood T-ALL: the partner effect changes sign with lineage | Epidemiology | 3 | 3/5 |
| KMT2A::MLLT1 outcome by age band: favourable in adult ALL, high-risk in childhood AML, and completely unstratified in the infants who are most of the disease | Epidemiology | 5 | 3/5 |
| KMT2A::MLLT1 versus KMT2A::MLLT3: paralogous partners whose chromosomes break on opposite sides of the same domain | Explainer | 3 | 4/5 |
| KMT2A::MLLT10 (MLL-AF10), t(10;11)(p12;q23) | Fusion | 6 | 4/5 |
| KMT2A::MLLT11 (MLL-AF1q), t(1;11)(q21;q23) — 28 patients, and not one functional experiment | Fusion | 7 | 3/5 |
| KMT2A::MLLT3 (MLL-AF9), t(9;11)(p21.3;q23.3) | Fusion | 6 | 5/5 |
| KMT2A::MLLT3 / t(9;11): the best-known partner prognosis claim, and the three cohorts that did not reproduce it | Epidemiology | 4 | 3/5 |
| KMT2A::MLLT3 across 612 genotyped patients: myeloid at every age, but 248 of them have ALL, and 157 of those are infants | Epidemiology | 6 | 4/5 |
| KMT2A::MLLT6 (MLL-AF17), t(11;17)(q23;q12-q21) — the bridge case: a leucine zipper on a DOT1L-complex subunit | Fusion | 6 | 3/5 |
| KMT2A::MYO1F, t(11;19)(q23;p13.2) — recurrent in infant AML, and never functionally tested | Fusion | 4 | 3/5 |
| KMT2A::SEPTIN11 (MLL-SEPT11) — the fusion that cytogenetically impersonates t(4;11) | Fusion | 5 | 3/5 |
| KMT2A::SEPTIN2 (MLL-SEPT2), t(2;11)(q37;q23) — the therapy-related septin | Fusion | 8 | 3/5 |
| KMT2A::SEPTIN5 (MLL-SEPT5 / MLL-hCDCrel-1), t(11;22)(q23;q11.2) | Fusion | 7 | 3/5 |
| KMT2A::SEPTIN6 (MLL-SEPT6), t(X;11)(q24;q23) and its cryptic insertion variants | Fusion | 8 | 4/5 |
| KMT2A::SEPTIN9 (MLL-SEPT9 / MLL-MSF), t(11;17)(q23;q25) | Fusion | 8 | 3/5 |
| KMT2A::TET1 (MLL-LCX), t(10;11)(q22;q23) — the fusion that throws away a second CXXC domain | Fusion | 4 | 3/5 |
| KMT2A::USP2 is invisible to karyotype and often to FISH, so these patients are misclassified as fusion-negative | Risk | 5 | 4/5 |
| KMT2A::USP2, inv(11)(q23.3q23.3) - the minor-BCR fusion that keeps the PHD fingers | Fusion | 13 | 3/5 |
| KMT2A::USP8, t(11;15)(q23;q21) - three patients, and the second instance of a deubiquitinase partner | Fusion | 5 | 2/5 |
| KMT2A's proximity promiscuity is BAIT-CLASS-SPECIFIC: it is recovered at twice its size-and-abundance prediction by RNA-binding-protein baits in a leukaemia cell and at exactly its prediction by transcription-factor baits in a kidney cell | Hypothesis | 2 | 1/5 |
| KMT2A*: a menin-blind, LEDGF-blind, SET-competent KMT2A protein made from out-of-frame reciprocal alleles | Protein | 4 | 3/5 |
| KMT2B (MLL2/MLL4) - the other protein menin binds, and the one this graph never wrote | Gene | 12 | 4/5 |
| KMT2B has no haematopoietic cell-state result, and two of the seven records that look like one are about a different gene in muscle | Analysis | 4 | 4/5 |
| KMT2B, AFF2, AFF3, AFF4 and ENL carry most of the contact residues of the two interfaces the fusion keeps (menin-KMT2A and AF9-AFF1), so a substitute is structurally possible and selectivity cannot be read from either surface; at the menin side KMT2B differs at W7 | Analysis | 3 | 3/5 |
| KMT2C (MLL3) - the fetal brake on MLL-rearranged leukaemia, and a 7q tumour suppressor chemotherapy selects against | Gene | 11 | 4/5 |
| KMT2D (MLL2/MLL4) - the gene named in this graph's menin-resistance entry, written here for the first time | Gene | 12 | 3/5 |
| KMT2E (MLL5) - the family member with a dead SET domain, and the exclusion from COMPASS is justified | Gene | 5 | 3/5 |
| Knock a tag-plus-degron cassette into the endogenous KMT2A::AFF1 allele in SEM - one construct that makes five claim classes attributable | Experiment | 5 | 3/5 |
| Knock down CDK13 and CDK12 side by side in lineage-matched KMT2A and non-KMT2A lines, and ask whether the DepMap signal is real | Experiment | 3 | 3/5 |
| Knock S395A into the MLLT3 half of a KMT2A::MLLT3 model and ask whether it becomes chemotherapy-resistant | Experiment | 2 | 3/5 |
| KOPB-26 (CVCL_7972): a t(9;11) B-ALL line from a 13-month-old, and the model for 42% of this partner's patients that nobody uses | Explainer | 6 | 3/5 |
| KOPN-8 (CVCL_1866): the field's default KMT2A::MLLT1 line, and its fusion protein has no YEATS domain | Explainer | 6 | 4/5 |
| Kotecha group, Perth: the infant KMT2A-rearranged laboratory this graph had cited once | Group | 6 | 4/5 |
| KPNA2 / importin-alpha-1 (P52292) - the classical NLS receptor in the pan-MLL-fusion core, and the ONLY karyopherin of any kind in the whole 960-protein network | Gene | 4 | 3/5 |
| KRAS - the commonest co-mutation in a disease that has almost none, and it is usually in a minority of the cells | Gene | 15 | 4/5 |
| KRAS as a co-mutation in KMT2A-r leukemia — the single most frequently co-mutated gene, and it still cannot start the disease | Gene | 6 | 4/5 |
| Kura Oncology — ziftomenib (KO-539): an adults-only sponsor that quietly supplies infant trials | Group | 8 | 4/5 |
| LAMP5 (BAD-LAMP) - a direct MLL-fusion target gene, a proposed immunotherapy antigen, and a brain protein | Gene | 4 | 4/5 |
| LAMP5 was proposed as an immunotherapy target for MLL-rearranged leukaemia without a normal-tissue filter; two atlases independently put it above 290 in the basal ganglia, and it is not partner-specific either | Analysis | 6 | 3/5 |
| LAMP5-directed therapy for KMT2A-rearranged leukaemia would meet the basal ganglia, in a disease treated in infants and routinely treated into the CNS | Risk | 4 | 3/5 |
| LAMP5, a surface antigen this project named as a fusion-enriched candidate, is 19.6x higher in normal cerebral cortex than in bone marrow - worse than every one of the 22 chromatin targets previously scored, including MEIS1 | Analysis | 1 | 3/5 |
| LARP7 - the clamp on the 3' end of 7SK, whose human loss-of-function phenotype is dwarfism and intellectual disability rather than cancer | Protein | 6 | 4/5 |
| LARP7's measured readout is P-TEFb release and Pol II CTD Ser2 phosphorylation, not a histone mark - and the one compound shown to act through it disrupts the particle rather than the protein | Mechanism | 2 | 3/5 |
| Last-exon indels that truncate the ZNF384 C-terminus phenocopy the fusion - so the fusion partner may not be the necessary element | Mechanism | 5 | 3/5 |
| Latency: months from the fusion forming in a fetus to leukaemia in an infant, against years or a decade for every other backtracked fusion | Epidemiology | 5 | 4/5 |
| LDB1 (Q86U70) - and the sarcoma fusion keeps the part that self-associates while losing the LIM interaction domain entirely | Gene | 3 | 3/5 |
| LDB1::KMT2A - the clearest statement in this literature that a sarcoma fusion keeps KMT2A exons 4 to 36 and discards exons 1 to 3 | Fusion | 5 | 3/5 |
| Ledger: every module the KMT2A half loses, with coordinates, how each was confirmed, and whether its loss has been shown to matter | Analysis | 13 | 4/5 |
| LEDGF as a survival factor rather than a tether: it is upregulated in chemoresistant AML blasts, protects against daunorubicin, and knocking it down sensitises MLLr lines | Mechanism | 4 | 3/5 |
| LEDGF does NOT hold the fusion on chromatin: knocking it down INCREASES fusion occupancy, and an IBD-binding-dead fusion still binds its targets | Mechanism | 3 | 4/5 |
| LEDGF IBD to KMT2A: TWO motifs, not one - IBM1 at 124-133 and IBM2 at 147-152, and the Kd this graph recorded as missing is 14.7 uM | Interface | 6 | 4/5 |
| LEDGF occupancy under revumenib: the measurement the graph called missing exists, in one 2025 preprint, and it goes the way the tenfold cooperativity predicts | Mechanism | 4 | 3/5 |
| LEDGF PWWP chemistry exists after all - 68 fragment hits, double-digit micromolar leads - and the pocket has a structural ceiling the NSD PWWPs do not | Target | 4 | 3/5 |
| LEDGF/p75 is required in the leukaemic cell and dispensable in ADULT MOUSE HAEMATOPOIESIS - not in the normal organism, which its germline knockout does not survive | Mechanism | 3 | 4/5 |
| LEF1 — the Wnt/β-catenin DNA-binding factor of the T-lineage, named as an MLL-AF4-specific interactor in a T-ALL cell line and with essentially no B-lineage or KMT2A literature | Gene | 5 | 3/5 |
| LEO1 — the weakest-evidenced entry in the PAF1 complex, and the gene whose Ensembl id this project already got wrong once | Protein | 5 | 2/5 |
| LEPR - the marker that defines the SCF-supplying perivascular niche cell, the receptor for an adipocyte signal that blunts cytarabine, and a gene_exact query that returns the wrong protein first | Gene | 4 | 3/5 |
| let-7 microRNA family (12 HGNC loci) - the effector LIN28B blocks. CORRECTED IN-SESSION: the headline 'zero papers in KMT2A leukaemia' was a NAME-LIST ARTEFACT; searching MLL instead of KMT2A returns three, one of them directly on point | Non-coding | 7 | 4/5 |
| Leukaemia cutis: the skin nodules that can be the first sign of infant leukaemia | Explainer | 4 | 3/5 |
| Leukaemia diagnosed in the first month of life: a different presentation and a different prognosis | Explainer | 6 | 4/5 |
| LIN28B - a one-row BioID prey of KMT2A that a 2026 Blood paper shows is REQUIRED for KMT2A::AFF1 to transform human fetal cells | Gene | 5 | 3/5 |
| LIN28B and IGF2BP3 are co-regulated members of ONE onco-fetal module in infant leukaemia - which strengthens the graph's existing scepticism about IGF2BP3 rather than weakening it | Explainer | 3 | 3/5 |
| LIN28B has THREE published signs in myeloid leukaemia - oncogene, tumour suppressor, and differentiation agent - and the design quality runs opposite to the direction the index-fusion story needs | Explainer | 5 | 3/5 |
| LIN28B has two routes - blocking let-7, and binding mRNAs directly - and in KMT2A::AFF1 every published mechanism is the direct-mRNA one (let-7 IS measured in mouse MLL-fusion AML: in-session correction) | Mechanism | 6 | 3/5 |
| LIN28B localization - a nucleolar pool that sequesters pri-let-7, a predominantly cytoplasmic steady state with cell-cycle-dependent nuclear entry, and NO measurement in any haematopoietic cell | Mechanism | 3 | 3/5 |
| LIN28B-dependent fetal B- and NK-lymphopoiesis - the NORMAL state the leukaemia requirement is parasitic on, and the reason the therapeutic window is narrow by construction | Cell state | 3 | 3/5 |
| Lineage drift - the partial state between B-ALL and AML, and the fact that nobody has published the ORDER in which markers change | Explainer | 5 | 3/5 |
| Lineage switch as a menin-inhibitor escape route — documented in a patient on revumenib, and invisible to every resistance-mutation screen | Resistance | 5 | 3/5 |
| Lineage switch as antigen escape from CD19-directed therapy in KMT2A-rearranged leukemia | Risk | 12 | 4/5 |
| Lineage switch in KMT2A-rearranged leukemia — the same clone changes what kind of blood cell it is | Mechanism | 10 | 4/5 |
| Lineage switch to myeloid leukaemia under CD19-directed therapy in ZNF384-rearranged ALL - and in the one cohort that caught both families, the ZNF384 switch looked mutationally NOTHING like the KMT2A ones | Risk | 5 | 3/5 |
| Lineage-split dependency for the round 5 panel: 23 genes, 2 myeloid-identity artefacts caught, and 3 survivors of which one has no literature at all | Analysis | 3 | 3/5 |
| Lineage-split DepMap: neither USP2 nor MAML2 is a dependency in KMT2A-rearranged lines, and USP22 is | Analysis | 2 | 3/5 |
| Live DepMap on fourteen genes: CDK6's pan-essentiality is a lineage artefact of pooling, and not one gene of the homeodomain cofactor code is a dependency anywhere | Analysis | 2 | 4/5 |
| LMNA - LEDGF is a prey of the nuclear-envelope MARKER bait, so this row is a statement about address, not about complex membership | Gene | 4 | 2/5 |
| LMO2 (rhombotin-2) - a bridging LIM-only protein, higher in pro-B and MLL-rearranged B-ALL, anti-selective in KMT2A-rearranged lines, and a physical partner of the KDM5A module that NUP98::KDM5A retains | Gene | 6 | 3/5 |
| Looking for a second handle on the retained fragment, and not finding one | Analysis | 3 | 0/5 |
| Losing the AF10 PZP reader is not a missing function - it is a removed brake, and putting it back cures the fusion | Mechanism | 4 | 4/5 |
| Lost from the KMT2A half: both taspase1 cleavage sites (D2666 and D2718) - the fusion is never processed | Mechanism | 9 | 4/5 |
| Lost from the KMT2A half: PHD2 (aa 1479-1533), an E3 ubiquitin ligase that limits KMT2A's own activity | Mechanism | 2 | 3/5 |
| Lost from the KMT2A half: PHD3 and the bromodomain are one cassette, not two modules (aa 1566-1765) | Mechanism | 4 | 4/5 |
| Lost from the KMT2A half: the four-residue HCF-binding motif (DHNY, aa 1799-1802) | Mechanism | 2 | 4/5 |
| Lost from the KMT2A half: the FYRN-FYRC clamp (2018-2074 / 3666-3747) that holds wild-type KMT2A together | Mechanism | 6 | 4/5 |
| Lost from the KMT2A half: the MOF/KAT8 contact - required in the cell, but not shown to matter to the fusion | Mechanism | 3 | 4/5 |
| Lost from the KMT2A half: the SET domain (aa 3829-3945) - the lost module whose loss demonstrably does not matter | Mechanism | 4 | 4/5 |
| Lost from the KMT2A half: the transactivation domain (aa 2829-2883) and its CBP contact | Mechanism | 5 | 4/5 |
| Lost from the KMT2A half: the WIN motif and the whole WRAD interface (aa 3762-3767, Arg3765) | Mechanism | 8 | 4/5 |
| Low-grade endometrial stromal sarcoma is a family of NuA4-acetyltransferase-to-Polycomb fusions, and that is why one of MBTD1's two fusions looks nothing like the other | Explainer | 7 | 3/5 |
| LPP (lipoma-preferred partner) - a KMT2A fusion partner in acute monoblastic leukaemia whose day job is adhesion mechanotransduction, and which is barely expressed in leukocytes | Gene | 5 | 3/5 |
| LRRK2 - the AFF4 row is one of 78 hits on an in-vitro protein array, but the protein has a real AML literature that arrived through USP7 and interferon, not through the interactome | Protein | 5 | 2/5 |
| LSD1/KDM1A inhibition — a differentiation therapy with real clinical pharmacodynamics and no randomised proof | Target | 2 | 3/5 |
| LUZP1 / fimbacin (Q86V48) - the weakest index-fusion call of the nine, and the strongest non-index call: p = 0.127 against MLL-AF4 and 2.6e-10 against MLL-ENL | Gene | 3 | 2/5 |
| LYAR (Q9NX58) - a zinc-finger nucleolar growth regulator cloned from a T-cell leukaemia line, in six of seven MLL-fusion interactomes, and the one member of this block whose discovery system is the same lineage as the AP-MS host | Gene | 5 | 2/5 |
| Lymphoid-primed multipotent progenitor (LMPP) — the bi-potent cell that explains how one fusion makes two lineages | Cell type | 5 | 3/5 |
| Lymphoid-style versus myeloid-style consolidation — the question asked twice in 1,100 infants, and answered no both times | Explainer | 4 | 4/5 |
| M-808 — a covalent menin-MLL inhibitor with a co-crystal, five years before the graph noticed it | Drug | 1 | 0/5 |
| MAML2 (mastermind-like 2) - the Notch co-activator that is a KMT2A partner in leukaemia and in thymoma | Protein | 8 | 3/5 |
| MAML2 exon 2: the strongly preferred 3' acceptor, the same in leukaemia, thymoma and salivary-gland tumours | Breakpoint | 6 | 3/5 |
| MAP3K14 (NIK) — the one node in this pathway where ACTIVATION, not inhibition, is the proposed therapy, and the one that also damages normal stem cells | Protein | 5 | 4/5 |
| MAP7D1 (Q3KQU3) - the strongest index-fusion p-value of the nine deferred pan-MLL-fusion preys, on a protein UniProt places entirely outside the nucleus | Gene | 3 | 2/5 |
| MAPK7 (ERK5) - a DOT1L partner on one 1:365 spoke of one atlas pulldown, and a kinase with real leukaemia literature that has never been connected to DOT1L | Gene | 4 | 2/5 |
| MAPRE1 / EB1 (Q15691) - a microtubule plus-end tracking protein that is BOTH a pan-MLL-fusion prey and a genuine KMT2A fusion partner in pro-B ALL | Gene | 3 | 2/5 |
| MAT2A - the enzyme that makes the methyl donor, and the one metabolic dependency in this disease with two independent papers and a lymphoid PDX result | Protein | 7 | 4/5 |
| MBD1 - one protein with a methyl-CpG reader and three CXXC fingers, only the third of which binds unmethylated CpG, and whose CXXC fails the MLL-AF9 swap | Protein | 7 | 3/5 |
| MBD3 (O95983) - the methyl-CpG-binding subunit that does NOT bind methylated DNA, and a validated KMT2A::AFF1-selective CRISPR vulnerability that is absent from every column of the pan-fusion interactome | Gene | 7 | 3/5 |
| MBM2, the second menin-binding motif of KMT2A (residues 23-40): 26-fold weaker than MBM1, never separately co-crystallised, and the only part of the menin grip a drug is not aimed at | Interface | 4 | 4/5 |
| MBTD1 - the H4K20me1/me2 reader inside NuA4/TIP60, the quiescence brake on adult haematopoietic stem cells, and the 3' partner of ZMYND11::MBTD1 whose methyl-lysine cage the fusion carries and does not use | Gene | 13 | 4/5 |
| MBTD1 is the effector-recruiting half of a leukaemia fusion and the addressing half of a sarcoma fusion while donating nearly all of itself to both - so the junction, not the parts, assigns the role | Analogy | 8 | 3/5 |
| MBTD1::EZHIP (MBTD1-CXorf67), t(X;17)(p11.2;q21.33) - MBTD1's other fusion, in which a NuA4 subunit delivers an H3K27M-mimicking PRC2 poison to low-grade endometrial stromal sarcoma | Fusion | 13 | 3/5 |
| MCL1 - named in 34 entries of this graph with no entry of its own until now; a mitochondrial survival protein high in infant KMT2A-rearranged ALL, druggable, and so far undruggable in patients | Protein | 10 | 4/5 |
| MCL1 plus BCL-2 plus dexamethasone: a triple combination that matched induction chemotherapy in infant PDX models | Target | 4 | 3/5 |
| MCM2 (P49736) - replicative helicase subunit and parental-histone chaperone in the pan-MLL-fusion core, and a live gene_exact collision with MCM7 | Gene | 4 | 3/5 |
| MEAF6 - a 191-residue subunit shared between the NuA4/TIP60 and MOZ/MORF acetyltransferase complexes, whose only two UniProt localisations both cite papers that are not localisation studies | Gene | 6 | 3/5 |
| Measure ABCA1, ABCG1 and SREBF1 before and during menin inhibition - a three-transcript panel on samples that already exist | Experiment | 2 | 1/5 |
| Measure all three H3K79 states on a real scale, across a dose series and after a menin inhibitor - the measurement this whole field has been doing by proxy | Experiment | 4 | 3/5 |
| Measure H3K27me3 after a menin inhibitor - the free pharmacodynamic nobody has read, and the one experiment that separates two mechanisms | Experiment | 4 | 1/5 |
| Measure H3R2 and H4R3 methylation states at KMT2A-fusion targets by isomer-resolving mass spectrometry, and test the gate by writer perturbation read out on the enzyme's product - the experiment that has never been done in any fusion | Experiment | 6 | 3/5 |
| Measure IRX1 transcript and KMT2A-N oncoprotein occupancy in the SAME KMT2A::EPS15 blast - the one cell where expression-without-occupancy is most likely and has never been paired | Experiment | 2 | 3/5 |
| Measure replication stress directly in KMT2A-rearranged cells instead of inferring it from a dependency ranking | Experiment | 5 | 3/5 |
| Measure the clearance clock directly: SNAP-tag H3.3 pulse-chase at KMT2A::AFF1 target genes, with and without DOT1L inhibition, in cycling and arrested cells | Experiment | 4 | 1/5 |
| Measure the free-versus-7SK-bound P-TEFb split in KMT2A::AFF1 cells - the experiment this whole beat turns on, which has never been done | Experiment | 5 | 3/5 |
| Measure the menin-KMT2B affinity nobody has measured, and the four clinical inhibitors' IC50 against it | Experiment | 5 | 3/5 |
| Measure the one number the whole YEATS-selectivity argument turns on: what fraction of ENL and of AF9 is in SEC, in SEC-L2, in SEC-L3 and free — with an exchange control, because the question may not be well posed | Experiment | 2 | 3/5 |
| Measure the pausing index at KMT2A::AFF1 target genes — the one number the whole pausing argument turns on, and it has never been reported | Experiment | 3 | 3/5 |
| Measure the RAS allele fraction in CSF blasts and in paired marrow blasts from the same infant on the same day | Experiment | 4 | 1/5 |
| Measured against a technical floor of 4-10% from two independent input pairs, PCGF1 loss lowers baseline fusion occupancy at the top-FLAG sites by 16.3% and changes the DOT1L inhibitor's effect on that occupancy by 22.8% - while leaving the menin inhibitor's effect unchanged at 1.3%. In the knockout SGC0946 displaces more fusion than VTP-50469 does, which is the opposite of the control | Analysis | 1 | 3/5 |
| Measured genome-wide, not just at the locus: the median WITHIN-CONDITION replicate disagreement between two ChIP-seq tracks at a 146 bp window is 23.48 percentile points across 56,171 CTCF anchors and 12 replicate pairs, rising to 57-83 points at the 90th percentile of anchors - and the KMT2A exon-11 element sits at the 35.8th percentile of that distribution, so it is NOT unusually noisy, 146 bp windows are | Explainer | 2 | 3/5 |
| Measured in six ENCODE cell types against every conservative-IDR CTCF anchor of the same cell: the KMT2A exon-11 anchor sits at the 70.6th percentile of CTCF occupancy (range 28.2-81.8, fold over the anchor median 0.69-2.37) - a called peak in 6 of 6 cells and an ORDINARY one, which fails the instrument control the corpus pre-registration wrote for this very experiment | Non-coding | 2 | 4/5 |
| Measured: the cell-type, cell-state and epigenetics literature for KMT2A and MEN1 was NOT missing from this corpus - 7 of 16 load-bearing papers were already cited, one of them 32 times, and 0 of 16 were in gene-kmt2a | Analysis | 1 | 4/5 |
| Measuring every PI-named axis structurally and by content: the type fields understate coverage by a median of 19.5x and by up to 81x, no axis falls below 18% of the corpus, and 'which axis is thinnest' is retired as a beat selector because it reports a lower bound as though it were the truth | Analysis | 1 | 4/5 |
| Mechanism class 1 — chromatin and elongation hijack (KMT2A-r, NUP98-r) | Mechanism | 6 | 4/5 |
| Mechanism class 2 — transcription-factor corruption (RUNX1::RUNX1T1, PML::RARA, ETV6::RUNX1, CBFB::MYH11) — a balance, not a pure dominant negative | Mechanism | 8 | 4/5 |
| Mechanism class 3 — constitutive kinase activation (BCR::ABL1, NPM1::ALK, ETV6::NTRK3) | Mechanism | 7 | 5/5 |
| Mechanism class 4 — condensate-driven transcriptional rewiring (NUP98-r, EWSR1::FLI1) | Mechanism | 4 | 3/5 |
| Mechanism class 5 — enhancer hijacking (inv(3) GATA2/EVI1 — and DUX4-r, which only half belongs here) | Mechanism | 5 | 4/5 |
| MECOM (EVI1) - a cell-of-origin memory that MLL-AF9 maintains but cannot install, present in about 43% of MLL-rearranged AML and marking the chemoresistant half | Gene | 5 | 4/5 |
| MED12 - a named menin-associated protein that restrains menin's transcriptional output, and the anchor of the CDK8 module a KMT2A-r AML paper co-targets | Protein | 7 | 3/5 |
| MED19 - the Mediator subunit curated against an engineered MLL-AFF4 fusion protein, and the one REST uses to deliver G9a | Protein | 9 | 3/5 |
| MED23 — rank 16 of 17,728, survives the lineage split with the B-lineage half stronger, and is not absent from the leukaemia literature after all | Protein | 6 | 3/5 |
| MED23 confirmed, and the zero-record claim corrected: it is not literature-free in leukaemia, an shRNA screen already found it | Analysis | 4 | 3/5 |
| MED26 — a common-essential Mediator subunit with a solved 87-residue domain and no ChEMBL target entity at all | Protein | 10 | 4/5 |
| Mediator's KMT2A signal is in its pan-essential core, CDK8 is expressed and not required at all, and MED13L is rank 9 while its paralogue MED13 is rank 13,569 | Analysis | 5 | 0/5 |
| MEF2C — an output-program transcription factor, the second-strongest leukemia co-dependency, and a gene humans cannot spare one copy of | Protein | 14 | 3/5 |
| MEF2C loses occupancy under VTP-50469 in all three human MLL-rearranged lines (MLL1-N 0.18 / 0.25 / 0.04 over floor), which resolves Q117's one locus-level disagreement with the published account in the paper's favour and localises the disagreement to the murine system | Analysis | 1 | 3/5 |
| Megakaryocyte — the platelet factory whose loss causes the bruising that brings these children in, and which also holds stem cells still | Cell type | 3 | 4/5 |
| Megakaryocyte-erythroid progenitor (MEP) — the branch KMT2A fusions almost never take, which is why it was a usable control | Cell type | 3 | 4/5 |
| Meiotic recombination: hundreds of deliberate DNA breaks per cell, made by a topoisomerase relative, at sites chosen by a single zinc-finger protein | Mechanism | 7 | 5/5 |
| MEIS1 — rate-limiting for MLL leukemia stem cells, a surviving co-dependency, and embryonic-lethal when removed | Protein | 14 | 4/5 |
| MEIS1's 'nucleus' is a profile prediction, not a measurement - and a homeodomain-less isoform is cytoplasmic and does the opposite job | Mechanism | 5 | 3/5 |
| Mel Greaves (Centre for Evolution and Cancer, ICR London) — natural history, in-utero origin and the prevention question | Group | 4 | 3/5 |
| Melphalan - the third agent in Interfant-06 conditioning, dosed per square metre in babies who are dosed per kilogram for everything else in the same week | Drug | 3 | 3/5 |
| MEN1 / menin — the adaptor the fusion cannot work without | Protein | 17 | 4/5 |
| MEN1 and CDK9 each carry exactly one genome-wide-significant in-gene common variant and PSIP1 two, so GWAS says almost nothing about on-target liability - yet the revumenib label lists hyperparathyroidism, the organ MEN1 loss famously affects | Analysis | 2 | 3/5 |
| MEN1 drug-interface mutations — the first proof that a chromatin drug can drive Darwinian escape in patients | Resistance | 3 | 4/5 |
| MEN1-AKT1 is ONE BRET well from a mutation screen, for the E17K allele only - declined | Interface | 3 | 2/5 |
| MEN1-BRAF V600E: four methods and an endogenous menin lane - the only one of the nine that is a real observation, and it is still a property of the allele | Interface | 3 | 3/5 |
| MEN1-CD226 is two proteome-scale AP-MS maps, both spoke-expanded, both in cell lines that do not express CD226 - declined | Interface | 4 | 2/5 |
| MEN1-EGFR is ONE BRET well from the extended-driver arm of a mutation screen, for L858R only - declined | Interface | 3 | 2/5 |
| MEN1-FBXW7 is four alleles of ONE BRET assay, all typed 'mutation with no effect' - declined, and it is the most insidious class | Interface | 3 | 2/5 |
| MEN1-PIAS4 - DECLINED. The single supporting publication is a PARP-1 heat-shock sumoylation study in which menin is never named, and the row is a HeLa co-IP passenger | Interface | 4 | 2/5 |
| MEN1-PTEN is ONE BRET well from the extended-driver arm, for R173C only - declined | Interface | 3 | 2/5 |
| MEN1-SMAD4 is four alleles of ONE BRET assay, all 'mutation with no effect' - declined, and the real menin-TGF-beta literature is elsewhere | Interface | 3 | 2/5 |
| MEN1-SPOP is four alleles of ONE BRET assay, all 'mutation with no effect' - declined, with a nuclear-speckle confound | Interface | 3 | 2/5 |
| MEN1-ZC3HC1 is one spoke-expanded BioPlex row in HCT116, and UniProt records ZC3HC1 weakly or not expressed in leukocytes - declined | Interface | 3 | 2/5 |
| MEN1, DOT1L and LEDGF dependency in the only CALM-AF10 cell line DepMap has screened | Analysis | 2 | 2/5 |
| Menin and LEDGF hold WILD-TYPE KMT2A on chromatin; for the fusion LEDGF is functionally required but positionally dispensable | Mechanism | 6 | 5/5 |
| Menin binds RPA2 directly, the contact maps to RPA2 aa 43-171 across its low-affinity ssDNA site, and three MEN1 patient missense mutations abolish it - a 2003 finding that this graph had never cited despite menin being its central node | Interface | 6 | 3/5 |
| Menin builds bone early and blocks it late: two opposite jobs in the same lineage | Mechanism | 4 | 3/5 |
| Menin CUT&RUN in an IRX1-high KMT2A::AFF1 blast — the missing track in every public deposit | Experiment | 3 | 3/5 |
| Menin dependence of a non-elongation KMT2A fusion has never been demonstrated — the counted absence, and what the pivotal trial actually enrolled | Analysis | 7 | 4/5 |
| Menin dependence of KMT2A::MLLT1: real, repeatedly demonstrated, and always as one lane of a partner panel | Explainer | 6 | 4/5 |
| Menin dependence of KMT2A::MLLT3: the fusion the co-IP was done on, the largest named partner in the pivotal trial, and still no published response rate | Explainer | 4 | 4/5 |
| Menin dependence varies 2.83x across KMT2A::AFF1 lines and the spread survives at three donors - but RS4;11 is last on KMT2A itself, so the heterogeneity is largely fusion-dependence heterogeneity, and DAXX is the one gene decoupled from it | Analysis | 2 | 3/5 |
| Menin dependency tracks the availability of an intact menin-binding motif, in cis or in trans — not the fusion family | Hypothesis | 4 | 1/5 |
| Menin displacement is a poor pharmacodynamic proxy for disabling the fusion, and the degron shows both halves of why: removing the fusion barely moves menin genome-wide, while the menin inhibitor that moves menin leaves half to three-quarters of the fusion's own chromatin sites occupied | Risk | 2 | 3/5 |
| Menin does NOT leave chromatin when the fusion is removed: three hours after MLL::AF9 is degraded to 2.5-7.1% of its own chromatin sites, menin still holds 80.0% of its strongest peak calls genome-wide - so menin occupancy is not a readout of fusion occupancy, and a menin inhibitor that displaces menin is doing something fusion loss does not do | Analysis | 3 | 3/5 |
| Menin does not outlast the fusion under revumenib in primary infant material - 0.586 against 0.485 at oncoprotein peaks, a ratio of 1.21 against a pre-registered threshold of 1.5 - so the fusion-independent menin plateau seen after a degron does not reproduce here | Analysis | 3 | 3/5 |
| Menin has never been tested against SET::NUP214 - a bounded absence in three independent registers: literature, cell-line dependency data, and the founding paper's own blots | Analysis | 4 | 4/5 |
| Menin has no subnuclear compartment, and nobody has looked - the whole published record is two biochemical fractionations, both DNA-damage papers, and no microscopy at all | Mechanism | 4 | 4/5 |
| Menin holds KMT2A and KMT2B, and the graph has been written as if it held one | Mechanism | 6 | 4/5 |
| Menin inhibition collapses the serine/one-carbon/ASNS programme in KMT2A::AFF1 cells - PHGDH -3.24, PSAT1 -2.40, ASNS -1.72, flat in a wild-type line - so it should re-sensitise KMT2A-rearranged ALL to asparaginase, a combination PubMed has zero records for | Hypothesis | 6 | 3/5 |
| Menin inhibition in the gut, not the islet: MI-463 raises GLP-1 from intestinal L cells | Mechanism | 1 | 3/5 |
| Menin inhibition is a reshuffle, not a subtraction: four proteins are documented to GAIN chromatin or persist under the drug, and none of them is the fusion | Mechanism | 5 | 4/5 |
| Menin inhibition makes adult human beta cells divide in a dish - the hardest thing in beta-cell biology | Mechanism | 2 | 3/5 |
| Menin inhibition recruits PRC1 to the BENC MYC enhancer cluster and evicts BRG1, exactly as CBFbeta-SMMHC inhibition does in inv(16) | Hypothesis | 5 | 1/5 |
| Menin inhibition removes the fusion from its strongest sites without relocating it to a new programme, and PRC1.1 fills in only where the eviction is complete - so the drug's chromatin action is subtraction plus local substitution, not redistribution | Hypothesis | 3 | 1/5 |
| Menin inhibition reported to induce CLEC12A and sensitise KMT2A-r and NPM1-mutant AML to CLEC12A-directed CAR cells (2026 preprint, not peer reviewed) | Mechanism | 3 | 2/5 |
| Menin inhibition restores graft-versus-leukaemia only where MHC class II is limiting - so the post-transplant maintenance rationale may hold in myeloid disease and fail in B-precursor infant ALL | Hypothesis | 2 | 1/5 |
| Menin inhibitors are prescribed on 'KMT2A-rearranged', a category that contains proteins as different as KMT2A::AFF1 and KMT2A::USP2 | Risk | 5 | 3/5 |
| Menin inhibitors should leave half the H3K79 methylation standing - and if they do not, the menin-interface model is wrong somewhere | Hypothesis | 3 | 1/5 |
| Menin is a brake the beta cell releases on purpose: pregnancy and glucose both lower it | Mechanism | 3 | 3/5 |
| Menin is a corepressor of the LXR sterol sensors - one paper supplies three of this graph's twelve missing partners, and the function has never been written down here | Mechanism | 6 | 3/5 |
| Menin is dispensable for blood at rest and required for blood under stress - and that is a cell state, not a hedge | Cell state | 1 | 4/5 |
| Menin is required in neural crest for the palate to close - and both menin inhibitors cause cleft palate in animals | Risk | 3 | 3/5 |
| Menin is the best handle on KMT2A::AFF1 because of where the break falls, not because menin is biologically special | Hypothesis | 4 | 1/5 |
| Menin is the best-observed of the six core proteins and the only one whose interval separates from the rest - the interface the programme is built on is the one the record actually supports | Analysis | 5 | 3/5 |
| Menin is the switch that lets TGF-beta turn parathyroid hormone down - and it works on secretion, not just growth | Mechanism | 2 | 3/5 |
| Menin loses half its promoter signal where the fusion sat, and nothing where it did not | Analysis | 4 | 4/5 |
| Menin persists on chromatin after the fusion is degraded because LEDGF/PSIP1 supplies a fusion-independent tether - the authors' own proposal, never tested, and the single cheapest experiment that would change how menin displacement is interpreted as a drug readout | Hypothesis | 4 | 1/5 |
| Menin primacy was established on the der(11) product alone and has never been tested against the der(4) product | Hypothesis | 6 | 1/5 |
| Menin represses GLP1R - the receptor a whole class of diabetes drugs exists to switch on | Mechanism | 3 | 3/5 |
| Menin represses NF-kB transactivation — through a mapped central region, a SIRT1 cofactor, and an RPA2 off-switch, in every tissue except the one this project cares about | Mechanism | 6 | 4/5 |
| Menin residue numbers: the resistance literature (G331R) and the crystal structures (residue 326) disagree by exactly five | Explainer | 3 | 4/5 |
| Menin stimulates homology-directed repair through Chk1 and the region required is 1-228: a 2010 paper that is cited in no entry of this graph and in no reference list of the 2026 paper that reports the same conclusion | Mechanism | 4 | 3/5 |
| Menin-bound genes are the RNA-processing and DNA-repair machinery, H2AK119ub-only genes are neuronal and developmental, and 'menin target' is therefore a much weaker label than this graph treats it as | Analysis | 3 | 4/5 |
| Menin-FANCD2: one 2003 co-immunoprecipitation, a curated sufficient region of menin 214-390, and nothing since | Interface | 4 | 3/5 |
| Menin-JunD: the same pocket, the same drug, the opposite job | Interface | 4 | 4/5 |
| Menin-SETD2, mapped to the NTD and Palm and tooled with a peptide at menin 231-248: the third partner assigned to the same half of menin, and the writer arm of the HR scaffold | Interface | 3 | 3/5 |
| Menin, ENL and DOT1L are CUT&Tag and the four KMT2A antibodies are CUT&RUN, run three weeks apart - so every menin-versus-fusion comparison in this pair crosses both assay and batch | Analysis | 2 | 4/5 |
| Menin's 33 curated partners, enumerated: 10 written, 10 discarded as mutation-directed or single-method, 3 that are not proteins, and what was read and rejected | Analysis | 4 | 4/5 |
| Menin's departure is partial where the fusion's loss is total, so the two are not stoichiometrically coupled | Mechanism | 4 | 3/5 |
| Menin's nucleosome grip (8GPN): a three-patch surface at menin 353-362, 428-442 and 556-587 that holds H3, H4 and H2B - and touches H2A at exactly one residue | Interface | 2 | 4/5 |
| Menin's other address list: the same complex that switches on HOXA in blood writes H3K4 methylation onto the CDK inhibitors p27 and p18 in endocrine cells | Mechanism | 4 | 4/5 |
| Menin's two nuclear localisation signals, 479-497 and 588-608: mapped in 1998, verified residue-for-residue today, annotated by UniProt nowhere - NLS-1 in no structure at all, NLS-2 resolved in one | Interface | 5 | 4/5 |
| MEPCE - absent from this graph until now, and a deeper pan-dependency than BRD4 | Protein | 5 | 4/5 |
| MEPCE caps 7SK before assembly and then stops being an enzyme inside the particle - so its epigenetics annotation is a methyltransferase that methylates an RNA phosphate, which is exactly the case a mark-name regex mislabels in both directions | Mechanism | 1 | 3/5 |
| Metabolic enzyme enumeration in KMT2A-rearranged leukaemia: the instrument, its positive controls, seventeen bounded absences - and the counted zero that would have been wrong | Analysis | 3 | 4/5 |
| Methotrexate - 5 g/m2 through kidneys that are still maturing, and the one backbone drug the canonical infant sensitivity study never tested | Drug | 4 | 3/5 |
| METTL14 — the other half of the m6A writer, with a real AML mechanism and zero KMT2A-specific records | Gene | 4 | 3/5 |
| METTL3 — the m6A writer with a clinical-grade inhibitor, an MLL-rearranged AML mechanism, and a B-lymphoid signal that goes the wrong way | Gene | 9 | 3/5 |
| MHC class I is a bivalent gene set, and a menin inhibitor derepresses it - shown in K-562, SCLC and neuroblastoma, and measured on HLA-A in primary AML, but never once in a KMT2A-rearranged cell | Mechanism | 4 | 3/5 |
| MI-2-2 was doing a weak version of the same thing - 5.8x enriched overlap with the potent inhibitor, 75% concordant - and the selectivity claim it left behind gets STRONGER when low-expressed probes are filtered out, 9.6x to 22.1x | Analysis | 2 | 3/5 |
| Michael Cleary (Stanford) & Akihiko Yokoyama (National Cancer Center, Tsuruoka) — the groups that discovered the menin requirement itself | Group | 4 | 4/5 |
| microRNA genes silenced by CpG hypermethylation in t(4;11) infant ALL — the non-coding genome the fusion switches OFF | Non-coding | 2 | 3/5 |
| miR-196b — the HOXA-cluster microRNA that is a direct KMT2A-fusion target and a genuine double agent | Non-coding | 7 | 4/5 |
| miR-9 — the most MLL-specific microRNA in AML, encoded at three separate loci nobody has disambiguated | Non-coding | 6 | 3/5 |
| Mitochondrial complex I plus venetoclax in KMT2A-rearranged paediatric AML - a genotype-stratified in vivo PDX result, on a drug whose adult clinical development stopped for toxicity | Target | 3 | 3/5 |
| Mitoxantrone - the Interfant-06 protocol says it is less cardiotoxic than daunorubicin, and the largest survivor cohort ever assembled says it is about seventeen times worse per milligram | Drug | 5 | 4/5 |
| Mixed donor chimerism under three years of age - the same drug exposure ablates less marrow in a younger child, and dosing cannot fix it | Risk | 2 | 3/5 |
| Mixed phenotype acute leukaemia (MPAL) and acute leukaemia of ambiguous lineage | Disease | 2 | 3/5 |
| Mixed-phenotype acute leukemia and KMT2A rearrangement — plasticity caught in the act | Mechanism | 10 | 4/5 |
| ML-2 (KMT2A::AFDN, a non-elongation partner) is the line where menin eviction is weakest (retains 37.2% of its own top windows against 20.5% and 13.0%) and where the DOT1L track moves most of any track in the beat (retains 31.6%, 13.69 percentile points below a rank-matched null at p = 3e-10) - the opposite pattern to what an AF9/ENL-free fusion would predict | Analysis | 1 | 2/5 |
| MLL fused to MURINE Af4 in human CD34+ cells — the model that works, and the swap that makes it work | Explainer | 1 | 4/5 |
| MLL fusions engage NuRD's remodelling arm without its deacetylase arm - and if so, every 'NuRD is repressive' inference in this graph is pointing the wrong way | Hypothesis | 3 | 1/5 |
| MLL was reported at regions attached to the nuclear envelope in 2000, which is indirect evidence at the lamina that this graph currently records as absent | Mechanism | 3 | 3/5 |
| Mll-AF4 mouse genetics — B-lineage tumours, long latency, and never infant pro-B ALL | Explainer | 3 | 4/5 |
| MLL-AF9 leukaemia destroys the nerves that run its own niche — a mechanism class this graph had nothing on | Mechanism | 3 | 3/5 |
| MLL1 stays on condensed mitotic chromosomes and tethers menin there — a menin-dependent function absent from this graph until cycle 34 | Mechanism | 2 | 3/5 |
| MLL2 and MLL4 each name two different genes, and the ambiguity is in the papers, not in the databases | Explainer | 8 | 4/5 |
| MLLT1 (ENL) refutes the YEATS parallel: the reader is retained in 84% of patients and is required for leukemogenesis | Mechanism | 3 | 4/5 |
| MLLT1 / ENL — the reader that beat its own paralogue, with a degrader already in hand | Protein | 6 | 4/5 |
| MLLT10 (AF10) — DOT1L cofactor and KMT2A fusion partner | Gene | 2 | 5/5 |
| MLLT10 (AF10): the discarded PZP reader — the one partner where loss is proven to be the oncogenic event | Mechanism | 3 | 4/5 |
| MLLT10 / AF10 — domain architecture and residue coordinates | Protein | 7 | 4/5 |
| MLLT10/AF10: twenty observed phosphosites, twelve PIKK motifs, and not one kinase-site relation in the literature - a bounded absence | Analysis | 3 | 4/5 |
| MLLT11 / AF1q — a 90-residue protein with no chromatin domain and no oligomerisation module, KMT2A partner in t(1;11)(q21;q23) | Protein | 10 | 4/5 |
| MLLT3 (AF9): the YEATS acetyl-lysine reader is discarded in ~92% of MLL-AF9 patients — same shape as PZP, but the causal test has never been run | Mechanism | 3 | 3/5 |
| MLLT3 / AF9 — a famous fusion partner that is not a dependency, and a hub domain that is | Protein | 10 | 4/5 |
| MLLT3 is the commonest partner in therapy-induced KMT2A leukaemia: 49 of 142, and 47 of those are t-AML | Epidemiology | 2 | 4/5 |
| MLLT3 runs normal stem-cell self-renewal and is required in essentially no leukaemia line — the inverted case | Mechanism | 3 | 4/5 |
| MLLT6 (AF17) — the fourth KMT2A fusion partner inside DotCom, and the only one no cell needs | Protein | 8 | 3/5 |
| MLLT6 / AF17 — domain architecture, and where the leucine zipper actually is | Protein | 2 | 3/5 |
| MME / CD10 (CALLA) - the marker this disease is defined by NOT having, and the promoter is methylated shut rather than simply not yet switched on | Gene | 8 | 4/5 |
| Model: interface hotspot prediction - trainable in general, pure extrapolation here, because SKEMPI contains zero menin entries | Analysis | 2 | 4/5 |
| Model: predicting who responds to a menin inhibitor - no patient-level data is public, so this cannot be trained either | Analysis | 5 | 4/5 |
| Model: resistance-mutation prediction - cannot be trained. There are six patient-observed labels in the world, and a base-editor screen already does the job better | Analysis | 3 | 4/5 |
| MOF/KAT8 is required by both KMT2A::MLLT3 and NUP98::HOXA9 — which is why it is the wrong kind of convergence | Mechanism | 5 | 3/5 |
| MOLM13 (KMT2A::MLLT3) is the only line in GSE127507 with a matched input in BOTH conditions, and it gives the one differential-input-controlled measurement in the series - MLL1-N occupancy at its own top 0.1% of bins is unchanged (share ratio 0.9438, input 0.9542, input-corrected 0.9891) with ZERO gained bins genome-wide, while menin retains only 13.0% of its own top windows | Analysis | 2 | 4/5 |
| Monoblast — the immature monocyte that names FAB M5a, the dominant morphology of congenital KMT2A leukaemia | Cell type | 5 | 4/5 |
| Monocyte — the graph's most-discussed undefined cell identity, and the confound sitting under its own DepMap haem signal | Cell type | 6 | 4/5 |
| Most gene-body 'AFF1-exclusive' calls in GSE252378 are a fold-change threshold cutting an oncoprotein-level gradient - and IRX1 is the one member where the non-AFF1 samples are genuinely at background | Hypothesis | 2 | 3/5 |
| Move the cohesin degron into a cell where the element actually breaks: RAD21-AID in Nalm6 or CD34+, sBLISS plus both END-seq variants, with the fusion readout in the same cells | Experiment | 2 | 1/5 |
| MRD as a trial endpoint in KMT2A-rearranged leukaemia: high negativity rates, and almost none of them say which assay | Explainer | 10 | 3/5 |
| MRD by fusion transcript: fast, standardised, partner-limited - and structurally blind to KMT2A* | Explainer | 7 | 4/5 |
| MRD by genomic breakpoint: the only assay in this disease that is fusion-specific by construction | Explainer | 8 | 4/5 |
| MRD by Ig/TCR rearrangement: the standard in ALL, and the assay infant KMT2A-rearranged disease strains hardest | Explainer | 9 | 4/5 |
| MRE11 (P49959, 708 aa) - the nuclease that makes the first cut of end resection, named in 10 entries of this graph and never written; DepMap mean -0.542 with 56% of 1,258 lines below -0.5, the deepest dependency in the whole resection cascade | Gene | 2 | 3/5 |
| MS2133 - the first molecule to degrade DOT1L rather than inhibit it | Drug | 2 | 3/5 |
| MSI2 (Musashi-2) — sustains the MLL stem-cell programme in mouse, and the myeloid DepMap arm disagrees in sign | Gene | 4 | 3/5 |
| MSL1 - the MSL scaffold that carries MOF and MSL2 to HOXA9 and MEIS1, with zero records against KMT2A and a mapped, drawable domain architecture | Protein | 9 | 3/5 |
| MSL2 — the second H2B ubiquitin ligase, sitting inside the MOF complex the KMT2A fragment contacts | Protein | 7 | 3/5 |
| MTA2 / MTA1L1 (O94776) - the NuRD scaffold that clamps HDAC1, recruited in T lymphocytes by BCL11B, and absent together with MTA1 and MTA3 from every column of the pan-MLL-fusion interactome | Gene | 8 | 3/5 |
| MTHFD1 (P11586) - the inverse case: the deepest leukaemia dependency in the serine/one-carbon panel, and the drug does not touch it | Gene | 4 | 3/5 |
| MTHFD2 (P13995) - the one panel member with a published MLL-AF9 in-vivo survival result, and the serine gene that behaves exactly like an ISR gene | Gene | 4 | 3/5 |
| MTUS2 (TIP150) - a microtubule plus-end tracking protein with 153 partners in the one yeast screen that reported it binding AFF4 | Protein | 4 | 1/5 |
| Multipotent progenitor (MPP) — the stage where the undifferentiated KMT2A-r infant leukaemias map | Cell type | 5 | 4/5 |
| MV4-11 (CVCL_0064) — KMT2A::AFF1, yes, but a ten-year-old's acute monocytic leukaemia with FLT3-ITD | Explainer | 2 | 5/5 |
| My own pre-registered reagent gate was the wrong test: it demanded a within-sample ordering from a class defined by a between-sample difference, and it failed by 2.5% | Explainer | 1 | 4/5 |
| MYB — rank 17 of 17,728 for KMT2A selectivity, and the only node in this beat where partial, transient suppression eradicated leukaemia without stopping normal blood production | Protein | 4 | 4/5 |
| MYBBP1A - the let-7-independent effector through which LIN28B suppresses MLL-rearranged AML, and a nucleolar MYB co-repressor that reads H3K9me2 | Gene | 3 | 3/5 |
| MYC - named in a hundred entries of this graph and, until now, written in none | Gene | 6 | 3/5 |
| MYC reactivation through PRC1.1 loss — a named, druggable bypass out of menin dependence | Resistance | 3 | 3/5 |
| Myeloid-directed antigens (CD33, CD123) — the only immunotherapy axis that survives lineage switch | Target | 6 | 3/5 |
| Myeloid-primed blasts are already present at diagnosis of KMT2A-rearranged B-ALL and expand under immunotherapy — the single-cell demonstration this graph recorded as not existing | Mechanism | 3 | 4/5 |
| MYH11 — domain architecture and residue coordinates | Protein | 9 | 3/5 |
| MYH9 (non-muscle myosin IIA) — the best-validated menin partner nobody in this field talks about, and the only one that maps to menin's N-terminus | Protein | 4 | 3/5 |
| MYO1F — unconventional myosin IF, a KMT2A partner with neither a transactivation domain nor a dimerisation domain | Protein | 6 | 3/5 |
| N-of-1 and n-of-few: the custom-therapy route, and what it actually costs | Explainer | 3 | 3/5 |
| NASP - the soluble histone reservoir, and the only gene in this beat with a real selective difference at a pan-essentiality shallow enough to interpret | Gene | 9 | 2/5 |
| Native E. coli asparaginase - the second-largest in-vitro resistance signal in infant ALL, and a different product from the pegylated one four doses later | Drug | 6 | 4/5 |
| NBN / nibrin (O60934, 754 aa) - the MRN subunit whose loss causes a leukaemia-predisposition syndrome and yet is almost dispensable in DepMap: mean -0.047 against MRE11's -0.542 in the same complex, the same call and the same release | Gene | 2 | 3/5 |
| NCI TARGET — a finished paediatric leukaemia genomics resource, not an active partner | Group | 6 | 4/5 |
| NCOA6 (ASC-2) - the subunit that gives MLL3 and MLL4 their target genes, and a recorded near-absence in leukaemia | Gene | 3 | 3/5 |
| NCT05631574 (COVALENT-102): the third solid-tumour menin-inhibitor trial, missing from this graph because its drug is called BMF-219 - terminated after 13 patients for a strategic reason, explicitly NOT for efficacy or safety | Trial | 2 | 5/5 |
| Necessary is not explanatory: four different questions that a knockout answers as if they were one | Explainer | 6 | 4/5 |
| Neither infant sample has an IgG control, and neither of their two sequencing batches contains one - so every number from this pair is confounded with chromatin accessibility | Analysis | 3 | 4/5 |
| Neither rival mechanism leaves its fingerprint, and the best correlate of Fanconi dependency is menin | Analysis | 5 | 0/5 |
| NEITHER, and it is the closest call this project has had: KAP1/TRIM28 reads the 90.62nd, 81.85th and 89.45th percentile of MCF-7 CTCF anchors at the exon-11 element in three of four tracks - satisfying the first clause of the pre-registered PRESENT rule - and the six-non-anchor-interval clause blocks it at 65.87 | Analysis | 2 | 3/5 |
| NELF — the brake that has to come off for elongation, absent from the KMT2A literature, and less required in KMT2A-rearranged lines than in any other leukaemia | Protein | 6 | 2/5 |
| NELFB (COBRA1) — the NELF scaffold, and the single least KMT2A-selective gene of the sixty least selective in the genome | Protein | 5 | 2/5 |
| NELFE (RDBP) — the RNA-binding subunit of the pausing brake, and the alias that inflated a record count fifty-fold before it was caught | Protein | 5 | 2/5 |
| Nestin+ mesenchymal stem cell — the niche cell that MLL-AF9 leukaemia wakes up and then loses | Cell type | 4 | 3/5 |
| Neuron - the off-target cell type that defines what KANSL1 loss costs a human being | Cell type | 2 | 4/5 |
| Newborn screening for leukaemia fusions: verdict NOT FEASIBLE TODAY, and the reason is arithmetic plus the absence of anything to offer a positive | Target | 6 | 4/5 |
| NF1 - the only tumour-suppressor loss in this disease, and it is a deletion, so a mutation panel cannot see it | Gene | 9 | 3/5 |
| NF1 in KMT2A-r leukemia — one homozygous deletion, one missense, and the only loss-of-function co-lesion in the disease | Gene | 4 | 2/5 |
| NFKB1 (p105/p50) — the only menin-NF-kB subunit with a co-immunoprecipitation, and the arm the MLL leukaemia data points at | Protein | 8 | 3/5 |
| NFKB2 (p100/p52) — menin binds the non-canonical subunit too, and activating that arm SUPPRESSES MLL-AF9 leukaemia | Protein | 8 | 3/5 |
| NFKBIA (IkB-alpha) — the switch itself. This graph has entries for everything the switch controls and none for the switch | Protein | 4 | 3/5 |
| NFYC / NF-YC - a histone-fold transcription factor whose partner subunit carries an H2B-like ubiquitination, and the most selective of the eleven TF baits that reached KMT2A | Gene | 8 | 2/5 |
| NG2 in KMT2A-rearranged patients replicates in two independent TARGET profiles - 3 of 4 and 9 of 13 above the 90th percentile of everyone else - but it is bimodal, and the 552-fold median ratio I first computed is an artefact of a near-zero denominator | Analysis | 3 | 3/5 |
| NG2 is absent from the candidate leukaemia stem-cell populations in t(4;11) ALL and 11q23 AML, so an NG2-directed therapy would debulk the disease and leave the fraction that initiates relapse | Hypothesis | 3 | 3/5 |
| NG2 reads the fusion's transcriptional programme, not the DNA lesion - so a menin inhibitor should erase the graph's best diagnostic marker while the rearrangement stays put | Hypothesis | 6 | 1/5 |
| NG2/CSPG4 is the one antigen in the whole surfaceome that KMT2A::AFF1 itself drives - and it is a pericyte and vascular protein, at 124.5 nTPM in normal blood vessel and 246 TPM in tibial artery | Target | 10 | 3/5 |
| NG2+ periarteriolar pericyte — the cell that holds blood stem cells asleep, and the one MLL-AF9 leukaemia destroys | Cell type | 4 | 3/5 |
| NHLH1 / HEN1 / NSCL1 - a TAL1-family bHLH factor found by cross-hybridising with the T-ALL oncogene, whose knockout mouse is normal and whose only imaging call puts it in the GOLGI | Gene | 9 | 2/5 |
| Niche biology HAS been measured in KMT2A-rearranged disease - but in the index fusion itself there is essentially one marrow-niche molecular experiment, from 2011 | Analysis | 5 | 4/5 |
| Niche components considered and not written: what the search actually returned for E-selectin, CAR cells, osteoclasts, marrow macrophages and the rest | Analysis | 3 | 4/5 |
| Niche proteins enumerated and NOT written in this tranche, and four symbol traps measured while doing it - three of them new to the registry | Analysis | 5 | 4/5 |
| Niche-mediated chemoprotection in KMT2A-rearranged leukaemia — real for cytarabine, unsupported for menin inhibitors, and the one hypoxia experiment points the other way | Mechanism | 4 | 3/5 |
| NIN (ninein) - a centrosomal scaffold recorded as a DOT1L partner under a UniProt isoform that UniProt itself calls dubious | Gene | 4 | 2/5 |
| Nine of the seventeen core promoters have a non-AFF1 sample within 10% of the threshold, and one has a non-AFF1 sample STRONGER than its own weakest AFF1 call | Analysis | 1 | 4/5 |
| Nine survivors in ten carry a long-term complication, and it is worse the younger they were | Risk | 4 | 4/5 |
| NIPBL - the cohesin loader, the cleanest degron result in the whole architecture literature, and a second bounded absence in this disease | Gene | 5 | 2/5 |
| NLRC5 - the MHC class I transactivator, and the route by which interferon activates class I when KMT2A and KMT2B are both gone | Gene | 9 | 3/5 |
| No acetyl-dead and no acetyl-mimetic KMT2A was ever put in a methyltransferase assay - the link from K1130/K1133 to catalysis runs entirely through SIRT1, and that is a weaker claim than the abstract makes it sound | Analysis | 1 | 5/5 |
| No BRCA1, BARD1, EXO1, DNA2, HP1-gamma or KDM5A has ever been localised at the KMT2A locus, in any cell type: 21 queries, every querytranslation read back, 0 on-topic records - and the absence splits THREE ways by class, which is what decides what it costs to close | Analysis | 4 | 4/5 |
| No experiment has ever ASKED whether MTA2, MBD3, GATAD2A or SIN3A binds a KMT2A fusion - four of them were nonetheless in the lysate of a seven-fusion pulldown, and the class of that absence is measured-not-reported, not never-measured | Analysis | 3 | 3/5 |
| No fusion oncoprotein in any family has a published replication-protein-A measurement: 23 queries across five fusion families and four spelling variants each, every querytranslation read back, zero records - so the PI's analogy dimension for RPA has no comparator at all, and the index fusion's single locus-level result is the entire field | Analysis | 3 | 4/5 |
| No gene-body-scale IRX2 measurement exists in this project - the one scale that could attribute the signal is the one nobody computed | Analysis | 2 | 4/5 |
| No H3K9me3 writer and no H3K9me3 reader has ever been localised at the KMT2A locus IN THE PUBLISHED LITERATURE, in any cell type: 20 queries, 5 alias spellings, 0 on-topic records - and CORRECTED 2026-09-22: the SUV39H1 half is no longer unanswerable from archives. ENCODE still holds zero SUV39H1 experiments (verified by three routes with controls), but GEO holds two deposits, and Q114 read both at this locus and found the writer ABSENT | Analysis | 3 | 4/5 |
| No HA library exists in the AFF4 sequencing batch, so AFF4 is excluded from the peak partition by name | Analysis | 3 | 3/5 |
| No HDAC-inhibitor result in this disease attributes to an HDAC enzyme - the only per-enzyme evidence is genetic, and it says the enzyme is not fusion-specific | Analysis | 7 | 4/5 |
| No histone-mark readout has ever been measured after perturbing ANY NuRD or Sin3 subunit in a KMT2A-rearranged cell - the two complexes whose entire job is acetylation have zero acetylation data in this disease | Analysis | 4 | 3/5 |
| No IDH inhibitor has ever been reported in KMT2A-rearranged leukaemia: 4 literature records, all reviews, and 1 registry record, an adult master protocol - and the first version of this query returned a false zero | Analysis | 3 | 3/5 |
| No infant or childhood KMT2A-rearranged cohort has REPORTED IDH status — and at least one has certainly MEASURED it | Analysis | 2 | 3/5 |
| No junction-specific antibody exists for any KMT2A fusion - and synovial sarcoma shows exactly what one would buy | Analysis | 3 | 4/5 |
| No KMT2A fusion junction peptide has ever been reported - the one measurement that would prove the protein exists has not been published | Analysis | 3 | 4/5 |
| No KMT2A-rearranged haematopoietic cell line in CCLE expresses IRX1 - including all four KMT2A::AFF1 lines MV4-11, NALM-19, RS4;11 and SEM at 0.0000-0.0053 RPKM | Analysis | 2 | 3/5 |
| No menin inhibitor has ever enrolled a KMT2A-rearranged solid tumour, and the one solid-tumour menin trial that read out was terminated for lack of efficacy | Analysis | 4 | 4/5 |
| No menin interaction outside the chromatin complex has ever been tested in a haematopoietic cell - 0 of 9, and the compartment is the wrong one in every case | Analysis | 2 | 5/5 |
| No menin-inhibitor or DOT1L-inhibitor trial has ever named this fusion - and the DOT1L trials excluded it by construction | Trial | 7 | 5/5 |
| No menin-inhibitor trial measures homocysteine or any amino-acid endpoint across 57 records - while a recruiting infant-ALL trial already gives PEG asparaginase and ziftomenib together | Analysis | 2 | 3/5 |
| No name-based test can clear a gene symbol, and GAPDH is the proof: 48 files, zero name support, unambiguously the real gene - so the triage is one-sided, 145 REAL and 144 ABSTAIN | Analysis | 1 | 3/5 |
| No orthogonal validation exists for any of the 110 MLL-AF4-specific partners, as far as four declared bounds can see — and the one partner the paper itself followed up, SETD2, is on the opposite list, shared by all seven fusions | Analysis | 4 | 3/5 |
| No preprint in this graph is carried at strong or established - and the audit that found that first misclassified Genes & Development as a preprint | Analysis | 1 | 3/5 |
| No proximity, degron or tiling-CRISPR study has ever been run on WRAD in KMT2A-fusion leukaemia | Explainer | 3 | 3/5 |
| No published biology exists for AFF1-AS1 under any name - and the 2026 review of non-coding RNAs in KMT2A-rearranged ALL does not mention it | Analysis | 2 | 4/5 |
| No published experiment combines an AKAP95 perturbation with any menin or DOT1L inhibitor - bounded by an enumerated 92-record literature, not by a keyword zero | Analysis | 3 | 4/5 |
| No second driver means no second target - the quiet genome forecloses the combination logic that works in every other leukaemia | Mechanism | 6 | 4/5 |
| No two entries name the same gene - 574 symbol-shaped entries, zero duplicate groups - and only two use a symbol HGNC does not approve: gene-kdm3c is JMJD1C and gene-bod1l is BOD1L1 | Analysis | 1 | 3/5 |
| No washout, withdrawal, release or drug-removal sample exists in any of GSE260742's 158 records, so the third clause of hyp-q117's prediction 5 - that the programme returns on drug withdrawal - cannot be scored from the deposit that prediction names, and closing it needs a wet experiment rather than a download | Analysis | 1 | 4/5 |
| Nobody has convincingly found the H3K79 eraser - and that constraint sets the clock on every DOT1L inhibitor | Mechanism | 6 | 3/5 |
| Nobody has ever asked whether a KMT2A-rearranged sarcoma needs menin: zero records, and the reason is that no model exists | Analysis | 4 | 4/5 |
| Nobody has ever looked at whether a KMT2A fusion is at PML nuclear bodies - a counted zero, with the one biochemical hint pointing yes | Mechanism | 3 | 4/5 |
| Nobody has ever published a menin experiment in CALM-AF10 - counted, controlled and dated | Analysis | 2 | 4/5 |
| Nobody has ever run proximity labelling on a KMT2A fusion, and the interaction records that look like they did are RBP-atlas preys from HEK293 | Experiment | 2 | 3/5 |
| Nobody has ever shown 14-3-3 binding directly to KMT2A: five records across every paralogue alias, and one of them is about AF4 | Analysis | 2 | 4/5 |
| Nobody has ever stratified any KMT2A::MLLT1 outcome or drug-response analysis by reciprocal or spliced status - a measured absence, with the queries | Explainer | 4 | 3/5 |
| Nobody has reported what a menin inhibitor does to CXCR4: zero papers name menin and CXCR4 together, and the RNA-seq that would answer it is already public | Analysis | 6 | 4/5 |
| Nobody knows which way to push H2Bub in this disease, and the only available compound pushes it upward | Hypothesis | 4 | 1/5 |
| Nobody needs to enrol anyone: the PTH question is a regression on data that already exists | Analysis | 2 | 3/5 |
| NOLC1 / Nopp140 (Q14978) - a nucleolar and Cajal-body phosphoprotein in the pan-MLL-fusion core, and the first physical bridge to this graph's nucleolar convergence | Gene | 4 | 2/5 |
| Non-elongation KMT2A partners considered and not written: what the searches actually returned, partner by partner | Analysis | 5 | 3/5 |
| None of the 166 leukaemia-family GWAS in the Catalog names KMT2A, MLL, 11q23 or infants, although ETV6::RUNX1, TCF3::PBX1 and hyperdiploid ALL each have their own scans - and a 987-case scan could only detect odds ratios of about 1.4-1.6 or more | Analysis | 2 | 4/5 |
| None of the five selective unwritten interactors survives a null, and FANCD2 - the one that carried a story - is the second weakest of them at p = 0.12 | Analysis | 3 | 0/5 |
| None of this graph's 2,196 cited papers is retracted - and I nearly reported that from a query that could not have found one | Analysis | 1 | 4/5 |
| NOP2 / NSUN1 / p120 (P46087) - the 28S rRNA m5C4447 methyltransferase in the MLL-fusion nucleolar block, present in the index fusion's column at p = 0.0223, and the gene whose PubMed token is two-thirds contaminated by its NSUN paralogues | Gene | 4 | 2/5 |
| Normal blood needs DOT1L too - lose it in an adult mouse and the marrow fails within weeks | Mechanism | 4 | 4/5 |
| Not one of the four studies in this dispute measured CTCF or cohesin occupancy in a human blood cell - so this beat read ENCODE instead, and the element is a STRONGER CTCF site in a B-lymphoblastoid line than in HCT116, with the summit at the same base | Analysis | 3 | 4/5 |
| Not one phosphorylation site has ever been mapped on a KMT2A fusion protein itself - every site in this beat is an inference across the junction | Analysis | 3 | 4/5 |
| Not re-bounded: an IDH-inhibitor name list crossed with KMT2A terms returns 489 full-text records and 131 even when tightened to the three approved drugs against the exact string KMT2A-rearranged, which is more than this beat could screen - the unrun step, stated with its size | Analysis | 1 | 3/5 |
| NOT YET REPLICATED (corrected cycle 97). Within the K562 map KMT2A's 25-of-50 promiscuity is explained by size (97.1st percentile falling to 90.7th among proteins its own length) and menin is under-reached at the 23.5th, surviving an abundance control. The replication attempt was UNINFORMATIVE, not negative: eleven of twelve other proximity panels do not sample the nucleus, and the one that does shows the same shape | Analysis | 1 | 5/5 |
| Nothing beats menin after all, and the statistic that said otherwise ranks narrowness | Analysis | 4 | 0/5 |
| Nothing connects ENL YEATS binding or ENL condensates to phosphorylation: zero records, and what that means for the phase-2 dossier | Analysis | 5 | 4/5 |
| Novartis 'compound 10' - a DOT1L methyltransferase inhibitor from Perner et al. (Blood 2020), active at 100 nM, whose chemical structure is not given in the GEO deposit and whose target engagement at that dose IS demonstrated in the same series by a 5.6-fold spike-in-normalised H3K79me2 collapse by day 3 | Drug | 3 | 3/5 |
| Novartis 'compound 11' - a DOT1L methyltransferase inhibitor from Perner et al. (Blood 2020), active at 100 nM, whose chemical structure is not given in the GEO deposit and whose target engagement is not measured anywhere in the series | Drug | 3 | 2/5 |
| NPM1 (nucleophosmin) — the nucleolar shuttle whose mutant form binds chromatin with KMT2A and buys the second menin-inhibitor indication | Protein | 11 | 4/5 |
| NPM1 (nucleophosmin) domain architecture | Protein | 2 | 4/5 |
| NPM1::ALK (NPM-ALK), t(2;5)(p23;q35) | Fusion | 6 | 5/5 |
| NPM1c and XPO1: one drug, one output, two incompatible mechanisms - is the mutant needed in the cytoplasm or on the chromatin? | Mechanism | 4 | 3/5 |
| NR1H2 / LXR-beta - the paralogue arm of the menin-LXR contact, present in both species and absent from the paper's conclusion | Gene | 5 | 2/5 |
| NR1H3 / LXR-alpha - the best-observed of the three MEN1 sterol partners, with both directions curated in two species, and menin as its corepressor | Gene | 6 | 3/5 |
| NR3C1 - the receptor the single most prognostic drug in this disease acts through, and the fusion suppresses it | Gene | 3 | 4/5 |
| NRAS - the other RAS, the one whose 0.3% clone came back, and a UniProt record that lists HRAS1 as its own synonym | Gene | 9 | 4/5 |
| NRAS as a co-mutation in KMT2A-r leukemia — the one co-lesion that is specifically enriched in t(4;11) | Gene | 5 | 4/5 |
| NSD1 - the H3K36 dimethyltransferase whose catalytic activity a NUP98 fusion cannot do without, and which cells can otherwise lose almost for free | Gene | 7 | 4/5 |
| NSD1 (nuclear receptor-binding SET domain protein 1) domain architecture | Protein | 1 | 4/5 |
| NSL complex - the MOF assembly that five NUP98 fusions bind alongside MLL1, and that competes with MLL/COMPASS for WDR5 | Protein | 7 | 3/5 |
| NTRK3 (TrkC neurotrophin receptor) domain architecture | Protein | 1 | 4/5 |
| NUCKS1 (Q9H1E3) - a RAD51AP1 paralogue that binds the same DNA with weaker affinity, and whose measured phenotype is mitomycin-C sensitivity rather than the D-loop binding this graph reached for | Gene | 2 | 3/5 |
| Nuclear import of every KMT2A fusion is a property of retained KMT2A sequence, and the determinant was mapped in 1997 to a region containing the AT-hook motifs | Mechanism | 5 | 3/5 |
| Nuclear matrix and mitotic chromosome scaffold — KMT2A sits with topoisomerase II, in the same place the gene breaks | Mechanism | 3 | 3/5 |
| Nuclear speckles — the compartment everyone assumes KMT2A::AFF1 uses, on evidence that skips AFF1 itself | Mechanism | 4 | 2/5 |
| NUDT21 / CFIm25 (O43809) - the CFIm subunit that picks poly(A) sites, in the pan-MLL-fusion core, and a paraspeckle protein | Gene | 6 | 3/5 |
| NUMA1 / NuMA (Q14980) - a nuclear-matrix protein that becomes the spindle pole, and the 5' partner of a variant APL fusion whose coiled-coil is required for oncogenicity | Gene | 5 | 3/5 |
| NUP214 / CAN - the cytoplasmic-face nucleoporin that CRM1 docks against, and the 3' partner of four leukaemia fusions | Gene | 11 | 4/5 |
| NUP50 / Npap60 (Q9UKX7) - a MOBILE nuclear-basket nucleoporin in the pan-MLL-fusion core, and the evidence says basket, not nuclear envelope | Gene | 3 | 3/5 |
| NUP98 - the mobile nucleoporin that leaves the pore to put H3K4me3 on haematopoietic promoters, and the shared 5' donor of seven fusions in this graph | Gene | 10 | 4/5 |
| NUP98 — domain architecture and residue coordinates (with the 1817/920 numbering trap resolved) | Protein | 8 | 4/5 |
| NUP98 FG condensates, audited assay by assay: no half-bleach has ever been done and no NUP98 fusion has ever been endogenously tagged | Mechanism | 8 | 3/5 |
| NUP98 fusions retain a 469-residue FG repeat region that carries ZERO annotated modification sites - the cleanest retained-portion PTM absence in the four fusion families checked | Analysis | 4 | 3/5 |
| NUP98 fusions share the menin dependency (confirmed preclinically) — and the partner-supplied reader/writer module is not why | Hypothesis | 6 | 4/5 |
| NUP98 is an eligibility criterion in 22 of 57 menin-inhibitor trials including a paediatric trial for that genotype alone - and NSD1 and KDM5A appear in none of them, so trials select on the fusion and never on its partner | Analysis | 2 | 3/5 |
| NUP98 rearrangements are 7.2% of paediatric AML and 1.6% of adult, with 35% five-year overall survival — and the partner changes everything | Epidemiology | 4 | 4/5 |
| NUP98::DDX10, inv(11)(p15q22) — the 'helicase' fusion whose helicase activity turns out not to be the point | Fusion | 5 | 3/5 |
| NUP98::HOXA9, t(7;11)(p15;p15) — the founding NUP98 fusion, and an incomplete oncogene | Fusion | 10 | 4/5 |
| NUP98::HOXD13, t(2;11)(q31;p15) — the myelodysplasia fusion, and a warning against targeting p53 | Fusion | 8 | 4/5 |
| NUP98::KDM5A (NUP98-JARID1A), t(11;12)(p15;p13) | Fusion | 7 | 4/5 |
| NUP98::KMT2A, inv(11)(p15q23) — the NUP98 fusion that contains KMT2A and is menin-inhibitor RESISTANT | Fusion | 4 | 3/5 |
| NUP98::NSD1 without FLT3-ITD loses its prognostic significance — the confound that undermines the fusion's own reputation | Epidemiology | 9 | 4/5 |
| NUP98::NSD1, t(5;11)(q35;p15.5) | Fusion | 8 | 4/5 |
| NUP98::TOP1, t(11;20)(p15;q11~q12) — the most precisely mapped NUP98 breakpoint, and the reciprocal that was wrong twice | Fusion | 6 | 3/5 |
| NUTM1 (NUT) - a testis-restricted, fully disordered protein that writes no mark and instead switches ON a writer, and the 3' partner of the KMT2A-wild-type infant B-ALL with the opposite prognosis | Protein | 11 | 4/5 |
| NUTM1-rearranged B-ALL - the KMT2A-wild-type arm of the same infant trials, with 4-year EFS of 100% against 36-37% next door | Disease | 10 | 4/5 |
| Occupancy-matched three-arm comparison of ziftomenib, revumenib and bleximenib on gamma-H2A.X resolution and HR efficiency in a KMT2A-rearranged B-lineage line, with the peptide competition as the biochemical pre-test | Experiment | 3 | 3/5 |
| Of 262 curated interactors this graph never wrote down, five are selectively required in KMT2A-rearranged lines - and one of them is FANCD2, which binds menin and sits inside a selectivity signal this project has failed four times to explain | Analysis | 4 | 0/5 |
| Of 62 registered menin- or DOT1L-inhibitor trials, 7 have stopped and none gave a safety reason - four were company or supply decisions - yet the same drugs carry dose-limiting differentiation syndrome and QT prolongation that the registry never mentions | Analysis | 4 | 3/5 |
| Of every antigen this project names, only NG2, LAMP5 and CD123 are present on all three KMT2A::AFF1 cell lines - CD19 is at 0.2 nTPM in MV4-11 and CD33 at 2.3 in RS4;11 | Analysis | 3 | 3/5 |
| Of the 58 two-patient AFF1-exclusive genes, four - not one - are called exclusive by both instruments, and the surviving IRX1 claim does not beat a patient-level null (p=0.092) [CORRECTED by q171] | Analysis | 3 | 2/5 |
| Of the 90 papers citing the discovery of KMT2A acetylation at K1130/K1133, the only three that mention MLL-rearranged disease or AFF1 are reviews, and none mentions menin - salvaged from an agent the session limit killed | Analysis | 2 | 4/5 |
| Of the menin co-dependencies, which are actually safe to hit? (run) | Analysis | 2 | 2/5 |
| Of three co-folding predictors run without alignments, only the single-sequence one (ESMFold2) recovers menin-MBM1 above shuffled-peptide controls, and its real peptides sit within 0.6 A (core) to 2 A of the deposited structures while shuffled peptides do not - on interfaces that were in its training data | Analysis | 3 | 3/5 |
| OGT - the O-GlcNAc transferase, a Polycomb-complexome bait that pulls down KMT2A, and already the metabolic dial on DOT1L in this graph | Gene | 5 | 3/5 |
| On an absolute scale, H3K79me2 in the index fusion falls 52-fold (EPZ5676) to 91-fold (compound 10) by day 9 and NOT ONE of 17,341 measurable genes holds its signal - the first absolute-scale chromatin statement this project has been able to make about KMT2A::AFF1 | Analysis | 3 | 4/5 |
| On one universe with one rule and a structure-respecting null, the two lineages of one infant overlap no more than two unrelated KMT2A::AFF1 infants do | Analysis | 3 | 4/5 |
| On the absolute scale the H3K79me2 gradient is real and it runs the other way from the share: the most heavily marked decile retains 0.8% and the least marked retains 31%, a 41-fold gradient - and every decile, in both lines and under both drugs, still loses | Analysis | 2 | 4/5 |
| One afternoon of titrations that closes a 1,300-fold question: tagless 1147-1203 against tagless 1147-1244, matched in every other respect | Experiment | 3 | 3/5 |
| One blot: phospho-eIF2alpha and ATF4 protein in RS4;11 under VTP-50469, with a dose-response and a DOT1L comparator arm | Experiment | 2 | 4/5 |
| One demethylase family sits at both ends of this disease - KDM3B gates whether KMT2A rearranges, JMJD1C is what the resulting fusion needs to survive - and a single compound hits both, so its therapeutic index runs in opposite directions in the two cell populations it reaches | Hypothesis | 5 | 1/5 |
| One domain, two names - and `MLL[tiab]` does not match `MLL1`. Two token traps, two missing affinity papers each | Explainer | 3 | 5/5 |
| One experiment that decides whether KDM4C is a target or the KDM4 family is: paralogue rescue of SD70 sensitivity in SEM | Experiment | 4 | 3/5 |
| ONE GEO series can carry TWO different chrom tables: GSE210480's H3K9 bigWigs declare hg19 + exactly 100,000 bp but its CTCF bigWigs declare EXACTLY hg19 with no padding - so a build check run on one file does not license the rest of the series | Explainer | 2 | 5/5 |
| One immunoprecipitation that decides whether 14-3-3 touches KMT2A at all | Experiment | 2 | 3/5 |
| One karyotype band, two partner genes: why t(11;19) and t(10;11) can cancel a real partner effect | Explainer | 5 | 3/5 |
| One laboratory holds up 92 entries, which counting papers could not show | Analysis | 5 | 0/5 |
| One paper holds up 70 entries, and one dataset holds up 167 | Analysis | 6 | 0/5 |
| One stain, in the right order: H3K27me3 across a low-grade endometrial stromal sarcoma series first, and the three MBTD1::EZHIP blocks second | Experiment | 5 | 3/5 |
| One trial, two published analyses, never crossed: gemtuzumab clearly helps KMT2A-rearranged children, and a common CD33 genotype abolishes gemtuzumab benefit — nobody has asked whether it abolishes it in them | Analysis | 3 | 4/5 |
| Only 2 of this graph's 26 bounded absences name a deposited dataset — the corpus asks whether a paper exists and almost never whether the data does | Analysis | 2 | 4/5 |
| Only 20% of this corpus's absences carry a machine-readable query, which I nearly published as an auditability crisis - and then read five of the other 80% and found every one bounded by a better instrument | Analysis | 1 | 3/5 |
| Only 4 of 43 open menin- or DOT1L-inhibitor trials admit infants under one year (9.3%), and only one (TINI-2) is infant-specific, though infants are about a third of the characterised KMT2A-rearranged population | Analysis | 2 | 3/5 |
| Only 69 of the 529 entries carrying absence_class are absence entries, and every conceptually novel token authors reached for - partially-measured, measured-and-contradicted, not-worth-measuring - is on an interface entry, where the thing being graded is not an absence at all | Analysis | 2 | 3/5 |
| Only a handful of loci lose fusion occupancy under a menin inhibitor, and they are the same few whether menin is drugged or deleted: MEIS1, MEF2C, JMJD1C - not HOXA, not MYB | Mechanism | 3 | 4/5 |
| Only BRD4 (mitotic chromosome) and CHD4 (mitotic spindle) of 31 fusion-pathway proteins carry the Human Protein Atlas cell-cycle flag (3.5% of all proteins), and the flag, defined by localisation to mitotic structures, does not mark TOP2A, a canonical G2/M gene | Analysis | 2 | 3/5 |
| Only one public B-lineage cohort annotates the KMT2A fusion PARTNER per sample beside an expression matrix - every other large paediatric leukaemia resource records only 'MLL yes/no' or the 11q23 band | Analysis | 2 | 3/5 |
| Only one query was broken, and it was dragging the whole figure down | Analysis | 2 | 0/5 |
| Open ground: the questions in this graph that nobody in the landscape appears to be working on | Hypothesis | 5 | 3/5 |
| Open trial map for KMT2A-rearranged and infant acute leukemia, September 2026 — what a clinician can actually enrol into today | Explainer | 2 | 4/5 |
| Ordering the fusions developmentally — which stage of blood formation each one hijacks, and at what age the child presents | Explainer | 8 | 3/5 |
| Orphan drug designation: what it actually gives a KMT2A programme, and what it bends | Explainer | 9 | 4/5 |
| Osteoblast — the bone-building niche cell whose expansion suppresses CML and makes MLL-AF9 AML worse | Cell type | 5 | 4/5 |
| Outcome in PICALM::MLLT10: children with ALL do reasonably well, children with AML do badly, and transplant does not rescue them | Epidemiology | 5 | 4/5 |
| Outside ENCODE the resection layer is not one absence but four: 31 BRCA1, 45 CBX3, 22 KDM5A, 14 MRE11 and 8 CtIP ChIP-seq experiments exist in ChIP-Atlas, DNA2 and RAD50 have one each, and only BARD1 and EXO1 have none in any of the three archives | Analysis | 4 | 4/5 |
| P-TEFb (CDK9 + cyclin T1) — the deepest dependency and the clearest therapeutic-index wall in the interactome | Protein | 6 | 4/5 |
| P-TEFb phosphorylates AFF4 and rearranges the complex the fusion hijacks | Mechanism | 3 | 3/5 |
| p279 and p318 are one patient in two lineage states, and collapsing them removes exactly one gene - NOP58 - from the recurrent core | Analysis | 2 | 4/5 |
| p279 and p318: one infant, two diseases, and an oncoprotein target map that does not carry over | Patient story | 2 | 4/5 |
| p279 carries the oncoprotein at HOXA AND at IRX1 — the published mutual exclusivity is not mutual exclusivity at chromatin | Analysis | 2 | 3/5 |
| PA2G4 / EBP1 (Q9UQ80) - the best-evidenced member of the MLL-fusion nucleolar block in the index fusion's own column (p = 0.014), and the only one with a published AML phenotype | Gene | 4 | 2/5 |
| Pablo Menendez & Clara Bueno (Josep Carreras Leukemia Research Institute, Barcelona) — cellular origin, fetal models and infant-specific drug resistance | Group | 4 | 3/5 |
| PAF1 — pan-essential subunit of a complex the fusion needs, where the window is in the interface and not in the protein | Protein | 6 | 4/5 |
| PAF1 and MED29 return the identical occupancy call in all 27 GSE252378 samples, because 86.5% of their promoter windows is the same DNA | Analysis | 2 | 3/5 |
| PAF1 is annotated as punctate everywhere in the nucleus EXCEPT the nucleolus - and a 2024 proximity map puts it in the nucleolus | Mechanism | 5 | 3/5 |
| PAF1C couples transcription to H2B ubiquitination - but the RTF1 half of that coupling is yeast-specific and contested in human cells, and PAF1C is one of the few complexes that genuinely binds the retained KMT2A fragment | Mechanism | 5 | 4/5 |
| PAF1c is needed by the normal stem cell and by the leukaemia, and the genes it regulates in each are different | Mechanism | 4 | 3/5 |
| Paired IRX1 RNA and KMT2A-N occupancy in the same non-AFF1 blasts: does the expression subgroup exist where the occupancy subgroup does not? | Experiment | 1 | 3/5 |
| PALB2 (Q86YC2, 1,186 aa) - the physical link that makes BRCA1 and BRCA2 one pathway, named in 4 entries and never written; DepMap mean -0.339, statistically indistinguishable from CBX1 and MEN1, and its entire KMT2A intersection is one Ewing sarcoma germline paper | Gene | 2 | 3/5 |
| Pallor and anaemia in infants: the number this graph quotes does not exist for babies | Explainer | 5 | 3/5 |
| Pallor and fatigue: the anaemia of a marrow taken over by leukaemia | Explainer | 3 | 3/5 |
| Pan-essentiality: checked for all eight, and cleared — but a shallow dependency is its own problem | Risk | 2 | 3/5 |
| Pancreatic neuroendocrine tumours in MEN1: the manifestation that kills, and the one the animal data points at | Disease | 6 | 4/5 |
| Panobinostat - the HDAC inhibitor this graph has reasoned about for cycles without having an entry for, with strong KMT2A-rearranged xenograft activity and a terminated adult trial | Drug | 4 | 3/5 |
| Panobinostat lowers H2B ubiquitination in MLL-rearranged ALL by suppressing RNF20/RNF40/WAC — the only clinical-stage agent that reaches this axis, and its one ALL trial was stopped for lack of efficacy | Mechanism | 3 | 4/5 |
| Papers we know exist, know matter, and cannot read | Explainer | 5 | 0/5 |
| Paralogue redundancy does NOT explain anti-selective DepMap results here: clearly selective genes carry paralogues at 30.6% against a 32.7% base rate, with no depletion | Analysis | 3 | 3/5 |
| Paraspeckles and NEAT1 — no KMT2A evidence at all, but a fusion oncoprotein in another leukemia uses NEAT1 as a differentiation brake | Mechanism | 4 | 2/5 |
| PARP1 - the target whose inhibitors this disease was specifically shown to resist, and which three later papers combine anyway | Gene | 10 | 3/5 |
| PARP16 - graded A- in the DOT1L pulldown, the best of the six, and a tail-anchored ER membrane protein that cannot be in the nucleoplasm | Gene | 6 | 2/5 |
| Partner import: when a mechanism measured in one fusion is asserted about another | Explainer | 5 | 4/5 |
| Partner-exclusivity does discriminate: of four comparator partner groups only AFDN fires, it is 4-of-4 AML, and lineage-matching collapses it to exactly chance while AFF1's class survives the same restriction | Analysis | 2 | 4/5 |
| Partner-protein occupancy is not fusion occupancy: every KMT2A::AFF1 chromatin claim resting on an AFF1, AFF4 or SEC-subunit ChIP is an upper bound that includes free complex | Hypothesis | 3 | 3/5 |
| Patricia Ernst (University of Colorado) — what normal KMT2A and menin actually do, which is the therapeutic-window question | Group | 3 | 4/5 |
| PAX5 - the most frequently hit non-KMT2A gene in infant KMT2A-rearranged ALL, and it is a deletion in one allele, not a mutation | Gene | 4 | 4/5 |
| PAXIP1 (PTIP) - the subunit that tells an MLL3/4 complex apart from a menin complex, and the only one with a leukaemic-niche phenotype | Gene | 4 | 3/5 |
| PBX proteins are not constitutively nuclear: a MEINOX partner keeps them there by blocking export - and nobody has ever looked at PBX3 in a KMT2A-rearranged cell | Mechanism | 3 | 2/5 |
| PBX1 — domain architecture and residue coordinates | Protein | 5 | 4/5 |
| PBX2 - an AFF4 co-purifying protein in two rounds of one AP-MS atlas, and the PBX paralogue the leukaemia literature explicitly excluded | Protein | 8 | 2/5 |
| PBX3 - the TALE cofactor the field says is non-redundant, and the experiment that says HOXA9 is the redundant one | Gene | 9 | 3/5 |
| PCGF1 — the PRC1.1 scaffold whose LOSS causes menin-inhibitor resistance, so it is a restraint on the leukaemia rather than a dependency of it | Protein | 10 | 3/5 |
| PCGF1 loss flattens the fusion's genomic distribution - the knockout-over-control share ratio rises monotonically from 0.810 at the highest-signal decile to 1.136 at the lowest while both input pairs stay flat - and the drug does something spatially different: VTP-50469 evicts almost only at the top 0.1% (0.7554 against 0.9937 at the decile below). The drug acts at the peaks, the genotype acts in the bulk | Analysis | 1 | 3/5 |
| Peak-call retention tracks peak strength, not fusion occupancy, and that inverts the answer | Analysis | 3 | 4/5 |
| Pegaspargase - the same enzyme wearing a polymer, dosed in units that are not the other product's units, and now dosed to a level in every group except infants | Drug | 4 | 4/5 |
| Pentimento and restoration — the fusion overpaints the cell, and cleaning reveals whatever was underneath | Analogy | 4 | 1/5 |
| PER-485 (CVCL_W984) — the relapse half of a matched infant t(4;11) pair, and it has lost CD19 | Explainer | 2 | 4/5 |
| PER-490 (CVCL_W986) — a KMT2A::AFF1 B-ALL line from a nine-day-old infant | Explainer | 4 | 5/5 |
| PER-494 (CVCL_A8JU) — infant t(4;11;7) line, and the one whose AFF1 was never demonstrated | Explainer | 2 | 4/5 |
| PER-785 (CVCL_IZ03) — infant t(4;11) line from a child who survived | Explainer | 2 | 5/5 |
| PES1 / pescadillo (O00541) - the missing PeBoW subunit of this graph's nucleolar block, pan-essential in 96.9% of DepMap lines, and the one myeloid experiment on it shows proliferation WITHOUT a differentiation block | Gene | 6 | 2/5 |
| Phase-2 dossier: CBX8 - the candidate this review would kill, and the reasons are all numeric | Target | 6 | 3/5 |
| Phase-2 dossier: DOT1L - perfect chemistry, a completed paediatric trial, and a target that has already had its answer | Target | 6 | 4/5 |
| Phase-2 dossier: KAT7/HBO1 - the only enzyme here with a real active site, a co-crystal inhibitor and a co-dependency that survives lineage adjustment almost intact | Target | 7 | 3/5 |
| Phase-2 dossier: the CXXC-DNA interface - two structures, a genetically validated requirement, and a selectivity problem that decides everything | Target | 6 | 3/5 |
| Phase-2 dossier: the ENL YEATS pocket - two co-crystals, nanomolar chemistry, and a co-dependency that only appears inside leukaemia | Target | 5 | 3/5 |
| Phase-2 dossier: the fusion junction - a negative feasibility finding, with the one surviving modality named | Target | 3 | 4/5 |
| Phase-2 dossier: the LEDGF/PSIP1 IBD - the best therapeutic index in the interactome, a solved structure, two hotspot residues, and three compounds in the world | Target | 8 | 3/5 |
| Phase-2 dossier: the menin MBM1 pocket - the only candidate here that is already de-risked, and therefore the only one whose gate is clinical | Target | 7 | 4/5 |
| Phase-2 dossier: the non-small-molecule modalities - degraders first, and the honest limits of each | Target | 3 | 3/5 |
| PHD3 and the CyP33 RRM: Kd 7-15 uM, and a 2023 ternary structure that settles the 2010 disagreement - H3K4me3 and the RRM CAN be held at once, and the real switch is RNA | Interface | 5 | 4/5 |
| PHD3 reading H3K4me3: Kd 4.3 uM for the PHD3-bromo cassette, 30 uM for PHD3 alone, two co-crystals - and the whole module is thrown away by the breakpoint | Interface | 3 | 5/5 |
| PHF1 (PCL1) - the PRC2 accessory subunit whose Tudor domain reads H3K36me3, and the 3' acceptor shared by three different NuA4-donor fusions in two different tumour types | Gene | 8 | 3/5 |
| PHGDH (O43175) - the largest menin-SELECTIVE fall in the whole serine panel, and the least essential gene in it | Gene | 9 | 3/5 |
| Phosphosite counts for the five 3' partners: the atlas beats UniProt 1.4-6.0x, and the retained/lost split is completely different for each partner | Analysis | 4 | 4/5 |
| PhosphoSitePlus returns HTTP 403 to its own homepage from this environment, so the PTM-database absence named by the cycle-65 census cannot be bounded there - and the positive control is what proves the 403 is a block and not an answer | Analysis | 3 | 4/5 |
| PICALM (CALM) - the clathrin-assembly adaptor that is the 5' partner of CALM::AF10 | Gene | 15 | 4/5 |
| PICALM / CALM - domain architecture, residue coordinates, and which parts the fusion keeps | Protein | 5 | 4/5 |
| PICALM::MLLT10 (CALM-AF10), t(10;11)(p13;q14) - the DOT1L-dependent HOXA fusion that contains no KMT2A | Fusion | 17 | 4/5 |
| Picking a GEO supplementary file by slot number instead of extension substitutes a depth-normalised bigWig for a raw fragment BED in 107 of this deposit's 171 records | Analysis | 1 | 5/5 |
| PIK3R1 in KMT2A-rearranged infant ALL - the only cooperating lesion in this disease that was functionally proved to be activating, and it is an ITD | Gene | 4 | 3/5 |
| Pinometostat (EPZ-5676) — the DOT1L inhibitor, and the most instructive failure in this field | Drug | 7 | 4/5 |
| PIP4K2A - the lipid kinase at a genome-wide childhood-ALL susceptibility locus, whose product is the ligand a PHD finger reads | Protein | 10 | 3/5 |
| Pituitary adenoma in MEN1: the third manifestation, and the one that matters most for a growing child | Disease | 3 | 4/5 |
| PKA phosphorylates menin at Ser487 and pulls it off chromatin - a kinase input on the drug target itself | Mechanism | 2 | 3/5 |
| Plain-English: chromatin and epigenetics — the sticky notes on the DNA, and which ones matter here | Explainer | 4 | 5/5 |
| Plain-English: what transcription elongation is, and why a traffic light explains this leukemia | Explainer | 3 | 5/5 |
| PLANNED: margin-ranked partner-specificity scan over all 6,049 occupied-anywhere promoters, with a depth control | Analysis | 1 | 1/5 |
| PLANNED: re-search the public PXD009338 raw files for the twelve corepressor subunits the published table truncated away - one compute job that closes twelve measured-not-reported absences and adjudicates the module-split hypothesis | Analysis | 3 | 3/5 |
| Planned: read CXCR4 and SYTL1 out of the menin-inhibitor transcriptomes that are already public, in the same contrast that shows HOXA9 and MEIS1 falling | Analysis | 4 | 1/5 |
| PLANNED: refit prey recovery on accessible lysine count instead of protein length, which separates the two mechanisms that could produce the size effect | Analysis | 1 | 3/5 |
| PLANNED: run the size-matched promiscuity correction for PSIP1 in the K562 BioID2 map, the way it was run for KMT2A - fully specified here so the next cycle executes rather than redesigns it | Analysis | 2 | 3/5 |
| Plasma cell - the end of the B lineage, and the only cell type in which ELL2 has a documented job | Cell type | 2 | 4/5 |
| Plasmacytoid dendritic cell — the interferon cell that KMT2A-rearranged leukaemia occasionally becomes, and is more often mistaken for | Cell type | 5 | 2/5 |
| Plerixafor (AMD3100, Mozobil) - a licensed CXCR4 antagonist that has never been given to an infant with leukaemia, and whose only paediatric efficacy study failed | Drug | 5 | 3/5 |
| PLK1 — nominated as an infant-restricted vulnerability, and one of the most essential genes in the genome | Gene | 2 | 0/5 |
| PML — domain architecture and residue coordinates | Protein | 7 | 4/5 |
| PML / TRIM19 (P29590) - the scaffold of PML nuclear bodies, co-purified with all seven MLL fusions, and never once studied as a KMT2A-fusion partner | Gene | 4 | 2/5 |
| PML K160 SUMOylation - the retained-portion PTM that became an approved therapy, and the benchmark every other retained site should be measured against | Mechanism | 6 | 4/5 |
| PML nuclear bodies and PML::RARA — the best-worked case of a fusion destroying a nuclear compartment, and what it actually predicts for KMT2A | Mechanism | 4 | 5/5 |
| PML::RARA, t(15;17)(q24;q21) | Fusion | 8 | 5/5 |
| POE 10-03 / NCT01319864 — the only completed paediatric trial of niche disruption, which mobilised blasts 3.4-fold and produced three responses in nineteen children, none of them in ALL | Trial | 2 | 4/5 |
| Point the EED inhibitor at the index fusion - a clinical-stage drug, a subunit with no paralogue, and zero leukaemia experiments | Experiment | 6 | 1/5 |
| Polycomb bodies — indirect evidence via CBX8, undercut by the finding that CBX8-PRC1 condensates are dissolved rather than built by the rest of PRC1 | Mechanism | 6 | 3/5 |
| Polycomb in KMT2A-r leukemia — core PRC2 required, EZH2 and BMI1 dispensable, and CBX8 acting outside its repressive role | Mechanism | 9 | 3/5 |
| Ponte-di-Legno non-infant KMT2A-r ALL (n=629): 5-year EFS spans 41.7% to 91.2% across partner-by-lineage cells | Epidemiology | 3 | 4/5 |
| Pooling the two AF4 antibodies, as the published analysis does, drops AFF1's fusion-site enrichment from 1.8-4.6x the null to 0.8-2.1x - below the H3K4me3 negative control in all three samples | Analysis | 2 | 4/5 |
| Portfolio theory — a hedge only works against uncorrelated risk, and nobody has estimated the correlation matrix of resistance routes | Analogy | 4 | 1/5 |
| POST HOC: against institution-matched, anchored comparators the same-patient pair has the LOWEST excess in all six factorial cells - which leans to q142, but was not pre-registered | Analysis | 2 | 3/5 |
| POU2AF1 (OCA-B / OBF-1 / BOB-1) - the B-cell-restricted OCT coactivator, in the Q152 AFF1-only core | Gene | 3 | 2/5 |
| PPIE (CyP33) — the off-switch the fusion throws away, and the reason PHD3 reinsertion kills transformation | Protein | 6 | 4/5 |
| PPIL4 - a spliceosomal cyclophilin whose BioID neighbourhood is the widest overlap with this graph's subject matter of any bait | Gene | 6 | 2/5 |
| PPP1R15A / GADD34 (O75807) - the eIF2alpha phosphatase adaptor, and KMT2A fusion proteins were shown to BIND it and block its apoptosis in 1999, a paper this graph has never cited | Gene | 4 | 3/5 |
| PRC1.1 — the complex this graph has been leaning on, now enumerated subunit by subunit, and the enumeration changes the conclusion | Protein | 13 | 3/5 |
| PRC1.1 is not both an effector and a resistance gene by coincidence: the two published readings are one activity measured from opposite ends | Hypothesis | 4 | 1/5 |
| PRC2 - the complex, not the subunit, is the unit every experiment in this disease actually resolves | Protein | 11 | 4/5 |
| PRC2 is the fusion's repressive arm, recruited through menin, and the index disease's version of it runs to HDAC7 | Hypothesis | 4 | 1/5 |
| PRDM9 - a germline risk mechanism for childhood ALL that does not reach KMT2A | Gene | 5 | 3/5 |
| Pre-B cell — the stage KMT2A::AFF1 leukaemia never reaches, and why that boundary is informative | Cell type | 5 | 4/5 |
| Pre-pro-B cell (murine Hardy Fraction A) - the stage before pro-B, with germline immunoglobulin genes, and the stage RYBP loss actually removes | Cell type | 4 | 4/5 |
| Pre-registration protects against moving the goalposts and does not protect against this: a blacklist added to fix an unrelated artefact moved a pre-registered count from 42 to 52 across a threshold of 50, flipping the verdict from FAIL to PASS without anyone touching the threshold | Explainer | 2 | 5/5 |
| Prediction 5 of hyp-q117 contains three separable claims - normal eviction, no silencing, and return on withdrawal - and the deposit it names supports one of them only through a clause it never states; the eviction and silencing clauses need tracks the NTvKO arm does not carry, and withdrawal is absent from all 158 samples | Analysis | 2 | 4/5 |
| Prednisolone - the active steroid, the drug every resistance experiment in this disease actually used, and the one given into the spinal fluid | Drug | 9 | 4/5 |
| Prednisone - the prophase drug, the prognostic factor, and a prodrug that has never itself been tested on a KMT2A-rearranged blast | Drug | 8 | 4/5 |
| Premise (iii) was not falsified at this locus - Gothe 2019 measures MLL breakage and MLL-AF4 fusion in the same cells and they move TOGETHER under TDP2 loss; what TDP2 actually falsifies is a premise about break FORMATION that the triad never stated | Analysis | 2 | 4/5 |
| Prevention by exposure avoidance: verdict NOT FEASIBLE, and the transplacental-exposure literature is much weaker than its prominence suggests | Target | 3 | 3/5 |
| Prey recovery in the two BioID depositions tracks SIZE and not abundance - and the interactome tail was being scored on the wrong side of the pair, because every one of the 22 partners is the BAIT and every core protein is the PREY | Analysis | 7 | 4/5 |
| Primary hyperparathyroidism in MEN1: the first and commonest consequence of losing menin | Disease | 4 | 4/5 |
| Prime, wash, divide, rechallenge - the one experiment that would turn 'DOT1L provides transcriptional memory' into a measurement, and it doubles as a dosing-schedule study | Experiment | 4 | 1/5 |
| PRKAR1A (P10644) - a PKA regulatory subunit in the pan-MLL-fusion core with no catalytic subunit anywhere in the network, and a fusion oncogene in variant APL | Gene | 3 | 2/5 |
| PRKDC / DNA-PKcs - the kinase that phosphorylates AF9 on the one regulatory residue the fusion keeps | Gene | 3 | 5/5 |
| PRMT1 — an MLL-fusion cofactor whose first-in-human inhibitor was terminated for lack of efficacy and toxicity | Protein | 10 | 4/5 |
| PRMT3 - the mostly-cytoplasmic ribosome methyltransferase that also writes the ACTIVATING mark on the residue PRMT5 represses, has an acute-leukaemia degrader, and is invisible to this project's own mark-query rule | Protein | 8 | 3/5 |
| PRMT5 - the type II arginine methyltransferase this graph has reached for sixteen times, whose mark on H3R2 RECRUITS WDR5 to chromatin | Protein | 8 | 3/5 |
| PRMT6 - the enzyme whose mark is MUTUALLY EXCLUSIVE with the MLL complex on the H3 tail, and which shuts HOX genes down by evicting WDR5 | Protein | 8 | 3/5 |
| PRMT7 - the enzyme whose class is still disputed, which represses a KMT2 enzyme by writing H4R3me2s, which is required for leukaemia stem cells in CML, and whose only H3R2 claim is the one this beat was dispatched to check | Protein | 11 | 3/5 |
| Pro-B cell — the stage at which KMT2A::AFF1 leukaemia is arrested, and the phenotype the diagnosis is made on | Cell type | 6 | 4/5 |
| Programmed DNA breaks - V(D)J and class switching - and the verdict on whether either one breaks KMT2A | Explainer | 6 | 3/5 |
| PROM1 (CD133) occupancy tracks HOXA occupancy at Spearman +0.952 — a second, independent marker of the same split | Analysis | 2 | 3/5 |
| PROM1 / CD133 - a direct MLL-AF4 target switched on by an intragenic H3K79me2/3 enhancer, and the one surface target in this disease with a published human-relevant kill | Gene | 6 | 4/5 |
| PROM1 occupancy tracks HOXA at +0.93 in KMT2A::AFF1 and not at all elsewhere; it is near-absent in KMT2A-AF9 and -AFDN despite high HOXA | Analysis | 1 | 3/5 |
| PROM1/CD133 is 5.27x higher in normal kidney than in bone marrow - worse than MEN1 on this project's own safety metric - and it was absent from the filter because that filter scored 22 chromatin targets and not one surface antigen | Analysis | 1 | 3/5 |
| PROM1/CD133 tracks the HOXA arm and ANTI-tracks the IRX1 arm in 48 KMT2A::AFF1 infant ALL cases - so the one surface target with a published human kill is depleted in the iALL-IRX1 subgroup | Analysis | 2 | 3/5 |
| PROPOSED: a side-by-side CHD4 co-IP in a t(4;11) B-ALL line and a KMT2A-wildtype B-ALL line, probing one subunit from each NuRD module - the first experiment that would ask whether a KMT2A fusion sees the whole complex | Experiment | 2 | 1/5 |
| PROPOSED: measure let-7 and restore it in the human fetal-liver KMT2A::AFF1 model - an axis measured in mouse MLL-fusion AML but never in the index fusion | Experiment | 4 | 3/5 |
| PROPOSED: run a second oncogene in LIN28B-null human fetal liver CD34+ cells - the control that decides whether the KMT2A::AFF1 transformation block is fusion-specific or just a broken progenitor | Experiment | 2 | 3/5 |
| PROPOSED: swap the partner, hold everything else - KMT2A::MLLT3 versus KMT2A::AFF1 in LIN28B-null human fetal liver CD34+ cells | Experiment | 3 | 3/5 |
| PRoXe — the one leukaemia xenograft repository that is actually public, and what that buys | Explainer | 2 | 4/5 |
| Proximally biased V(D)J and IGHV6-1 in KMT2A::AFF1: the Ig MRD target is a moving target, and the clinic had already moved | Explainer | 5 | 4/5 |
| Proximity-interactome beat: every query run, every paper rejected, and the one resource not reachable | Analysis | 4 | 5/5 |
| Proximity-labelling map of KMT2A::AFF1 — the experiment nobody has run in twenty years of interactome work | Experiment | 5 | 3/5 |
| PSAT1 (Q9Y617) - a DIRECT ATF4 target, and the gene that shows the brief's menin-selectivity claim was PHGDH's and not the pathway's | Gene | 7 | 3/5 |
| PSIP1 / LEDGF p75 — the tether with the best therapeutic index in the whole interactome | Protein | 6 | 4/5 |
| PSIP1 is a tumour suppressor in the lymphoid lineage next door: losing Psip1 ACCELERATES T-ALL in mice, while the same protein is a dependency in KMT2A-rearranged myeloid leukaemia | Risk | 3 | 4/5 |
| PSIP1 keeps R-loops off the genes it sits on, and removing it causes transcription-replication conflict, DNA damage and PARP-inhibitor sensitivity | Mechanism | 3 | 3/5 |
| PSIP1 makes two proteins and only one of them has the IBD: a p52 result is not a p75 result, and the knockout mouse removes both | Explainer | 6 | 4/5 |
| PSIP1-FASTKD2 declined: the bait is a mitochondrial matrix and nucleoid protein with two experimental localisations, the prey is nucleoplasmic LEDGF, and the row is one spoke-expanded BioID2 proximity in K562 | Interface | 5 | 3/5 |
| PSIP1-FOXK2: a single TAP row from the same TF atlas as the RBPJ decline - kept as a lead rather than declined, because FOXK2 is a chromatin-recruiting forkhead expressed in lymphoid cells and LEDGF is a chromatin-recruiting tether | Interface | 3 | 2/5 |
| PSIP1-GDF5 is a single DSSO crosslink in isolated U2OS nuclei with no bait on either side; GDF5 is a secreted cartilage growth factor, and the source paper itself attributes 30% of its cross-compartment links to contamination during nuclei isolation - declined | Interface | 4 | 2/5 |
| PSIP1-IGHMBP2 is a single DSSO crosslink in one detergent fraction of U2OS nuclei with no bait; unlike the other Fasci rows the compartments match, so this is declined on evidence depth alone - and IGHMBP2 is a fourth ribosome-biogenesis-adjacent protein on this list | Interface | 4 | 2/5 |
| PSIP1-PPP1R13B (ASPP1) is a single DSSO crosslink in unfractionated U2OS nuclei with no bait; both proteins are nuclear and both are stress-response regulators, so this is declined on evidence depth alone and is the most biologically coherent row in the beat | Interface | 4 | 2/5 |
| PSIP1-RBPJ - DECLINED. A 214-purification transcription-factor TAP atlas that this beat's own atlas heuristic failed to flag, and the Notch connection is the reason to say so out loud | Interface | 2 | 2/5 |
| PSIP1-SDC1 - DECLINED as an interaction, kept for the splicing thread: nuclear syndecan-1 co-IP in a mesothelioma line recovers LEDGF among an RNA-splicing-enriched network | Interface | 3 | 2/5 |
| PSIP1-TMEM214 is a DSSO crosslink in two preparations of isolated U2OS nuclei with no bait on either side; TMEM214 is an ER-membrane mediator of CASP4-dependent ER-stress apoptosis - declined | Interface | 3 | 2/5 |
| PSIP1-UTP3 is one spoke-expanded BioID2 proximity row in K562 with UTP3 as bait and PSIP1 as prey at miscore 0.27; PSIP1 is recovered by 9 of the 50 baits in that screen and only 2 of the 9 are nucleolar, which is the panel's own base rate - declined | Interface | 5 | 2/5 |
| PSPH (P78330) - the third serine-synthesis enzyme, high in Ewing sarcoma alongside PHGDH and PSAT1, and the one that does NOT fall in leukaemia | Gene | 4 | 3/5 |
| PTBP1 — the strongest RNA-layer dependency in KMT2A-rearranged lines, found by a domain-focused screen and missed by this beat's own gene panel | Gene | 9 | 3/5 |
| PTPN11 in KMT2A-r leukemia — named in every gene list, supported by almost no cases | Gene | 5 | 2/5 |
| PTPN11/SHP2 - non-recurrent in infant KMT2A-rearranged ALL, well drugged everywhere else, and the one leukaemia trial that carried a SHP2 inhibitor was withdrawn | Gene | 5 | 3/5 |
| PUBLISHED, DONE: human fetal liver CD34+ cells fail to transform on KMT2A::AFF1 induction without LIN28B (Ling et al., Blood 2026) - a dedicated human index-fusion experiment, read from the abstract only | Experiment | 4 | 3/5 |
| PubMed deletes zero-hit terms from an OR-group's querytranslation, so the translation is a free audit of which drug names in your list actually contributed - and five of mine contributed nothing | Analysis | 3 | 4/5 |
| Put both fusion proteins in the same cell and you get something neither produces alone | Mechanism | 4 | 3/5 |
| Put mutant IDH2 into SEM and ask three questions at once: does the unmethylated-CpG pool shrink, does the fusion move, and does its competitor move | Experiment | 4 | 1/5 |
| Put the same fusion in two cell types and degrade it, rather than cutting the gene | Experiment | 2 | 3/5 |
| Put three descriptions of the same address on one hg38 axis - the exon-11 CTCF site, the intron-10/exon-11 functional cut point, and the region that breaks more in patients who got a KMT2A fusion - and find out whether they are one element | Analysis | 4 | 3/5 |
| Q109 enumeration: the ten panel members that got no entry, the measurement that declined each, the papers read and not used, and four identifier traps measured on this panel | Analysis | 3 | 5/5 |
| Q117 predicted an MLL1 ChIP would diverge from FLAG at MYB and agree at MEIS1 - both halves fire in RS4;11 (MYB 1.21 against mouse 0.71, MEIS1 0.25 against 0.23), but the MYB divergence does NOT reproduce in MOLM13, which carries the same fusion as Q117's mouse, so the MYB difference is a partner difference and not an antibody artefact | Analysis | 1 | 3/5 |
| Q117's CpG-island falsifier reproduces in the human index fusion almost to the decimal - gained bins 5.66% on an island against a class-matched null of 4.23%, fold 1.34, Fisher p = 0.49, where Q117 got fold 1.35 and p = 0.53 - so the CXXC-redistribution model fails in human RS4;11 as it did in mouse | Analysis | 1 | 4/5 |
| Q117's prediction, run: an MLL1 N-terminal ChIP and a FLAG ChIP of the tagged fusion in the same murine cells diverge 1.83-fold at Myb (0.6645 against 0.3623) and agree to within 4% at Meis1 (0.112 against 0.1171) - the direction is exactly as predicted and the pre-registered numeric threshold for Myb still fails | Analysis | 1 | 4/5 |
| Q124's criterion H2 was written to be able to void Q124's own conclusion, and it cannot - because it is scored on a contrast in which the control genotype shows no effect to lose. Its raw arithmetic FIRES at 0.0813 against a 0.05 threshold, which reads as 'the knockout is a knockout' and is not evidence of anything | Explainer | 3 | 4/5 |
| Q142 and Q144 measured the same patient's lineage switch and disagreed in direction - 0.117 'less than unrelated' against 0.400 'keeps 1,894 of 2,045 calls' - and the beat with 351 pairs and a chance floor beats the one with three pairs and none, which retracts a headline I put in a king log | Analysis | 1 | 2/5 |
| q142's exact comparison - p279 against its own switched AML versus p279 against an unrelated infant - replicates in q144's own universe with q144's own rule, and q144 never made it | Analysis | 2 | 4/5 |
| q145's anti-correlation p = 0.0288 is a one-sided value; the two-sided exact p is 0.0576 and the rho reproduces exactly | Analysis | 1 | 5/5 |
| Q153's named threat, run: the reciprocal KMT2A-C arm shows the same bidirectional-promoter enrichment as the fusion-side N arm (44.86% against 43.86%), and IgG shows 33.86% - so the 2.03x is mostly accessibility, carries a real 7-point KMT2A-family component, and is not fusion-specific in any part | Analysis | 1 | 4/5 |
| q172's four-line index arm is three KMT2A::AFF1 lines from TWO donors plus an ENL line; dropping the ENL line moves MEN1 7.7x more than DAXX, and menin's lost significance is variance, not effect | Analysis | 4 | 4/5 |
| Q25 enumeration: what was searched, found, rejected and could not be read across the five 3' partners | Analysis | 4 | 4/5 |
| Q48 enumeration: every antigen, identifier and query this beat ran - including what was searched and rejected, and the three identifier traps found live | Analysis | 5 | 4/5 |
| Q50 enumeration: every query this beat ran, every zero it recorded with its bound, and the papers it read and did not use | Analysis | 3 | 5/5 |
| QKI - a KMT2A proximity row in K562, and a tumour suppressor whose loss concentrates in the HOXA subtype of T-ALL | Gene | 5 | 3/5 |
| Quiescence (G0) — the state 15 entries invoke to explain measurable residual disease, defined here for the first time | Cell state | 3 | 3/5 |
| Quiescence in the blood stem cell is actively held there by MLL1 - and losing MLL1 pushes the stem cell INTO cycle while pulling the progenitor OUT of it | Cell state | 3 | 4/5 |
| RAD21 - the cohesin subunit with the most break-prone sites in KMT2A-rearranged patients, and the degron experiment this graph keeps asking for | Gene | 12 | 3/5 |
| RAD50 (Q92878, 1312 aa) - the third MRN subunit, and the one that settles whether the complex is incoherent in DepMap: mean -0.114 with 5.2% of 1,257 lines below -0.5, so it sits with NBN and not with MRE11, yet it covaries with MRE11 across cell lines as tightly as BRCA1 does with BARD1 | Gene | 6 | 4/5 |
| RAD51 - the one repair protein measured AT the KMT2A translocation hotspot, and ATM controls how much of it loads there | Gene | 6 | 3/5 |
| RAG off-target activity: the dominant mutator in ETV6::RUNX1 ALL, and probably not the cause of KMT2A fusions | Mechanism | 5 | 4/5 |
| Raise a KMT2A::AFF1 junction-specific monoclonal by the published TEL 6F2 protocol - rat immunisation with a junction peptide, ELISA and western screen, then a ChIP test against the wild-type-parent controls that the ETV6::RUNX1 campaign never ran | Experiment | 2 | 3/5 |
| Raise H2Bub in KMT2A-rearranged cells with the existing USP22 macrocycles and see which way the disease moves | Experiment | 2 | 3/5 |
| Raising HEXIM1 to brake the fusion's output without touching the fusion - one supporting experiment, one chemical series, and no therapeutic window | Target | 6 | 2/5 |
| Raising MHC class I is not a free good: the same molecule is the inhibitory ligand that holds NK cells off, and in this fusion family it is an in vivo leukaemia dependency | Risk | 4 | 3/5 |
| RALGAPA2 (AS250) - the catalytic brake on RalA that behaves as a tumour suppressor, fused to KMT2A exon 22 in an osteosarcoma and predicted out of frame, which makes allele DISRUPTION the better hypothesis than a chimera | Gene | 9 | 3/5 |
| Ranked against four fusion families, the KMT2A acetylation site is the only candidate with no evidence on the fusion at all - and the strongest argument for it is one nobody has made | Analysis | 2 | 3/5 |
| Ranking bins by raw menin signal builds a class that the IgG control piles into eight to thirty-six fold - so the first version of our menin-bound contrast was measuring accessibility, and its own negative control said so before we believed it | Analysis | 2 | 4/5 |
| Ranking every KMT2A::AFF1 partner on dependency versus essentiality | Analysis | 2 | 3/5 |
| RARA — domain architecture and residue coordinates | Protein | 4 | 5/5 |
| Rash: the one presenting feature that gets commoner the younger the baby is | Explainer | 4 | 3/5 |
| RBBP4 - the shared histone-binding subunit that every leukaemia line needs, and whose identical-length paralogue cannot replace it | Gene | 6 | 4/5 |
| RBBP5 — a WRAD subunit that binds the one part of KMT2A every fusion throws away | Protein | 12 | 4/5 |
| RBBP5: the thinnest fusion literature of the four subunits, and one chromatin datum | Explainer | 10 | 4/5 |
| RBBP7 - the silent paralogue that is not silent, and the reason this project's paralogue rule finally produced a positive answer | Gene | 5 | 3/5 |
| RBBP8 / CtIP - the only unwritten core-complex partner with a DIRECT-interaction record, and the graph already held its mechanism without holding the protein | Gene | 10 | 4/5 |
| RBM15 — m6A adaptor, AMKL fusion partner, and a named hit in the only KMT2A-biased RNA-protein CRISPR screen | Gene | 10 | 3/5 |
| RBM15B — the bridge from the DOT1L mark to the RNA layer: it reads H3K79me2 and steers m6A to start codons | Gene | 6 | 3/5 |
| Re-adjudicating the standing weak spot: proximity labelling HAS sampled AFF1, KMT2A and five leukaemia fusions - just never a KMT2A fusion | Analysis | 5 | 4/5 |
| Re-analyse the eight unreported H3K9me3 samples in GSE210480 at the KMT2A breakpoint cluster region - compute only, and it decides whether the rearrangement brake is mark-specific | Analysis | 2 | 3/5 |
| Re-auditing every cached GEO deposit on three axes after the parser fix: 1,597 comparable title-versus-characteristics pairs across 40 series and 2,620 samples, zero disagreements - and nine series including the one this cycle's beats rest on are abstentions rather than passes, because a 0-of-0 is not a clean bill of health | Analysis | 1 | 4/5 |
| Re-bound at full text, where methods live: 20 records pair a WRAD subunit with a proximity-labelling method and a KMT2A term, 14 pair one with a tiling-CRISPR term, and none is a proximity, degron or tiling study of WRAD in a KMT2A-fusion line | Analysis | 2 | 3/5 |
| Re-bound at full text: 100 records pair an MLLT1 alias with reciprocal-fusion language and 8 with spliced-fusion language, and none stratifies a KMT2A::MLLT1 outcome, transcriptome or drug response by reciprocal or spliced status | Analysis | 2 | 3/5 |
| Re-bound at full text: 40 records pair an ENL alias with condensate and phosphorylation language, 11 of them congress abstract books, and none tests whether YEATS reader binding or ENL condensate behaviour is phosphorylation-gated | Analysis | 2 | 4/5 |
| Re-bound at full text: 65 records name CXCR4 and a menin inhibitor in the same document and the 50 read are all reviews of AML therapy - no study measures the CXCR4 axis under menin inhibition | Analysis | 1 | 4/5 |
| Re-bound at full text: AFF4 still has no haematopoietic cell-state result - the loose intersection is 265 records and the tight one 11, and every title read is a review, a complex-membership mention or a congress abstract book | Analysis | 1 | 3/5 |
| Re-bound at full text: ASH2L still has no haematopoietic cell-state result - the loose intersection is 429 records and the tight one 17, and every title read is a review, a complex-membership mention or a congress abstract book | Analysis | 1 | 3/5 |
| Re-bound at full text: ELL still has no haematopoietic cell-state result - the loose intersection is 1055 records and the tight one 17, and every title read is a review, a complex-membership mention or a congress abstract book | Analysis | 1 | 3/5 |
| Re-bound at full text: KMT2B still has no haematopoietic cell-state result - the loose intersection is 1065 records and the tight one 13, and every title read is a review, a complex-membership mention or a congress abstract book | Analysis | 1 | 3/5 |
| Re-bound at full text: no published experiment removes LEDGF from an established KMT2A-rearranged leukaemia in an animal - the tight intersection returns 12 records of which 6 are congress abstract books and none is a treatment experiment | Analysis | 1 | 3/5 |
| Re-bound at full text: no study of MLLT1/ENL function in cerebellum or developing brain exists, and 10 of the 22 full-text hits are congress abstract books - the weakest-bounded absence in the corpus is now the best-bounded of the four ENL ones | Analysis | 2 | 4/5 |
| Re-bound at full text: still no publication puts KDM2B's rDNA repression together with a KMT2A fusion's nucleolar residence - 27 records, 10 of them congress abstract books, the rest reviews - but KDM2B ChIP-seq in MLL-AF9 cells is now deposited, so the rDNA re-map has a second and better dataset | Analysis | 2 | 4/5 |
| Re-bound at full text: still nobody has asked whether a KMT2A fusion GAINS chromatin sites under a menin inhibitor - but the data to ask it are now deposited, 158 ChIP-seq samples including spike-in-normalised FLAG-MLLAF9 under VTP50469, so the class moves from never-measured to measured-not-analysed | Analysis | 4 | 4/5 |
| Re-bound at full text: the H3K79me2 decay half-life is still unmeasured - one paper in 12.4 million full texts contains the phrase 'half-life of H3K79me2', it is an unnumbered assertion citing a 2010 review, and the MLL::AF9 degron time-course that could have measured it uses the word zero times | Analysis | 3 | 4/5 |
| Re-bound at full text: the LEDGF-after-menin-failure intersection goes from 0 records at abstract level to 116 at full text and 90 with resistance terms, and the 50 read are review articles - no LEDGF-directed agent has been tested in a menin-inhibitor-resistant model | Analysis | 1 | 3/5 |
| Re-bound in the matching instrument: the Antibody Registry holds no junction-specific antibody for any KMT2A fusion under five spellings, while the same query template returns the synovial sarcoma clone as a positive control and turns up two leukaemia-fusion junction reagents nobody here had found | Analysis | 3 | 4/5 |
| Re-checking all 60 bounded-absence claims against the repaired citation index returns zero strong candidates - and that null is not reassurance, because the one absence known to be false ranks first for the wrong reason and its actual refutation is a deposit the method cannot see | Analysis | 1 | 4/5 |
| Re-founding the address argument: the CXXC domain cannot specify a location at any affinity, and a tighter one would be worse | Mechanism | 3 | 4/5 |
| Re-grade the interactome on PSI-MI method class instead of bait role - a dry experiment, and an EXECUTION of a prescription data/symbol-collisions.json already wrote down in cycle 57 and nobody has run | Experiment | 2 | 3/5 |
| Re-measured against IntAct the interactome is 103/217 (47.5%) covered, up from 41.0%, and the read queue is now ZERO - no partner with two publications or two baits lacks an entry, so the instrument's own ranking criterion has stopped selecting anything. It was also persisting the list of partners that DO have entries while counting and discarding the 105 that do not, which is the exact defect cycle 57 fixed for the other list | Analysis | 1 | 5/5 |
| Re-ran this corpus's literature bounds against the live index: 40 of 40 stored zeros still return zero, none has expired - and 19 stored 'queries' abbreviate their own clauses, so they were never runnable bounds at all | Analysis | 1 | 5/5 |
| Re-score all nine GSE260742 same-condition floors under two further external stratifiers already binned on disk - KDM2B DMSO and the Oct-2024 input - to decide whether the twentyfold arm span is a property of the replicate pairs or of the stratum definition. Zero downloads, one re-run of an existing script. | Experiment | 1 | 3/5 |
| Re-score every committed within-sample share ratio at S_FLAG against Q117's eviction quartiles - the bins are already on disk in five scratch directories, no download and no wet work - and start with the H3K79me2 PCGF1 arm, because cycle 83's central null is the one most likely to change | Experiment | 1 | 3/5 |
| Re-scored under the measure that passes a degron positive control, cycle 117's MLL1 two-by-two verdict does not merely survive - it strengthens from a 3.33-fold to a 4.64-fold separation between the menin inhibitor and the DOT1L inhibitor, because the MOLM13 arms do not show the peak-broadening that broke the metric elsewhere | Analysis | 1 | 4/5 |
| Re-supply the AF10 PZP module in cis to KMT2A::MLLT10 and ask whether transformation is suppressed | Experiment | 2 | 3/5 |
| Read all 76 archived CBX3 and BRCA1 tracks at the KMT2A exon-11 anchor at SIGNAL level against a CTCF-anchor-matched null, and score the anchor's rank among its own class in each - no wet work, no new data, and it decides whether the sub-IDR peak is a foothold or a threshold artefact | Experiment | 2 | 3/5 |
| Read at last, against a pre-registered class-matched null: in SU-DIPG13 and SU-DIPG36 the SUV39H1 CUT&RUN mean at the KMT2A exon-11 CTCF anchor is 0.0000 and 1.6660 - the first an EXPLICIT zero record, not missing data - and no one of the seven KMT2A intervals in either line exceeds 1.21x the genome-wide random-tile mean. The pre-registered NEGATIVE prior held. | Analysis | 4 | 3/5 |
| Read from deposited files today: the KMT2A exon-11 CTCF/cohesin element is a top-0.05% etoposide break site on chromosome 11 in a human B-cell-precursor line and in primary CD34+ marrow - and is NOT one in HCT116, the only cell line in which cohesin was ever degraded | Analysis | 4 | 4/5 |
| Read-through (cis-SAGe) chimeras: most 'fusions' called from RNA-seq in childhood ALL are normal conjoined genes | Mechanism | 8 | 4/5 |
| Reading the fusion interactome by COMPLEX rather than by protein — and the strongest signature in it is a known contaminant, which is what makes the rest readable | Analysis | 2 | 3/5 |
| Reading the same-source counter-evidence: 77 notes adjudicated, and the defect is not the one the metric measures | Analysis | 7 | 4/5 |
| Recalibrate the N/C oncoprotein threshold on the fusion-negative CD34+ control at the interval scale it will actually be used at, and report the false-positive count at every scale rather than one | Experiment | 1 | 4/5 |
| Reciprocal status is a different fact depending on whether you assay DNA or RNA, and the whole prognostic literature is RNA | Explainer | 5 | 4/5 |
| Redesign: the proximity-labelling map of KMT2A::AFF1 cannot be controlled with the wild-type allele - it has to be controlled with time | Experiment | 3 | 3/5 |
| Redone at 11x the power: at n=124 the truncating-ARID1A group IS materially lineage-concentrated (TVD permutation p = 0.00020, against p = 0.42 at n=11), so this time the lineage test had something real to remove - and the effect survives it at -0.2516. The missense null is tight, CI95 (-0.0242, +0.0473), excluding -0.10. And there are now 4 truncating-ARID1A leukaemia lines, one short of testable | Analysis | 1 | 4/5 |
| REFUTED IN THE CYCLE IT WAS WRITTEN - the proposal that fusion-driven and normal-tissue-clean surface antigens are disjoint in KMT2A::AFF1 because of what the fusion's output programme is; an expression-matched permutation says it is the base rate | Hypothesis | 4 | 3/5 |
| REFUTED THE SAME CYCLE: window displacement against the current annotation is 1.83%, not systematic - and the real blind spot it hid is one row per symbol at 14.69% | Hypothesis | 3 | 1/5 |
| Registry sweep: is there any CXCR4-directed trial in KMT2A-rearranged or infant leukaemia? There is not, and the one paediatric attempt closed with a single patient | Analysis | 3 | 4/5 |
| Regress prey abundance against interactor confidence class across all 1,330 baits of the Hein atlas - the data are already downloaded and the run is an afternoon | Experiment | 2 | 3/5 |
| REL (c-Rel) — the third canonical subunit, measured once and found unchanged, and named in zero papers in this disease | Protein | 4 | 2/5 |
| RELA (p65) — menin binds it and represses it, and it is required to keep MLL oncoproteins on chromatin | Protein | 11 | 4/5 |
| RELB — the NF-kB subunit that SUPPRESSES MLL-AF9 leukaemia, with a direct ChIP target list and a genetic rescue, which makes it the best-evidenced anti-leukaemic node in this beat | Protein | 5 | 4/5 |
| Releasing JunD does not merely de-repress it: JunD without menin becomes a growth promoter | Mechanism | 3 | 3/5 |
| Removing the fusion is a transcription event first and a chromatin event later, and the gap is enormous: nascent transcription changes within 15 minutes, while genome-wide RNA Pol II peak calls are 99.6% retained at 3 hours and not one active histone mark loses a peak call by 24 hours - the fusion's immediate job is licensing elongation, not building a chromatin landscape | Mechanism | 2 | 3/5 |
| Reopen PXD009338 at peptide level — the search results are already deposited, so no re-search is needed, but the deposit carries no sample-to-file mapping and that is the real cost | Experiment | 2 | 3/5 |
| Repairing 85 defective citation blocks, and the finding that the queue's own numbers were wrong in three directions at once | Analysis | 6 | 5/5 |
| Repeat the H3K79 partition in a human KMT2A::AFF1 line: menin inhibition and MLLT10 knockout, side by side with a KMT2A::MLLT3 line | Experiment | 4 | 3/5 |
| Repeat the one published RPA-at-the-KMT2A-breakpoint experiment in a haematopoietic cell, with an RPA-dose arm - the protocol is fully specified in a 2010 paper whose every arm used fibroblasts and a CML line, and whose primer sets, dose and controls are all published | Experiment | 3 | 3/5 |
| Replication stress and interstrand-crosslink repair as a cell state - an ATR dependency measured in mouse MLL-rearranged AML, and the same stress implicated in breaking the MLL locus in the first place | Cell state | 4 | 3/5 |
| Replication stress, AID, base-excision repair and endonuclease G cut the KMT2A locus | Mechanism | 3 | 3/5 |
| Repurposing approved IMPDH inhibitors (mycophenolate, mizoribine, ribavirin) in KMT2A-rearranged leukaemia - cheap, mechanistically attractive, and asking an immunosuppressant of a neutropenic infant | Target | 5 | 3/5 |
| Rerun the 2002 SPR with the two controls it did not have: cleave the GST, and put the protein on the chip instead of the DNA | Experiment | 2 | 3/5 |
| Resolve acetyl-K1130/K1133 occupancy on the fusion versus wild-type KMT2A in the same cell - the one experiment that makes a shared-sequence site interpretable | Experiment | 2 | 3/5 |
| Resolving all 3,438 cited DOIs, the last identifier class never checked here - 99.8% resolve, every apparent defect is a wrong DOI the corpus quotes in order to correct it, and the three that are genuinely unregistered turn out to carry a working PMID in the same block, because 99.7% of citations here carry two identifiers | Analysis | 1 | 4/5 |
| Resolving cycle 83's threat: the MLL1 channel moves under both drug classes and is therefore not diagnostic, but the MEN1 channel separates them completely - so 'menin displacement' remains a specific readout of menin-interface engagement and the corpus must stop treating the two channels as one | Mechanism | 4 | 3/5 |
| REST / NRSF - the transcription factor that delivers G9a to chromatin through MED19 and MED26, is a paediatric cancer gene, and is the worst search token in this corpus | Protein | 5 | 3/5 |
| Restore the AF9 YEATS reader in cis to MLL-AF9, and read out the ENL patients who already did the experiment for us | Experiment | 3 | 3/5 |
| Retained fetal programme — the infant-versus-adult stem cell difference, and the reason KMT2A::AFF1 needs no second mutation | Cell state | 3 | 4/5 |
| RETRACTED: 'Sixteen percent of GEO sample labels contradict their own metadata' was an off-by-one in my own parser - GEO's brief format puts the title before the accession, so every sample was scored against the next sample's title; the true rate is ZERO, the deposit named as worst offender has none, and the same bug made me 'correct' an agent whose accessions were right | Analysis | 1 | 2/5 |
| Retrospective paired-target MRD on stored Interfant marrows, stratified by IGHV usage | Experiment | 4 | 3/5 |
| Reversibility and kinetics — does the program collapse when the fusion is removed, and how fast? | Mechanism | 6 | 4/5 |
| Revumenib (SNDX-5613, Revuforj) — first approved menin–KMT2A interface inhibitor | Drug | 9 | 5/5 |
| Revumenib does not move H3K27me3 in MLL-fusion leukaemia, in vitro or in vivo: the absence narrows a THIRD time and the experiment's prior collapses | Analysis | 3 | 4/5 |
| RGPD8 is the top-ranked MLL-AF4-specific prey on 3 spectra, and 96.5% of its tryptic peptides are shared with seven near-identical paralogues — only 4 peptides in the whole protein could ever have discriminated it — declined | Interface | 5 | 2/5 |
| RING1 (RING1A) - the paralogue that is not RING1B, and the reason a substring search for 'RING1' in this graph returns the wrong gene | Protein | 7 | 3/5 |
| Risk: CLEC12A-directed therapy ablates normal granulocytes and disables an inhibitory brake on NET formation - the toxicity is mature-myeloid, not stem-cell | Risk | 5 | 4/5 |
| Risk: the class's pharmacodynamic logic measures menin and reports it as the fusion, in a drug class dosed in infants | Risk | 4 | 3/5 |
| RN7SK / 7SK snRNA - the 332-nucleotide brake on elongation, and the one molecule in this beat that every dataset this project uses is blind to | Non-coding | 5 | 4/5 |
| RNA m6A (METTL3/YTHDF/YTHDC1) in KMT2A-rearranged leukemia — the empty cell that turned out not to be empty | Mechanism | 3 | 3/5 |
| RNA-binding proteins set how much KMT2A::AFF1 protein a cell makes from its own fusion transcript | Mechanism | 6 | 3/5 |
| RNA-targeting the fusion transcript: verdict THE LEAST HOPELESS of the three fusion-level routes, blocked by delivery rather than by biology | Target | 3 | 3/5 |
| RNF2 (RING1B) — the one catalytic subunit shared by every PRC1 flavour, which is why the genetics point two ways at once | Protein | 8 | 3/5 |
| RNF20 (BRE1A) — the H2B ubiquitin ligase that MLL-rearranged leukaemia needs, and that DepMap says every other cancer line needs just as much | Protein | 9 | 4/5 |
| RNF40 (BRE1B) — the obligate partner of RNF20, and the one of the pair with a documented link to differentiation and bivalency resolution | Protein | 7 | 4/5 |
| Rob Pieters, Inge van der Sluis & the Interfant consortium (Princess Maxima Center, Utrecht) — the only global infant-ALL trial network | Group | 5 | 4/5 |
| Rolf Marschalek & Claus Meyer (DCAL, Goethe-University Frankfurt) — the world's KMT2A breakpoint dataset | Group | 4 | 4/5 |
| Romidepsin - the HDAC inhibitor with the best preclinical case in KMT2A-rearranged INFANT ALL specifically, and a mechanism that is not about histones at all | Drug | 4 | 3/5 |
| Route 5 rescued 2 of 32, and 21 of the 30 failures returned HTTP 200 with no article - each publisher failing at a constant, recognisable length | Analysis | 2 | 0/5 |
| RPA-coated single-stranded DNA is the structure that licenses ATR: ATRIP reads it, ATR is brought to the lesion, and CHK1 is activated - which is how this corpus's ATR and CHEK1 entries connect to the clamp that had no entry until now | Mechanism | 4 | 5/5 |
| RPA1 (RPA70) - the large subunit of replication protein A, which carries most of the ssDNA-binding folds and the N-terminal fold that hands the lesion to ATR | Gene | 7 | 4/5 |
| RPA1 and RPA2 are curated HGNC aliases of POLR1A and POLR1B, and RPA34 - a UniProt synonym of RPA2 - is an alias of POLR1G, so three of the ssDNA clamp's names point at RNA polymerase I subunits; the hazard is in symbol-based DATABASE lookups, not in PubMed, and the measured contamination says which | Analysis | 5 | 4/5 |
| RPA2 (RPA32) - the middle subunit of replication protein A, whose disordered N-terminus is the phospho-switch of the replication-stress response and whose 43-171 region binds menin | Gene | 7 | 4/5 |
| RPA2 is the only compartment-compatible candidate of the six and the corpus already has a KMT2A resection thread it would fit — but it is an abundant ssDNA-binding subunit on 6 spectra in a benzonase-treated lysate with no RPA1 or RPA3 co-recovered — declined, thread flagged | Interface | 5 | 2/5 |
| RPA3 (RPA14) - the 121-residue subunit of replication protein A, which has no annotated domain, no HPA localisation call and no connection to this disease at all | Gene | 4 | 4/5 |
| RPRM (reprimo) - the other half of menin's Ewing 2007 pair, a protein with no experimental localisation at all, and a promoter methylated in 45% of paediatric AML | Protein | 5 | 2/5 |
| RRP12 (Q5JTH9) - a pre-40S export factor in six of seven MLL-fusion interactomes but NOT in the index fusion's, and the block's only member with a recessive human disease published in 2025 | Gene | 5 | 2/5 |
| RRP9 / U3-55K (O43818) - the U3 snoRNP-specific core protein in four MLL-fusion interactomes but NOT the index fusion's, and the block's only member with a published acetylation switch | Gene | 4 | 2/5 |
| RS4;11 - the human KMT2A::AFF1 index-fusion line - has a deposited H3K79me2 pair, a MENIN pair, an MLL1-N pair, a DOT1L pair and an input under the same menin inhibitor in GSE127507. Every track needed to run this beat's test on the index fusion exists. The download is 1.99 GB measured by HEAD request, and nobody has run it. | Analysis | 2 | 4/5 |
| RS4;11 (CVCL_0093) — an ADULT KMT2A::AFF1 line, MSI-high, carrying NSD2 E1099K | Explainer | 3 | 5/5 |
| RS4;11 retains 2.5x more H3K79me2 than MOLM13 under EPZ5676 at every one of ten baseline deciles - and 0.71x under compound 10, with the sign reversing in deciles 5-10: the between-line difference survives the baseline confound and fails the drug replication, so it cannot be attributed to the fusion partner | Analysis | 2 | 3/5 |
| RSBN1 / KDM9 (Q5VWQ0) - an H4K20me2/me3 demethylase in the AFF4 proximity record, and the only read-queue partner that is a chromatin enzyme at all | Gene | 8 | 2/5 |
| RTF1 — the PAF1C subunit the graph was missing, on a complex that does bind the retained KMT2A fragment | Protein | 7 | 4/5 |
| Rule 62 applies to a genome browser: the UCSC search API returns several tracks and many rows per gene, 'take the longest' put Hoxa9 and Meis1 on chr1, only the refGene track carries the SYMBOL in posName, and xenoRefGene returns a human-aligned Six1 on mouse chr17 | Explainer | 2 | 5/5 |
| Rule 80 measured: the abstract index missed the best KMT2A measurement for three marks out of seven, and confirmed the absence for the other four | Analysis | 3 | 4/5 |
| RUN (by the King, cycle 159): the eight definitions span 55 points, from 36.8% to 78.8% on one population - every pre-registered reading fires, the beat is NOT refuted, and bare 'chromatin' alone moves it 25 points | Analysis | 1 | 3/5 |
| Run a fusion-specific and a total-AFF1 readout side by side in the same KMT2A::AFF1 nuclei, and report the two target sets rather than one | Experiment | 2 | 3/5 |
| Run in coordinates: the protective CTCF site and the patient break-prone window are ONE element, it is cohesin-bound, and the 'functional cut point' is 3.75 kb away - two of the graph's three exon-11s were the same exon and the third was not | Analysis | 9 | 4/5 |
| Run on the reciprocal KMT2A-C antibody instead of the fusion-side KMT2A-N, the same rule gives zero AFF1-exclusive recurrent gene bodies against a null of 0.52 - the gene-scale class is fusion-arm specific | Analysis | 2 | 4/5 |
| Run the menin inhibitor against CALM-AF10 next to a KMT2A-rearranged control - the missing two-week experiment | Experiment | 3 | 3/5 |
| RUN, and the absence closes: all 13 released ENCODE BRCA1, CBX3 and CBX1 ChIP-seq tracks read at the KMT2A locus with three nulls - zero called peaks in 13 of 13, the breakpoint cluster at 0.57-1.24x the genome, and the exon-11 CTCF element BELOW the median CTCF anchor of its own cell type in 10 of 13 | Analysis | 4 | 4/5 |
| RUN, by Q156, within the hour: the whole-table displacement audit - drift is 1.83%, the real blind spot is one row per symbol at 14.69%, and the case that motivated it is not displaced | Analysis | 3 | 4/5 |
| RUN, with its positive control: knocking down KDM4B and KDM4C together raises H3K9me3 at the +1 nucleosome of 2,000 active promoters by 35.7 percentile points, moves the KMT2A promoter's +1 nucleosome by the same 35.3, and moves the 90 kb KMT2A gene body 5.05 points the WRONG way - so the methyl-poor domain is not an erasure product | Analysis | 2 | 3/5 |
| RUN: endogenous HP1a/CBX5 is DEPLETED at the exon-11 anchor (median 23.94th percentile) and has the lowest KMT2A gene-body reading of any protein in the panel (30.16) - while the phosphomimetic Bio-ChIP mutant 4E reads higher than the phospho-compromised 4A at all seven intervals AND that difference falls inside the genome-wide interquartile range of the same comparison, so it carries no information | Analysis | 3 | 2/5 |
| RUN: G9a/EHMT2 reads the 95.8th percentile of 56,171 same-cell-type CTCF anchors at the KMT2A promoter in all four MCF-7 ChIP-seq tracks, and a median 33.42nd at the exon-11 anchor - so the cheapest test of hyp-q114's third prediction REFUTES it | Analysis | 3 | 3/5 |
| RUN: KAP1/TRIM28 has a called peak overlapping the KMT2A promoter in MCF-7 in both hormone conditions, 267 bp of it inside the K562 TRIM28 peak Q110 found - and its nearest chr11 peak to the exon-11 CTCF summit is 52,230 bp away | Analysis | 3 | 3/5 |
| RUN: KDM4B and KDM4C both read the 76.6th-79.7th percentile of MCF-7 CTCF anchors over the whole 90 kb KMT2A gene body - above the 25-track panel median of 61.39, LOCUS-WIDE ELEVATED - and both are ORDINARY at the exon-11 anchor with replicate spreads of 92.3 and 61.5 percentile points | Analysis | 3 | 3/5 |
| RUN: ten ENCODE peak sets and fourteen signal tracks read at the KMT2A locus in two blood cells - not one called peak for SETDB1, CBX5, CBX1, CBX3 or TRIM28 anywhere in the gene, while G9a/EHMT2 and TRIM28 both sit on the KMT2A PROMOTER and neither touches the breakpoint cluster region | Analysis | 3 | 3/5 |
| RUN: the eight unreported H3K9me3 samples of GSE210480, read at the KMT2A CTCF element - H3K9me3 does not move where H3K9me1 moves 3.9-fold, and the me1/me2 positive controls passed | Analysis | 3 | 4/5 |
| RUN: the IDR-free, signal-level re-read of the KMT2A exon-11 anchor against a class-matched CTCF-anchor census - the pre-registered prior of NEGATIVE HELD, both arms score FAILS on the pre-registered rule (BRCA1 median percentile 62.8 of 6 tracks, CBX3 55.9 of 3), and the one thing the prior did not predict is that 2 of 6 BRCA1 tracks sit above the 90th percentile and both are the non-blood cells | Analysis | 2 | 4/5 |
| Running the HOXA programme is not enough to need menin | Analysis | 1 | 2/5 |
| Running the wrong-paper check over the 17,925 PMID citations - the larger half of the corpus and the half where both documented failures happened - gives 100.0% year agreement and 99.7% on authors, one genuine defect, and shows the DOI side's 92% was an artefact of comparing against a single date field | Analysis | 1 | 4/5 |
| RUNX1 — activated by KMT2A::AFF1 and then bound by the reciprocal fusion, in the one published two-oncoprotein circuit in t(4;11) | Protein | 7 | 3/5 |
| RUNX1 — domain architecture and residue coordinates (with the RUNX1b/RUNX1c +27 offset) | Protein | 7 | 4/5 |
| RUNX1 K43 acetylation - a retained-portion site that AML1-ETO genuinely requires, in the 5' partner, with the 3' partner supplying the acetyltransferase in trans | Mechanism | 3 | 4/5 |
| RUNX1::RUNX1T1 (AML1-ETO), t(8;21)(q22;q22) | Fusion | 7 | 5/5 |
| RUNX1T1 (ETO / MTG8) domain architecture | Protein | 1 | 4/5 |
| RUNX2 - a direct KMT2A-chimera target and dependency in T-ALL, a patient-specific enhancer target in KMT2A::AFF1 B-ALL, and the gene a menin inhibitor represses to restore steroid sensitivity in t(4;11) infants | Gene | 9 | 4/5 |
| RYBP - the subunit that makes a variant PRC1 complex catalytically active, named by two entries in this graph and never written | Gene | 8 | 3/5 |
| S1PR4 - the third parenchymally clean surface protein in the screen, a leukocyte-restricted GPCR, and not fusion-specific either | Gene | 4 | 3/5 |
| S821 is not phosphorylated in any dataset we could query: the 14-3-3 motif candidate is dead as stated | Analysis | 3 | 4/5 |
| SALVAGED from a beat killed by a session limit: the PXD009338 spike control passes decisively, but AFF1 - the index fusion's own partner - has 33 PSMs and ZERO above the identity threshold, so that criterion cannot discriminate any of the six candidates | Analysis | 3 | 3/5 |
| SALVAGED from a beat killed mid-write: with direct DOT1L inhibition as the positive control that bounds the achievable effect, VTP-50469 achieves only F = 0.09-0.25 of it. SGC0946 strips H3K79me2 to 6.7-14.8% of DMSO; the menin inhibitor leaves 77-91%. And the bin-wise responses do not correlate (rho = -0.026) | Analysis | 1 | 3/5 |
| Salvaged from a session-limit death: the DMSO-versus-DMSO selection control cannot be run cleanly on GSE260742, because every same-condition vehicle pair is confounded - two differ about three-fold in aggregate signal and the only admissible same-mark pair crosses processing states (filt.bam.tdf versus tdf). Its automated verdict of MANUFACTURED is NOT supported, and the control remains UNRUN rather than passed or failed | Analysis | 1 | 3/5 |
| SALVAGED: in K562, which carries no KMT2A fusion at all, a menin inhibitor moves H3K79me2 as much as it does in fusion-bearing murine MLL-AF9 (V 0.8291 vs 0.7734, F 0.1831 vs 0.2500). Both the confirmation and the refutation fail to fire, and the refutation misses by 0.0057 - this is at-the-edge and must not be read as a clean negative | Analysis | 1 | 2/5 |
| SAM / methionine dependence - the one metabolic state in this graph demonstrated in KMT2A-rearranged lymphoblastic leukaemia itself, with a drug and a PDX behind it | Cell state | 3 | 4/5 |
| SAM supply sustains the KMT2A-rearranged hypermethylated state - the metabolic requirement that IS a consequence of the chromatin programme, and can be attacked as one | Mechanism | 3 | 3/5 |
| SAMHD1 - the dNTP hydrolase that is the real biomarker behind the IMPDH story, and the reason the KMT2A framing of that story does not hold | Protein | 5 | 4/5 |
| SATB1 - a nuclear-matrix and PML-body genome organiser with its own matrix-targeting sequence, the clearest subnuclear-localization entry in this beat, and a T-lineage factor that B cells do not need | Gene | 10 | 4/5 |
| SAVE (NCT05360160): the first prospective menin-inhibitor trial to report a NUP98-rearranged subgroup outcome | Trial | 4 | 3/5 |
| SBDS - a ribosome-maturation factor whose loss causes a leukaemia-predisposition syndrome, and whose BioID neighbourhood contains AFF1, KMT2A, CDK9, PAF1 and LEDGF | Gene | 7 | 2/5 |
| SCAF11 / SRrp129 (Q99590) - an SR-related protein that binds the RNA Pol II CTD, in the pan-MLL-fusion core, and alone among the SCAF family | Gene | 4 | 3/5 |
| SCF(Skp2) grips the retained fragment and the fusion escapes it - the clearest documented non-menin contact on that region | Interface | 3 | 3/5 |
| SCMC-L1 (CVCL_7125) — a four-month-old's KMT2A::AFF1 line carrying NSD2 E1099K | Explainer | 3 | 4/5 |
| Score the HSPC-like fraction on paired pre-treatment and on-treatment samples from KMT2A-rearranged patients receiving a menin inhibitor — a flow-first design with a single-cell confirmatory arm | Experiment | 2 | 3/5 |
| Scored against the literature: the composition half of the YEATS-selectivity objection holds and the selectivity half is refuted — a scaffold-blind probe already has an in vivo window in the index fusion with no HSPC toxicity | Analysis | 3 | 3/5 |
| Scored against the same DMSO in the same batch, degrading the fusion leaves 1.0% of its chromatin sites, the DOT1L+menin combination leaves 10.7%, the menin inhibitor alone leaves 51.7% and the DOT1L inhibitor alone 75.5% - and in a second independent batch the menin inhibitor again beats the DOT1L inhibitor on the fusion's own channel | Analysis | 2 | 3/5 |
| Scored at complex level, coherence predicts nothing (rho -0.016 over 719 complexes) - but the Fanconi core complex is 2nd of 719 and the HBO1/MOZ acetyltransferase modules are 1st | Analysis | 3 | 0/5 |
| Scored in the published criterion's own currency, the number of oncoprotein-target promoters runs 0 to 2282 across 27 KMT2A-rearranged patient samples - 20.01x between the 10th and 90th percentiles - and the spread widens to 61.10x after depth matching | Analysis | 2 | 4/5 |
| Scoring complexes instead of genes, and the controls disagree with each other (run) | Analysis | 1 | 3/5 |
| Scoring cycle 104's mark panel against a floor measured in its OWN arm: 9 of 10 mark-by-arm cells at D1 land inside the floor's own spread, so D1 is not resolvable from this deposit at all - and the same mark ratios give 0, 4 or 4 breaking marks depending only on which floor was imported, so cycle 104's pass, cycle 107's F1 and the GSE299100 beat's failure were all measuring the ruler rather than the marks | Analysis | 1 | 3/5 |
| Scott Armstrong & Andrei Krivtsov (Dana-Farber / Boston Children's) — the group that turned menin dependency into a drug | Group | 4 | 4/5 |
| scripts/is-symbol-covered.py returns 'no match' for BRAF, AKT1, EGFR, CD226 and IRF2 - all five have a declined interface entry. The `interface-` prefix in its PREFIXES list can never match anything. | Analysis | 2 | 5/5 |
| Searching 32 GEO series and 2,312 samples for a menin readout under DOT1L inhibition: exactly ONE distinct experiment exists, MOLM13_MEN1-ChIP_EPZ5676_4d at 100 nM, and it is the sample Q136 already used - so the deflationary reading of Q136 is blocked not by a missing assay but by a ~50-fold DOSE GAP, and Q136's drug-class conclusion rests on a single unreplicated sample in a single cell line | Analysis | 1 | 4/5 |
| SEC — the AFF1/AFF4-scaffolded super elongation complex, the particle KMT2A::AFF1 is a permanent subunit of | Protein | 5 | 5/5 |
| SEC-L2 — the AFF2-scaffolded super-elongation-like complex: P-TEFb plus ENL and AF9, and NO ELL | Protein | 3 | 3/5 |
| SEC-L2 and SEC-L3 contain ENL and AF9 exactly as SEC does, so AFF2 and AFF3 sit in complexes built around the same acyl-lysine readers as the index fusion's partner - and both entries carry no epigenetics annotation at all | Mechanism | 1 | 4/5 |
| SEC-L3 — the AFF3-scaffolded complex, and the only SEC-family member with a known physiological job: genomic imprinting and X inactivation | Protein | 5 | 3/5 |
| SELE (E-selectin) - the vascular-niche chemoresistance receptor with a clinical antagonist, zero KMT2A papers, and a paediatric trial that a company restructuring closed | Gene | 6 | 3/5 |
| Selective in the disease and quiet everywhere else: MYB comes out cleanest | Analysis | 3 | 0/5 |
| Selinexor (XPO1 inhibition) — a real paediatric response rate attached to an unproven mechanism in KMT2A-rearranged disease | Drug | 2 | 3/5 |
| SEM (CVCL_0095) — the workhorse, from a five-year-old, and microsatellite unstable | Explainer | 4 | 5/5 |
| SEM, the standard t(4;11) model line, has zero signal at IRX1 — every model of this disease is a model of one subgroup | Analysis | 4 | 3/5 |
| Separate AKAP95's two routes into the KMT2A axis - starting with one transfection that re-reads a thirteen-year-old control | Experiment | 2 | 3/5 |
| Separate ncBAF from canonical BAF in KMT2A-rearranged cells: paired degron, paralogue-pair CRISPR, and complex-resolved CUT&RUN | Experiment | 4 | 3/5 |
| Separate positioning from catalysis: an ASH2L mutant that keeps RBBP5 and loses DPY30 | Experiment | 3 | 3/5 |
| Separating CK2's two routes into KMT2A leukaemia, which every published experiment has confounded | Experiment | 2 | 3/5 |
| Separation-of-function RTF1 rescue in a KMT2A-fusion line: does the fusion need PAF1C for elongation, or for H2B ubiquitination? | Experiment | 2 | 3/5 |
| Separation-of-function test: does KMT2A::AFF1 need its C-terminal homology domain to dimerise? | Experiment | 7 | 3/5 |
| SEPTIN11 (septin-11) — KMT2A fusion partner at 4q21, adjacent to AFF1 | Protein | 4 | 3/5 |
| SEPTIN2 (septin-2 / NEDD5) — KMT2A fusion partner in t(2;11)(q37;q23) | Protein | 10 | 3/5 |
| SEPTIN5 (septin-5 / CDCrel-1) — KMT2A fusion partner in t(11;22)(q23;q11.2) | Protein | 4 | 3/5 |
| SEPTIN6 (septin-6) — cytoskeletal GTPase, KMT2A fusion partner in t(X;11)(q24;q23) | Protein | 5 | 4/5 |
| SEPTIN9 (septin-9 / MSF) — cytoskeletal GTPase, KMT2A fusion partner in t(11;17)(q23;q25) | Protein | 9 | 3/5 |
| Sequencing phase 2: the order to do things in, ranked by information per unit cost | Explainer | 3 | 3/5 |
| Sequencing-based MRD: better than flow in paediatric B-ALL, and applied to infant KMT2A-rearranged disease exactly once | Explainer | 5 | 3/5 |
| Serine/glycine dependence in MLL-ENL leukaemia, reached through a DIRECT fusion target gene - and the reason a PHGDH counted absence in this graph would have been wrong | Mechanism | 2 | 3/5 |
| SESN2 / sestrin-2 (P58004) - the ISR's exit into mTORC1: a leucine sensor that falls 1.4 log2 under either inhibitor, and the one panel member with a real structural record | Gene | 5 | 4/5 |
| SET / TAF-I beta - a histone chaperone that binds the retained N-terminus of MLL, co-activates HOXA with it, and is itself a HOXA-activating fusion partner that recruits DOT1L | Gene | 9 | 3/5 |
| SET / TAF-Ibeta domain map (Q01105, 290 aa) - dimerisation, earmuff, and the acidic tail that binds MLL | Protein | 7 | 3/5 |
| SET::NUP214 (TAF-Ibeta-NUP214, SET-CAN), cryptic del(9)(q34.11q34.13) - a HOXA-driving fusion of a histone chaperone to a nucleoporin, with no KMT2A and no menin-binding motif | Fusion | 9 | 4/5 |
| SET::NUP214 adult T-ALL is gamma-delta-lineage-restricted and resistant to steroids and chemotherapy early - the same cell state CALM-AF10 occupies | Cell state | 4 | 4/5 |
| SET::NUP214 has no address of its own: chromatin-bound CRM1 is already at HOX, and the fusion's FG repeats dock onto it | Mechanism | 3 | 4/5 |
| SET::NUP214 is KMT2A-free in its sequence but not in its mechanism: it binds and condenses wild-type MLL1, which reopens the menin question this beat was sent to close | Mechanism | 4 | 3/5 |
| SET::NUP214 is the second KMT2A-free HOXA fusion, and it converges on the same two proteins CALM-AF10 uses: CRM1 and DOT1L - and so does NPM1c, which IS menin-dependent (corrected 2026-09-21) | Mechanism | 4 | 4/5 |
| SET::NUP214 recruits DOT1L by a different surface from CALM-AF10 and KMT2A::MLLT10: the founding paper tested for AF10 in the complex and did not find it | Mechanism | 4 | 3/5 |
| SETD1A — a leukemia dependency whose enzyme activity turns out to be dispensable | Protein | 11 | 4/5 |
| SETD1B - the COMPASS paralogue round 4 deferred for want of a leukaemia paper, which had already been published: its SET domain sets H3K4me3 breadth and MYC in MLL-rearranged AML | Protein | 6 | 3/5 |
| SETD2 (Q9BYW2) - the H3K36 trimethyltransferase that binds all seven MLL fusions, and the only one of them with a published KMT2A::AFF1 dependency test | Gene | 6 | 3/5 |
| SETDB1 (Q15047, KMT1E/ESET) - the second H3K9me3 writer: it represses the fusion's own targets via the PAF1 complex, it is required in fetal liver HSPCs and in leukaemic stem cells, and it is a broad dependency in half the CRISPR panel - three published directions that do not agree | Gene | 10 | 3/5 |
| Settle the monocytic confound isogenically: degrade the fusion, read haem-gene dependency before lineage has time to move | Experiment | 4 | 3/5 |
| Settle the WRAD question: tagged co-IP plus degron-timed proximity across three fusion classes | Experiment | 4 | 3/5 |
| Seven KMT2A-rearranged sarcomas retain the menin-binding motif, three of them carry the complete leukaemic N-terminal module, and all sixteen partner names were in one unopened supplementary table | Analysis | 2 | 3/5 |
| Seventeen entries declare themselves part of a causal chain that does not exist, and the validator could not see it | Analysis | 1 | 4/5 |
| Severability (contract law) — what survives when a clause is struck, and what survives a KMT2A break | Analogy | 3 | 1/5 |
| SF3A3 / SF3a60 (Q12874) - a U2 snRNP splicing subunit in the pan-MLL-fusion core, and the paper's own named example of a NON-selective hit | Gene | 4 | 3/5 |
| SFPQ / PSF (P23246) - the last of 21 fusion-construct partners without an entry, and it is itself the 5' half of an ALL fusion that puts ABL1 in the nucleus | Gene | 6 | 3/5 |
| SGC-iMLLT - the MLLT1/MLLT3 YEATS chemical probe, and the 2026 paper that put it into KMT2A::AFF1 in vivo with a healthy-HSPC comparison | Drug | 4 | 3/5 |
| SGC0946 removes 86% of H3K79me2's share at the fusion's own sites and the four eviction quartiles are 0.1396 / 0.1453 / 0.1452 / 0.1360 - span 0.0036, Spearman +0.400, a bootstrap interval spanning zero - so a very large effect on this mark can carry no eviction-depth structure whatever | Analysis | 4 | 3/5 |
| SGF29 — a SAGA reader with a Tudor pocket, intermediate essentiality, and the best unexploited profile in this beat | Protein | 10 | 3/5 |
| SGK1 / SGK (O00141) - a MENIN-SELECTIVE upregulated kinase, a druggable AGC family member, and the panel's worst platform disagreement | Gene | 3 | 3/5 |
| SHMT2 (P34897) - the mitochondrial one-carbon step, and the paralogue that rises while it falls is why its loss may not matter | Gene | 5 | 3/5 |
| SIAH1 — the E3 ligase that degrades AFF1, and that the reciprocal AF4::KMT2A fusion escapes | Protein | 8 | 3/5 |
| SIAH1/SIAH2: the disposal route that destroys wild-type AF4 and that the reciprocal fusion escapes | Mechanism | 3 | 2/5 |
| SIAH2 — the second AFF1 E3 ligase, reported only alongside SIAH1 and never separated from it | Protein | 2 | 2/5 |
| Signalling co-mutations (RAS pathway, FLT3-ITD, WT1) under menin-inhibitor pressure | Resistance | 3 | 3/5 |
| Silmitasertib (CX-4945) - a CKII inhibitor that works on KMT2A-rearranged leukemia by strengthening the allele the fusion does not have | Drug | 2 | 3/5 |
| siMA6 confirmed junction-spanning by reconstruction - 8 KMT2A bases plus 13 AFF1 bases - and it targets the 1362/1363 breakpoint, not the one this graph modelled as canonical | Analysis | 2 | 0/5 |
| SIN3A (Q96ST3) - the scaffold of the OTHER HDAC1/2 corepressor complex, a 5' fusion partner in infant B-ALL and in myelodysplasia, and present in three MLL-fusion AP-MS columns but not the index fusion's | Gene | 11 | 3/5 |
| Single-cell CUT&Tag on p279 — is the double-positive blast one cell state or two clones? | Experiment | 2 | 3/5 |
| Sinusoidal obstruction syndrome after infant conditioning - an age signal, a regulatory exposure threshold, and a prophylaxis that failed its randomised trial | Risk | 4 | 3/5 |
| SIRT1 - not a fusion partner, the least required gene in KMT2A-rearranged lines, and the one target here where the direction of the drug is genuinely disputed | Protein | 7 | 3/5 |
| SIT1 - one of only three surface proteins in the screen that is both expressed in KMT2A::AFF1 lines and absent from normal parenchyma, and it is clean because it is leukocyte-restricted, not because it is leukaemic | Gene | 4 | 3/5 |
| Six countermeasures, no head-to-head — so rank their targets: CDK6 is 13th and CDK4 is 16,052nd | Analysis | 1 | 3/5 |
| Six files titled H2AK119ub rep1 are FLAG ChIPs, so prediction 5's eviction clause - declared UNREACHABLE by Q124 - was computable from bins already on disk. It is now scored and it CONFIRMS: VTP-50469 removes the same share of fusion occupancy in the PCGF1 knockout as in the control, 0.7655 against 0.7554, a 1.3% difference against 22.8% genotype variation on a control drug | Analysis | 1 | 3/5 |
| Six gene bodies are AFF1-exclusive and recurrent at gene scale; the authors' own pipeline confirms one of them, refutes three and has never measured two - and IRX1 is the one it confirms | Analysis | 3 | 4/5 |
| Six GSE260742 samples titled 'NTvKO ... H2AK119ub rep1' carry ChIP_FLAG filenames AND a ChIP_FLAG string in the TDF header their own depositors' igvtools wrote - two of three independent sources say FLAG, the shape test is near-indecisive, and the channel of half the replicate arm cannot be settled from the deposit | Analysis | 3 | 4/5 |
| Six of 85 proteins are both selectively required and drugged — and MEN1 is not close to the others | Analysis | 1 | 3/5 |
| Six relapses and a change of lineage: KMT2A::AFDN T-lymphoblastic lymphoma that came back as monoblastic leukaemia, and a seventh remission that held | Patient story | 2 | 3/5 |
| Six times the null pool, and the criterion I had been using turns out to be the problem (run) | Analysis | 1 | 3/5 |
| Six to twenty-four libraries in RS4;11: two DOT1L inhibitors titrated to equal spike-in-measured global H3K79me2 loss, three replicates per arm, plus the no-primary control that no public deposit contains - the smallest experiment that would convert four moderate entries in this beat into testable ones | Experiment | 2 | 3/5 |
| SKIC8 (formerly WDR61) — the last PAF1C subunit, and a gene-symbol trap worth recording | Protein | 6 | 4/5 |
| Skin first, blood later: a three-day-old referred for purple spots, with KMT2A::MLLT3 neonatal ALL | Patient story | 1 | 3/5 |
| SKP1 — a pan-essential housekeeping adaptor that is also a structural subunit of PRC1.1, which makes it the one PRC1.1 member that can never be a target | Protein | 5 | 4/5 |
| SKP2 - the substrate receptor that grips the retained fragment; two nodes in this graph already pointed at it as a free-text string with nothing to point to | Gene | 7 | 4/5 |
| SMARCA2 (BRM) - the paralogue nobody measured, and the reason a DepMap rank cannot predict what a BRG1/BRM inhibitor does | Protein | 11 | 3/5 |
| SMARCA4 (BRG1) - a tumour suppressor by mutation and a maintenance requirement by knockdown, and in KMT2A-rearranged lines the dependency data say it is not selective at all | Protein | 14 | 4/5 |
| SMARCB1 (BAF47/INI1/SNF5) - zero entries, zero mentions and, on the evidence, correctly so: it is lost in primary AML rather than required | Protein | 10 | 3/5 |
| SMARCC1 / BAF155 (Q92922) - the SWI/SNF core scaffold, in the pan-MLL-fusion core, and the missing gene entry in this graph's SWI/SNF beat | Gene | 3 | 2/5 |
| SMARCD1 (BAF60A) - rank 59 of 17,728, survives the lineage split, and had never been named in this graph or studied in this disease | Protein | 8 | 3/5 |
| SMARCD2 (BAF60B) - named in one KMT2A paper in the whole of PubMed, and the dependency it carries is myeloid identity, not the rearrangement | Protein | 9 | 3/5 |
| SMC1A - a bounded absence written with its query: eleven records, none about this disease, and the whole literature is Cornelia de Lange syndrome | Gene | 5 | 2/5 |
| SMC3 - the cohesin ATPase arm, the only subunit whose partial loss has been tested directly against a KMT2A fusion, and it was tolerated | Gene | 8 | 3/5 |
| SMNDC1/SPF30 - a Tudor-domain splicing factor recovering ELL, ENL, KMT2A, PAF1 and KAT7 | Gene | 3 | 2/5 |
| SMYD3 - a lysine methyltransferase with three claimed histone marks and one robust non-histone substrate, sitting on an HOXA9 feed-forward loop in MLL-AF9 AML and a fatty-acid-oxidation axis in CML stem cells, with zero interventional trials | Gene | 16 | 3/5 |
| SOCS2 (O14508) - a MENIN-INHIBITOR-SELECTIVE member of the signature, a cullin-5 E3 substrate receptor, and its likeliest upstream regulator is MEF2C rather than ATF4 | Gene | 5 | 4/5 |
| SON (P18583) - a nuclear speckle scaffold that BINDS MENIN and inhibits MLL complex assembly, and the one protein in this tranche the Skucha authors name in their own discussion | Gene | 4 | 3/5 |
| Sort KMT2A-rearranged blasts by cell-cycle state, then measure menin-inhibitor response — the one-week experiment nobody has run | Experiment | 3 | 3/5 |
| SPEN / SHARP / MINT (Q96T58) - the RNA-binding corepressor that silences the X chromosome, in the pan-MLL-fusion core | Gene | 3 | 2/5 |
| SPEN is the only member of the real-gap floor whose epigenetic readout is direct and published: its SPOC domain recruits NCoR/SMRT, NuRD and the m6A machinery to active enhancers and promoters, and it disengages from chromatin the moment silencing succeeds | Mechanism | 1 | 4/5 |
| SPI1 / PU.1 — a myeloid dependency that a KMT2A panel mistakes for its own | Protein | 7 | 3/5 |
| Spike-in-normalised menin CUT&RUN in a KMT2A::AFF1 degron line, with replicates and a PSIP1 arm | Experiment | 3 | 3/5 |
| Spike-in-normalised menin CUT&RUN with paired N- and C-terminal KMT2A antibodies in an infant KMT2A::AFF1 sample, on and off drug, in the same disease state | Experiment | 3 | 3/5 |
| Spike-in-normalised paired KMT2A N- and C-terminal CUT&RUN, with a fusion-junction readout, in a HOXA-negative KMT2A-rearranged blast beside a HOXA-positive one from the same institution and batch | Experiment | 2 | 3/5 |
| Spliced and balanced KMT2A::MLLT1 do not automatically make the same oncoprotein - unless you restrict the comparison, which nobody has | Explainer | 4 | 4/5 |
| Spliced KMT2A fusions join to partner exon 2 — with the per-partner counts, and a correction | Breakpoint | 3 | 4/5 |
| Spliced KMT2A fusions: breaks upstream of the partner's exon 1, and the reciprocal-free natural experiment | Breakpoint | 4 | 3/5 |
| SPP1 (osteopontin) - the endosteal matrix protein whose knockdown prolongs survival in MLL-AF9 mice, and the one KMT2A::AFF1-specific paper about it cannot be read | Gene | 5 | 3/5 |
| SPRED1 - the RAS/MAPK brake whose deletion marks relapse in paediatric B-ALL, third-widest margin in the Q152 AFF1-only core | Gene | 3 | 2/5 |
| SRCAP - the other H2A.Z-loading motor, whose entire PubMed intersection with MLL is five neurodevelopmental gene panels | Gene | 3 | 3/5 |
| SREBF1 / SREBP-1 - the weakest of the three MEN1 sterol partners, because it is simultaneously the pathway's readout | Gene | 7 | 2/5 |
| SS18 - a SWI/SNF subunit that is itself a fusion partner in another cancer, and a lineage-independent dependency in KMT2A-rearranged lines | Protein | 10 | 3/5 |
| SSRP1 - the small FACT subunit, and the only protein in this beat that binds a confirmed KMT2A-fusion interactor directly (LEDGF/p75, via HMG box to PWWP) | Protein | 8 | 3/5 |
| St. Jude Cloud and the Pediatric Cancer Genome Project — raw paediatric leukaemia genomes a small lab can get without a collaboration | Group | 4 | 4/5 |
| STAG2 - the cohesin subunit that defines secondary AML, and the one whose loss a KMT2A fusion does not care about | Gene | 8 | 0/5 |
| STC2 / stanniocalcin-2 (O76061) - the second largest effect in the signature (-4.40 log2), a SECRETED glycoprotein, and its localisation rests on curator inference alone | Gene | 4 | 4/5 |
| Step 1 — How the fusion finds its genes: AT-hooks and the CXXC domain reading unmethylated CpG | Mechanism | 5 | 4/5 |
| Step 1: the blood count and the blood film | Explainer | 5 | 4/5 |
| Step 2: flow cytometry and the CD10-negative pro-B fingerprint | Explainer | 7 | 4/5 |
| Step 3 — The hijack: the fusion drags the super elongation complex to paused RNA polymerase II | Mechanism | 5 | 5/5 |
| Step 3: the G-banded karyotype and t(4;11)(q21;q23) | Explainer | 5 | 4/5 |
| Step 4 — The histone mark: DOT1L and H3K79me2/3 at fusion target genes (and why global expression barely moves) | Mechanism | 9 | 5/5 |
| Step 4: the split-signal FISH nucleus - one fusion, one green, one red | Explainer | 5 | 4/5 |
| Step 5 — The output program: HOXA9/HOXA10/MEIS1/PBX3 plus MEF2C, MYB, BCL2, FLT3 and PROM1/CD133 | Mechanism | 8 | 5/5 |
| Step 5: molecular confirmation and naming the partner | Explainer | 5 | 4/5 |
| Step 6 — The consequence: self-renewal held on, differentiation never fires | Mechanism | 5 | 5/5 |
| Strand-resolved transcription across the AFF1 / AFF1-AS1 / C4orf36 promoter - the only measurement that can say which gene the signal belongs to | Experiment | 2 | 3/5 |
| Stratify an existing menin-inhibitor cohort by reciprocal fusion status | Experiment | 3 | 3/5 |
| Stratifying by eviction depth does NOT rescue H3K79me2 as a resistance-detecting readout: at the most-evicted quartile the PCGF1-knockout and the control are 0.6123 against 0.5860, a difference of 0.0263, while the whole genotype effect sits at the LEAST-evicted quartile (-0.1401) - the opposite of eviction-graded | Analysis | 3 | 3/5 |
| Stratifying the MOLM13 co-occupied bins by signal amplitude qualifies this beat's own headline: at the strongest tenth the MLL1-N channel falls to 0.5304 and H3K79me2 to 0.7614, so 'MLL1-N does not move' and 'the mark does not move' are both properties of the aggregate - while the ordinal swap that refuted the four-way ordering survives in every stratum | Analysis | 1 | 4/5 |
| Subclonal cooperating lesions lost at relapse - what was actually measured, and why 'lost' is the wrong word | Mechanism | 5 | 4/5 |
| Subtraction is a partner class, not a curiosity — and the class is defined by compartment, not by sequence | Hypothesis | 4 | 3/5 |
| Sumitomo Pharma — enzomenib (DSP-5336): one trial, adolescents at 12 years and 40 kg, no paediatric programme | Group | 3 | 3/5 |
| Summit containment passes the positive control that the bin-overlap measure failed, in all three HA batches | Analysis | 3 | 4/5 |
| SUMO1 - not a complex partner of LEDGF but a modifier of it, and the interactome row cannot tell you which | Gene | 9 | 3/5 |
| SUPERSEDED IN PART, CYCLE 56 - the MI-2-2 response is ~9x fusion-selective (that stands), but 'does not touch HOXA or MEIS1' was a fact about a weak compound: VTP-50469 collapses MEIS1 -5.25 log2 in the same line | Analysis | 6 | 3/5 |
| SUPT16H (SPT16) - the large FACT subunit: pan-essential, an anti-dependency in KMT2A-rearranged lines, and drugged in MLL-r leukaemia by a compound that works through p53 | Protein | 7 | 3/5 |
| SUPT4H1 (SPT4) — zero papers linking it to KMT2A, and the 138th most KMT2A-selective gene out of 17,728 | Protein | 6 | 2/5 |
| SUPT5H (SPT5) — the pausing factor the KMT2A field has never studied, and the counted absence that undercuts 'the fusion hijacks pause release' | Protein | 9 | 3/5 |
| SUPT6H (SPT6) - the histone chaperone that rides with RNA polymerase II, which puts it closer to the fusion's proposed mechanism than anything else in this beat | Gene | 8 | 3/5 |
| SUV39H1 (O43463, KMT1A) - the H3K9me3 writer: a menin effector whose binding region OVERLAPS the drug pocket at its N-terminus, a tumour suppressor in MLL-AF9 AML, recruited to double-strand breaks by CTCF, and never localised at the KMT2A locus in any cell type | Gene | 16 | 3/5 |
| SUZ12 - the scaffold that holds PRC2 together and decides which PRC2 it is, required in this disease and studied in it exactly once | Gene | 7 | 3/5 |
| Swap the AFF1 C-terminus onto a KMT2A-AF9 backbone and score IRX1 occupancy: the direct test of partner causality | Experiment | 2 | 3/5 |
| SWI/SNF enumeration for KMT2A-rearranged leukaemia: every subunit searched, every count dated, and what was read and rejected | Analysis | 4 | 4/5 |
| SWI/SNF split by sub-complex and by lineage: every KMT2A-selective subunit is in the ncBAF module and none is in canonical BAF | Analysis | 4 | 3/5 |
| Switching menin inhibitors: four substitutions defeat all of them, three defeat only some, and the map now exists | Resistance | 4 | 4/5 |
| Switching menin off reverses diabetes that is already there - in three different diabetic mouse models | Mechanism | 2 | 4/5 |
| Sympathetic nerve fibre in bone marrow — the wiring that sets the niche's daily rhythm, through beta-3 in health and beta-2 in leukaemia | Cell type | 4 | 3/5 |
| SYNCRIP (hnRNP Q) — required for MLL leukaemia stem cells in one paper and a tumour suppressor deleted in T-ALL in another | Gene | 5 | 3/5 |
| Syndax Pharmaceuticals — revumenib (SNDX-5613), the only menin inhibitor licensed down to infancy | Group | 6 | 4/5 |
| Systematic enumeration of menin-inhibitor resistance mechanisms: seven entries written, thirteen candidates rejected with reasons | Analysis | 7 | 4/5 |
| t(11;19) is the largest named partner group in the revumenib registration trial - and the trial never resolves whether those patients have MLLT1 or ELL | Epidemiology | 3 | 4/5 |
| t(6;11) makes four fusion genes, not two, and the PHD/bromodomain cassette is what opens chromatin in all of them | Explainer | 3 | 3/5 |
| t(9;11) is the reciprocal-POSITIVE arm: 2 of 612 patients are spliced, against 241 of 460 for t(11;19) | Explainer | 2 | 4/5 |
| t(9;11): the reciprocal product is made, is engineered into every genome-editing model, and has never been separately tested | Explainer | 3 | 3/5 |
| TAF15 (RBP56, TAF2N) - the FET-family, prion-like partner that donates a low-complexity N-terminus to ZNF384 | Gene | 5 | 4/5 |
| TAF15::ZNF384 - the FET-partner version, where the naming order in the literature is a trap and the founding experiment says the transactivation domain is not doing the work | Fusion | 5 | 4/5 |
| Tag endogenous KMT2B in an index-fusion line and measure what revumenib does to it - the experiment the reagents have blocked | Experiment | 4 | 3/5 |
| Tag the endogenous KMT2A::AFF1 allele in RS4;11 and ChIP the tag with and without VTP-50469 alongside MENIN and MLL1-N in the same chromatin - the one experiment that converts every occupancy claim in this literature from a reagent statement into a fusion statement | Experiment | 2 | 3/5 |
| Target safety triage v2: constraint with its uncertainty attached (run) | Analysis | 4 | 3/5 |
| Targeted PRM for the KMT2A::AFF1 junction peptide - the experiment that makes every other attribution claim testable | Experiment | 3 | 3/5 |
| Targeting LIN28B - the essential-function and wrong-sign risks are established by the SAME paper that makes it interesting, and the sign may reverse with lineage | Risk | 3 | 3/5 |
| TASP1 (taspase1) - the protease that cuts KMT2A, and the timer the fusion escapes | Protein | 8 | 4/5 |
| Taspase1 and its two KMT2A cleavage sites: an enzyme-substrate interface with four apo structures, one co-crystal with a small molecule, and no structure with MLL at all | Interface | 4 | 4/5 |
| Taspase1 is what turns the reciprocal product into an oncoprotein - and it is a conditional oncogene because of it | Mechanism | 4 | 3/5 |
| Tazemetostat - an approved EZH2 inhibitor, and the drug this disease's own biology predicts will not work | Drug | 7 | 3/5 |
| TB051939 is rank 12 of 26 and owns fewer singletons than its even share; the library that owns 22.4% of singletons destroys no exclusivity at all; and dropping any single comparator moves the exclusive set by a median of 2 genes | Analysis | 3 | 4/5 |
| TB920488, the other HOXA-negative IRX1-negative blast, has the highest GMP-over-B-lineage ratio of any B-lineage sample in the deposit - and it fails both the matched null and the N-over-C test | Analysis | 2 | 3/5 |
| TBL3 / UTP13 (Q12788) - a UTP-B ribosome-biogenesis subunit in the pan-MLL-fusion core, whose loss in zebrafish severely reduces T cells and haematopoietic stem/progenitors | Gene | 4 | 2/5 |
| TBX21 (T-bet) - the Th1/NK master regulator, the third lymphoid gene in the Q152 AFF1-only core and the one that makes the B-lineage reading fail | Gene | 2 | 2/5 |
| TBXT / brachyury - the notochord master regulator, and one of only two of 102 transcription-factor baits whose neighbourhood contained DOT1L | Gene | 7 | 2/5 |
| TCF3 (E2A) — domain architecture and residue coordinates | Protein | 8 | 4/5 |
| TCF3::HLF (E2A-HLF), t(17;19)(q22;p13) | Fusion | 8 | 4/5 |
| TCF3::PBX1 (E2A-PBX1), t(1;19)(q23;p13.3) | Fusion | 6 | 4/5 |
| TCF3::ZNF384 - the partner whose contribution is now actually demonstrated: steroid resistance, and it is not shared with EP300::ZNF384 | Fusion | 6 | 4/5 |
| TCF7L2 - the protein IntAct's 'DOT1L-TCF4' row is actually about, and the Wnt effector that DOT1L and AF10 coactivate | Gene | 8 | 3/5 |
| TCOF1 / treacle (Q13428) - the Treacher Collins nucleolar phosphoprotein in the MLL-fusion nucleolar block, the block's only link to rDNA damage signalling through NBS1, and the only member whose loss causes a named human developmental syndrome | Gene | 5 | 2/5 |
| TDP2 - the protein-adduct remover named in this graph's own mechanism entry and until now having no entry of its own | Gene | 7 | 4/5 |
| TDP2 unglues trapped topoisomerase II from the KMT2A locus - it suppresses translocations overall and manufactures one rare junction class | Mechanism | 5 | 3/5 |
| TDRD3 (Q9H7E2) - the reader the new H4R3me2a entry could not name, and it brings TOP3B to the MYC promoter and keeps R loops off it | Gene | 4 | 3/5 |
| Ten affinity measurements for this contact and not one uses a fusion protein, full-length KMT2A or a nucleosome | Analysis | 2 | 4/5 |
| Ten of menin's 33 IntAct partners come from one BRET screen for MUTATION-created interactions — and five are gains caused by a named allele | Analysis | 4 | 4/5 |
| Term structure of risk — a steeply falling hazard curve is a statement about heterogeneity, not about time | Analogy | 3 | 1/5 |
| TERT — telomerase, switched on by the index fusion through HOXA7 | Gene | 2 | 0/5 |
| Tested in an independent deposit with an epitope-tagged fusion: of the pivotal paper's three named losers under a menin inhibitor, MEIS1 and JMJD1C reproduce and MEF2C does not; of its three named retained loci, the HOXA cluster reproduces and MYB does not - and GAPDH, the negative control, loses half its share too | Analysis | 3 | 3/5 |
| Testing every pattern against the sentence it must not match | Analysis | 2 | 0/5 |
| Testing my own diagnosis from last cycle: 809 of 1,052 entries that state a quantity in prose already carry it as typed data - 76.9% - so the corpus was machine-readable, the detector was simply weak, and the reporting field I imposed on every future beat rests on a different and narrower justification than the one I gave | Analysis | 1 | 4/5 |
| Testing this corpus's own recorded refusals instead of its gap list overturned the first refusal tried, and the refusal had named the falsifier itself | Analysis | 2 | 4/5 |
| Testing whether every citation points at the paper it claims: 314 scoreable blocks, 242 scoring below 0.3 on title overlap, and every low scorer read is CORRECT - because this project's citation title is a descriptive sentence by house style, which means a PMID pointing at the wrong paper is undetectable by any automated check over the corpus alone | Analysis | 1 | 4/5 |
| TET1 (LCX / CXXC6) - a CXXC reader that is also a KMT2A fusion partner, and whose leukaemic fusion throws its own CXXC domain away | Protein | 15 | 3/5 |
| TET2 is NOT a CXXC protein - its CXXC domain is a separate gene, and it is DEPLETED in KMT2A-rearranged AML rather than enriched | Protein | 7 | 4/5 |
| TET3 - the CXXC reader whose domain prefers 5-carboxylcytosine, and the only CXXC-family gene ever found mutated in a KMT2A-rearranged cohort | Protein | 6 | 3/5 |
| Th17 cell - the mature CD4 T-helper subset whose differentiation and maintenance require MENIN, which makes it the clearest published on-target normal-tissue liability of the menin interface | Cell type | 4 | 4/5 |
| The '0.400, keeps 1,894 of 2,045 calls' in the dispatch brief is two independent per-sample call counts read as a retention ratio; the intersection is 1,116 of a 2,812 union | Analysis | 2 | 4/5 |
| The 'infant ALL' PDX panel with four KMT2A::AFF1 models — one of which the full text calls adult | Explainer | 3 | 4/5 |
| The 'named but unwritten' queue flags ALL EIGHT of this project's negative-control loci plus one alias-filed entry - 20.5% of it, after I corrected my own reimplementation which had double-counted collisions the tool already blocks | Analysis | 3 | 4/5 |
| The 'never duplicate an entry' rule has held across 1,761 entries - and the audit that checked it would not have caught the near-duplicate that prompted it | Analysis | 1 | 3/5 |
| The 'raw library promoter mean' that two cycles treated as library coverage tracks the in-promoter fragment FRACTION at Spearman +0.993 and true sequencing depth at only +0.292, and the oncoprotein share correlates with true depth at -0.255 | Analysis | 3 | 4/5 |
| The 'sixteen percent of GEO sample labels contradict their own metadata' finding is a one-line off-by-one: 2,280 of 2,280 titles were attributed to the wrong sample, and with the record boundary fixed the rate falls from 96 of 586 comparable pairs (16.4%) to 7 of 656 (1.1%) - and all seven, read by hand and named here, are tokeniser artefacts rather than contradictions | Analysis | 2 | 4/5 |
| The "second breakpoint cluster region" of KMT2A (Meyer 2019): the founding report of BCR2, not a third cluster | Breakpoint | 3 | 4/5 |
| The 0.069 chance floor quoted beside the 0.400 same-patient Jaccard is the cohort MEDIAN's null, and this pair's own floor is 0.267 | Analysis | 2 | 4/5 |
| The 1 kb bin-overlap retention measure this project uses for eviction FAILS a degron positive control: it reports the fusion as still occupying 40-93% of its own sites in cells where the fusion has been destroyed, because a collapsing ChIP signal makes MACS call FEWER but 1.9x WIDER peaks - so it fails hardest exactly where the protein is most completely gone | Analysis | 2 | 4/5 |
| The 110 MLL-AF4-specific preys are 14.5% mitochondrial and 34% nuclear; the 42 pan-fusion preys are 2.4% mitochondrial and 88% nuclear — Fisher p = 0.042 on a nuclear-extract pulldown | Analysis | 2 | 4/5 |
| The 17-promoter AFF1-only recurrent core is not more recurrence than a label permutation of the same matrix gives | Analysis | 3 | 4/5 |
| The 2.03-fold over-representation of shared windows among fusion-occupied promoters is generic promoter activity, not a fusion preference - and if it is not, the rule is finding something different from what it claims | Hypothesis | 3 | 1/5 |
| The 2015 paper did not discover the KMT2A acetylation site - it inherited it from the 2009 Choudhary acetylome, which was run in a cell panel that includes MV4-11, a KMT2A::AFF1 line | Analysis | 5 | 3/5 |
| The 24 genes that respond to BOTH menin inhibitors in RS4;11 are led by the ATF4 stress programme - CHAC1 -5.11, STC2 -4.40, TRIB3 -3.10 - and CHAC1 and TRIB3 are named zero times in this graph | Analysis | 5 | 3/5 |
| The 297 absence-bearing entries that are not named absence-* split cleanly by entry type: the 109 gene and protein entries are bounded by title/abstract search (7 of 7 hand-read), the analyses are bounded by deposited data (0 of 6), and the weighted abstract-level share is 60% - indistinguishable from the 59% measured on the 39 named ones | Analysis | 3 | 3/5 |
| The 2x2 paralogue swap: separate 'is the reader there' from 'which backbone is it on', in one background with matched expression | Experiment | 5 | 1/5 |
| The 3.7% was mostly the query: DOT1L recall is 19.6% once you ask about leukaemia | Analysis | 2 | 4/5 |
| The 332 AFF1-only promoters are BELOW chance: a label-permutation null over the same occupancy matrix expects 426, so the figure the IRX1 partner-specificity line rests on is not an enrichment - and my own brief told the agent the opposite | Analysis | 2 | 4/5 |
| The 332-promoter AFF1-only set is BELOW the count a random eight-sample arm produces (null 425) | Analysis | 2 | 4/5 |
| The 41 residues after the CXXC fold (1204-1244) carry a substantial part of the fusion's DNA grip, and removing them is why the structural literature's affinity is so low | Hypothesis | 3 | 1/5 |
| The 50-RBP BioID2 proximity map in K562 - the first modern proximity dataset this graph can reach, and AFF1 is in it as prey | Analysis | 4 | 4/5 |
| The 7SK elongation brake is not an off-chromatin reservoir: 7SK occupies enhancers and super-enhancers genome-wide, recruits BAF and repositions nucleosomes - which means NOT APPLICABLE is the wrong epigenetics annotation for LARP7, MEPCE and HEXIM2, and BOUNDED ABSENCE is the right one | Mechanism | 1 | 4/5 |
| The 7SK snRNP - a stable RNA core with a reversibly docked kinase, which is why the reservoir is a switch and not a sink | Protein | 7 | 5/5 |
| The 82.9% population scored twice as many defect-shaped notes as the same-source one, and reading six of them says the comparison is confounded by our own DepMap numbers | Analysis | 3 | 0/5 |
| The absence-class checker globbed a filename instead of the field, so it walked 40 of 243 entries and reported them as the whole population - and the 40 it called invalid turn out to be two independently re-invented vocabularies | Analysis | 1 | 5/5 |
| The ABT1/KRR1/UTP3 nucleolar triple: pre-registered, then adjudicated - it is not three proteins on two baits but a seven-member ribosomal block in one screen plus one hit in a neighbourhood that shows no nucleolar enrichment, and two of the four pre-registered discriminators were void exactly as the pre-registration predicted | Analysis | 6 | 3/5 |
| The active chromatin landscape does not lose a single peak call within 24 hours of the fusion being destroyed: H3K79me2 holds 99.7% at both 3 h and 24 h, H3K9ac 100.0% at both, H3K27ac 83.3%/67.2%, H3K4me3 99.6%/78.9% - while the authors, measuring signal at fusion target genes, report a marked H3K79me2 reduction by 24 h | Analysis | 2 | 3/5 |
| The adult-type model answers PLK1 inhibition by making more PLK1 and AURKA | Mechanism | 1 | 0/5 |
| The AF9 acetylation arm: PCAF at K339, HDAC5 gated by CaMKII - a kinase-controlled switch the fusion throws away | Mechanism | 3 | 3/5 |
| The AFF-family N-terminus on cyclin T1: Kd 10 nM, a 2.94 A crystal, and every number in it measured on AFF4 rather than on AFF1 | Interface | 6 | 5/5 |
| The AFF1 promoter window holds three genes' TSSs, not two, and the third is protein-coding - Q153's 92.5% is confirmed and its two-gene framing is not | Analysis | 4 | 4/5 |
| The age confound: a partner arm and an age arm are nearly the same arm | Explainer | 4 | 4/5 |
| The age of the marrow, not only the age of the cell, decides whether MLL-rearranged leukaemia comes out myeloid or lymphoid | Mechanism | 2 | 3/5 |
| The AHD inhibitor's deposited arm is MOLM-13 and its in vivo arm is nowhere: a half-resolution that names the limit exactly | Analysis | 3 | 4/5 |
| The AML-over-ALL retention ratio is 93.5% denominator: the GMP-like numerator barely moves across 23 samples while the B-lineage denominator varies fourteenfold, so the ratio measures loss of the B-lineage class and not gain of the GMP-like one | Analysis | 2 | 4/5 |
| The analysis that would settle it: a partner-by-lineage interaction term in pooled individual-patient data | Experiment | 3 | 3/5 |
| The anchor-matched ranking, run: the KMT2A exon-11 CTCF anchor is rank 58 of 1,625 anchors matched on baseline strength - the 3.6th percentile - and the matched MEDIAN anchor also falls to 0.63x, so 'CTCF falls only at the KMT2A anchor' is refuted while 'the KMT2A anchor loses more than most' survives weakly | Analysis | 3 | 4/5 |
| The anti-MLL-C ambiguity is not a t(4;11) problem - it has three sources, and one KMT2A fusion family is measurably cleaner than the rest | Explainer | 3 | 4/5 |
| The ANZCHOG infant cohort: 119 babies, with the presenting features actually tabulated | Explainer | 3 | 4/5 |
| The apoptotic priming state — KMT2A-rearranged infant ALL is the one childhood ALL subgroup that is BCL-2-dependent rather than BCL-XL-co-dependent, and BH3 profiling is how that was measured | Cell state | 3 | 4/5 |
| The assumption the whole project rests on, tested at last: menin dependency is fusion-specific (run) | Analysis | 1 | 3/5 |
| The ATF4/ISR collapse under menin inhibitors reports loss of the KMT2A-fusion transcriptional programme by ANY route, not engagement of the menin interface - and the loss is of ATF4 activity, not ATF4 | Hypothesis | 3 | 3/5 |
| The atlas heuristic is scoped to six baits instead of to publication scale, so it misses HuRI, OpenCell and five other proteome-wide screens - 49.5% of rows credited with a 'focused' publication have only atlas support, and all five of q178's credible interactors fail | Analysis | 2 | 4/5 |
| The authors' own deposited table puts menin at 0.87 of its diagnostic-sample signal over their oncoprotein-target peaks, in the sample their text describes as having menin reduced to undetectable levels - the two statements are about different denominators, and only one of them travels | Analysis | 3 | 4/5 |
| The authors' signal floor removes 92% of non-occupied genes from the menin table, and all of the occupied ones survive | Analysis | 3 | 4/5 |
| The B-ALL and the AML of one infant share no more fusion-occupied promoters than two unrelated infants do - lineage, not patient identity, sets where KMT2A::AFF1 sits | Analysis | 3 | 3/5 |
| The bait/prey grade this project uses to triage the interactome systematically discards its strongest evidence, because the strongest methods have no bait | Hypothesis | 4 | 3/5 |
| The bigWig refusal of cycle 57 is overturned: pybigtools installs on this box under Python 3.12, reads GEO tracks by HTTP range request without downloading them, and passes the control loci the refusal itself demanded | Analysis | 2 | 5/5 |
| The binary ladder for AFF1: does the index fusion's partner touch P-TEFb without AFF4, and does it touch AFF4 at all? | Experiment | 3 | 3/5 |
| The bite-back of striking a target: a wrong strike costs a cure and generates no data that it was wrong | Risk | 5 | 4/5 |
| The bite-back surface: LEDGF tethers CtIP to active chromatin and is required for DNA-end resection and homologous recombination | Mechanism | 5 | 4/5 |
| The blind spot is closed: all four K1130-and-leukaemia full-text hits are reviews restating the source paper, and the citation-network bound survives 26 nomenclatures rather than five | Analysis | 3 | 4/5 |
| The bone-marrow niche — the address a blood stem cell lives at, which 26 entries in this graph invoke and none had defined | Explainer | 7 | 4/5 |
| The bounded-absence population went 39 to 73 in two days, and the abstract-level defect class went from 26 of 39 to 2 of 34 (Fisher p = 1.3e-5) | Analysis | 3 | 4/5 |
| The brake pad is actively thinned: autophagy degrades HEXIM1 in MLL-fusion and NPM1c AML cells | Mechanism | 3 | 3/5 |
| The cannot-be-occupied floor never binds at gene-body scale in any of the 27 samples, so q147's gene-scale rule is a bare 2.0x gate - and the max-versus-95th-percentile difference between q147 and q152 is immaterial there | Analysis | 2 | 4/5 |
| The case that the KMT2A-fusion condensate is an artefact — what 1,6-hexanediol, overexpressed tags and in-vitro droplets actually prove | Mechanism | 7 | 4/5 |
| The CD24-positive pre-leukaemic state — what the index fusion makes before it makes leukaemia | Cell state | 1 | 3/5 |
| The CD34+ oncoprotein-negative sample that calibrates the published N/C threshold is in GSE159608, not GSE252378 - so the 1.75 threshold cannot be re-derived from the deposit that carries the 27 patients it is applied to | Analysis | 3 | 4/5 |
| The cell CALM-AF10 arrests: an early T-precursor in adults and a TCR-positive thymocyte in children - two states, split by age (corrected 2026-09-21) | Cell state | 3 | 4/5 |
| The cell types that need MLL1 are the uncommitted ones - dependence ends exactly where lineage commitment begins | Mechanism | 3 | 4/5 |
| The chain's biggest risk is generalising a myeloid mouse result to infant B-ALL, and the graph cannot measure how much of it does | Analysis | 3 | 4/5 |
| The cheap experiment nobody has run: an MLL1 C-TERMINAL ChIP beside the standard N-terminal one in a single human KMT2A-rearranged line under a menin inhibitor - the C-terminus is lost in the fusion, so the difference of the two tracks is the fusion, with no tag and no knock-in | Experiment | 1 | 3/5 |
| The cheapest missing experiment in this beat: put revumenib on a parathyroid cell | Experiment | 3 | 3/5 |
| The cheapest study that would settle this: nine assays and a hand radiograph, on children already being followed | Experiment | 3 | 3/5 |
| The cheapest unrun test in this beat's queue: GSE260742 deposits an H3K79me2 ChIP under the DOT1L inhibitor SGC0946 in the same murine MLLAF9 cells as its FLAG and MLL1 tracks, which removes the catalysis directly instead of indirectly and would separate 'the mark is stable' from 'residual DOT1L is sufficient' - one download | Analysis | 1 | 3/5 |
| The check I called decisive was not: the haem signal is still open (run) | Analysis | 2 | 3/5 |
| The check this project named nine cycles ago and never ran: the 34 least-verified papers in the corpus are attached to the right claims, and every low-scoring pair is support living in a supplement or a structure rather than an abstract | Analysis | 2 | 3/5 |
| The chromatin compartment that the field treats as 'the fusion's sites' is smaller and less shared in MOLM13 than in RS4;11: 467 of 1,389 MLL1-N-top bins also carry top menin (33.6%) against 692 of 1,390 (49.8%), and the MLL1-N and H3K79me2 compartments barely overlap in either line | Analysis | 1 | 4/5 |
| The chromatin exchange at a menin-inhibited fusion site, measured in one experiment: H2AK119ub and H3K27me3 in, H3K4me3 out, in proportion to how much fusion left - and PCGF1 loss attenuates the in-fill without abolishing it | Mechanism | 2 | 3/5 |
| The citation index built to stop false gap claims made one: its regex matched prose but not the schema's own pmid field, missing 73.7% of the corpus's citations, and the single-cell gap it selected was refuted by a paper already cited in fourteen entries | Analysis | 1 | 4/5 |
| The class I and class II arms of menin inhibition are different mechanisms - the class I effect was tested against viral mimicry and NF-kB and excluded both | Mechanism | 3 | 3/5 |
| The clearance clock has machinery, and the machinery says the clock does NOT stop in a non-dividing cell - a postmitotic heart replaces its histones with a half-life of about two weeks | Mechanism | 4 | 3/5 |
| The clearest clinical rationale for a LEDGF agent - second line after menin-inhibitor failure - has never been tested, and one 2025 measurement now argues against it | Analysis | 4 | 3/5 |
| The clinical outcome data do not support a single KMT2A class, and they do not refute the menin interface either | Hypothesis | 5 | 1/5 |
| The clock/SIRT1-regulated MLL1 acetylation site maps to KMT2A K1130 and K1133 in human numbering, just N-terminal to the CXXC and 208 residues before the breakpoint cluster - so it is retained in every KMT2A fusion | Analysis | 2 | 4/5 |
| The clustered PHD fingers (KMT2A aa 1416-1640) are a chromatin-targeting module and the canonical t(4;11) junction removes them by ten residues | Mechanism | 3 | 3/5 |
| The CNS-adapted state — leukaemia-propagating cells reprogrammed by the central nervous system niche, and worse at restarting systemic disease afterwards | Cell state | 2 | 3/5 |
| The cohesin-degron break map was run in the one human cell line where the KMT2A element does not break - so premise (i) is not underpowered, it is unaddressed | Analysis | 2 | 4/5 |
| The cohort paper this graph said had certainly measured IDH status was opened: 96,537 characters of full text contain IDH1 zero times, IDH2 zero times, TET2 zero times and DNMT3A zero times, so the measured-not-reported class is confirmed by reading rather than by inference | Analysis | 2 | 4/5 |
| The comparator arm was never screened for pathway-equivalent lesions — and it made us understate our own result | Analysis | 1 | 4/5 |
| The comparison that founded 'the CXXC contact is too weak' puts a 300 mM NaCl protein-DNA measurement against a 50 mM NaCl protein-peptide measurement | Analysis | 4 | 4/5 |
| The compound in the only infant menin-inhibitor occupancy sample is revumenib, named in the abstract - and neither the dose nor the duration of exposure is recorded in the paper, the GEO record or the authors' repository | Analysis | 4 | 4/5 |
| The computed-but-unread scan ran, passed its own declared informativeness control at 60.3% cited, and produced a headline nobody can act on: 36,110 uncited values across 182 results files, dominated by ranks, taxids and chromosome extents. The useful population is not 'uncited numbers' but 'PRE-REGISTERED quantities that went uncited', which is what the one real instance actually was | Analysis | 1 | 5/5 |
| The comutation confound: KRAS, DNMT3A, TP53 and KMT2A-PTD track with partner and carry prognostic weight of their own | Explainer | 4 | 3/5 |
| The confounder every previous analysis flagged and none removed, removed (run) | Analysis | 1 | 3/5 |
| The convenient deposited promoter table finds 3 gained windows where the genome-wide re-binning finds 53, because 83% of the gained set is not at a RefGene TSS - so the processed file that makes this dataset cheap to re-use is structurally blind to the answer | Analysis | 1 | 4/5 |
| The corpus citation index reads `PMID nnnnnnnn` in prose and never the `pmid` citation field — it sees 1,908 of 3,991 papers, undercounts 872 of the rest, and its headline single-cell absence was an artefact | Analysis | 5 | 5/5 |
| The corpus holds 42 of 42 pan-fusion partners and 1 of 110 MLL-AF4-specific ones — the inverse of the standing priority, and every mechanism that produced it was a reasonable local decision | Analysis | 3 | 4/5 |
| The cost of surviving: late effects carry a lifetime bill nobody has costed for infants | Explainer | 3 | 3/5 |
| The cost the hospital never sees: half of families spend more than 15% of their income | Explainer | 2 | 4/5 |
| The counter-argument: the menin field is an adult field, and the infant studies were withdrawn | Explainer | 5 | 4/5 |
| The counter-note defect detector mistakes cross-referencing for unsupported assertion, which is why the different-source rate looked twice as bad | Analysis | 2 | 3/5 |
| The coverage checker the standing brief mandates overwrites its own HGNC index mid-loop, so every symbol after the first no-match is answered wrongly - and the wrong answer is 'treat any answer as unsafe' | Analysis | 3 | 5/5 |
| The coverage guard withheld 30 of 351 pairs and named every one: 26 contain 152985, which calls zero promoters, and a Jaccard with a zero-call sample is a division, not a measurement | Analysis | 2 | 4/5 |
| The coverage tool's id arm cannot reach five of its nine prefixes - 225 entries - and the prose arm covers for it in 338 of 338 cases, so the reported false clear happens only under a flag that disables the prose arm | Analysis | 2 | 4/5 |
| The CRISPR-ChIP H3K79 partition is a mouse MLL-AF9 result: resolved from GEO after the full text proved unreachable | Analysis | 6 | 5/5 |
| The CRM1 address is not a menin-free address: NPM1c reaches HOXA the same way and NPM1c AML is menin-inhibitor-sensitive in the clinic | Analysis | 3 | 3/5 |
| The cross-entry contradiction screen does not work, and the reason is that this graph writes carefully | Analysis | 2 | 4/5 |
| The CSF1R-positive fetal lymphoid-primed multipotent progenitor — a fetal-restricted subset of LMPPs that makes AML rather than ALL when KMT2A::MLLT3 is switched on, and exists in human embryos | Cell type | 2 | 3/5 |
| The CTCF licensing cascade: CTCF recruits HP1-gamma, KAP1, SUV39H1, SETDB1 and KDM5A to a break, that repressive chromatin licenses EARLY BRCA1/BARD1, and early BRCA1/BARD1 licenses EXO1/DNA2 long-range resection - measured entirely in U2OS and HEK-293T, with engineered breaks and one etoposide arm | Mechanism | 4 | 3/5 |
| The CTCF site in KMT2A exon 11 - a conserved insulator element sitting exactly on the functional cut point of the breakpoint cluster region, whose occupancy decides whether the locus rearranges | Non-coding | 4 | 3/5 |
| The curated interaction database knows less about AFF1 than this graph does | Analysis | 3 | 0/5 |
| The CXXC domain (aa 1147-1195, PDB 2KKF) is a chromatin address, not a compartment address — CpG mutants lose transformation but keep their subnuclear position | Mechanism | 4 | 3/5 |
| The CXXC-DNA affinity is a ten-point ladder from 44 uM to 33 nM, not two numbers 1,300-fold apart, and every step but the last is under 5.5-fold | Analysis | 7 | 4/5 |
| The DAXX requirement in B-lineage KMT2A-rearranged lines is a telomere phenotype, not a fusion-target phenotype - and the two non-KMT2A lines in the deep group are the test | Hypothesis | 3 | 1/5 |
| The days-long experiment that would close or confirm the imprinting liability: allele-specific XIST and MEG3 readout in cells treated with a YEATS antagonist | Experiment | 2 | 3/5 |
| The decisive experiment: acute degron removal of IGF2BP3, IGF2BP2 and both, read on self-renewal and xenograft initiation rather than bulk dropout | Experiment | 6 | 3/5 |
| The decisive test that needs no new data: overlay the 12,443-anchor CTCF-loss ranking on the copy-number changes Gray 2023 reports, and ask whether the 280 anchors that lose CTCF as hard as KMT2A also amplify | Experiment | 2 | 3/5 |
| The deferred KMT2A partners: what the counts actually are, what was written, what was rejected, and three numbers the previous enumeration got wrong | Analysis | 6 | 3/5 |
| THE DEFLATING NULL, RUN: matching on gene length AND MCF-7 expression roughly HALVES the H3K9me3 depletion over the KMT2A gene body - from the 7.6th-15.0th percentile of class-matched CTCF anchors to the 18.2nd-23.4th of 385 matched transcribed gene bodies - so the methyl-poor breakpoint domain is partly a fact about transcription and does not dissolve into one | Analysis | 3 | 3/5 |
| The dependencies this project keeps failing to see are the buffered ones: paralogue redundancy and guide placement, not absence of biology | Hypothesis | 5 | 3/5 |
| The deposit names its first replicate "paired" and its later ones rep1/rep2/rep3, so GSM8123403 "H2AK119ub paired" and GSM8123420 "H2AK119ub rep2" are one condition in two replicates - which this project has called "the two processing conventions" since cycle 88. GSE260742 holds 17 genuine same-condition replicate groups, 13 of them histone marks, refuting the claim repeated since cycle 100 that it has none and never will | Analysis | 1 | 4/5 |
| The deposit paper's own supplementary table calls IRX1 an oncoprotein target in exactly p279, p318 and p454 - the same three samples this project reached by a different instrument | Analysis | 5 | 4/5 |
| The deposit this graph filed as 'four SUV39H1 ChIP-seqs' is actually 77 samples in MCF-7 carrying the ENTIRE H3K9 axis in one cell type and one pipeline - writer SUV39H1, writer G9a/EHMT2, reader HP1-alpha/CBX5 (wild-type AND two phospho-mutants), co-repressor KAP1/TRIM28, erasers KDM4B and KDM4C, the mark H3K9me3, and an shKDM4B+shKDM4C eraser-knockdown arm | Experiment | 2 | 4/5 |
| The deposit's two lineage-switching patients behave in opposite directions: the untreated pair keeps 1126 of its 2045 oncoprotein-target promoters across the switch, while the menin-inhibited pair falls from 345 to zero - so lineage switching does not by itself clear the oncoprotein | Analysis | 2 | 3/5 |
| The deposited dm6 spike-in table covers the eighteen H3K79me2 samples and nothing else - the ten MEN1 and DOT1L ChIPs in the same series have no fly chromatin, so every occupancy number from them is a within-sample contrast and no gain-or-loss statement on an absolute scale is available | Analysis | 2 | 5/5 |
| The deposited GSE127507 processed signal table is an Excel export in which every value at or above 1,000 is a quoted comma-separated string, so a plain numeric parse silently zeroes 34,955 of 386,298 cells - and those cells are the entire top of all eighteen distributions | Analysis | 1 | 5/5 |
| The deposited RS4;11 H3K79me2 table in GSE149183 is two-thirds MOLM13: 38,580 of its 57,794 rows are byte-for-byte identical to the MOLM13 file, so the index fusion is measurable at only 19,214 TSS entries | Analysis | 3 | 5/5 |
| The depth-matched discriminator I called the only available test: thinning 44 of 54 libraries down to A73051's in-promoter fragment count moves their oncoprotein share by a median of +0.0003, 39 of 39 hold and 0 collapse - so depth could never have explained A73051, and my cycle-135 worry was misconceived rather than merely wrong | Analysis | 1 | 4/5 |
| The differentiation block — what it actually is, operationally, in KMT2A::AFF1 leukaemia | Cell state | 7 | 4/5 |
| The dispatch brief scoped this deposit's oncoprotein-score arm at two patients and a cell line; it is 27 patient samples across six fusion partners, and the scoping error was inherited from a beat that only needed three of them | Analysis | 1 | 5/5 |
| The DOT1L inhibitor removes menin from fusion promoters too, which a pure interface model does not predict | Analysis | 3 | 3/5 |
| The DOT1L partner IntAct calls TCF4 is TCF7L2 - the second UTP18/WDR5-class symbol mis-assignment found in this interactome, and gene-tcf4 is declined | Analysis | 5 | 4/5 |
| The DOT1L-AF10 octamer - the second route to H3K79 methylation, required in MLL-AF10 and absent from KMT2A::AFF1 | Mechanism | 5 | 4/5 |
| The DOT1L–ubiquitin and DOT1L–acidic-patch interfaces: two non-catalytic surfaces that MV4;11 cells cannot do without | Interface | 3 | 4/5 |
| The druggable node in the homeodomain code is the MEIS1-PBX3 interface, not the HOX-PBX one - and it is the only one nobody has attacked | Hypothesis | 6 | 1/5 |
| The early lymphocyte precursor (ELP) state — what KMT2A-rearranged infant B-ALL scores as against a developing bone marrow reference, and why it is earlier than the pro-B arrest this graph also records | Cell state | 2 | 4/5 |
| The easy null was not the problem, and nothing in 2,018 genes beat menin | Analysis | 1 | 3/5 |
| The EGR1 promoter fails its own IgG control — an attractive claim withheld because a pre-declared control said no | Explainer | 2 | 4/5 |
| The element carries an equally strong CTCF/cohesin peak in HCT116 and in a B-lymphoblastoid line, yet breaks in one and not the other - so occupancy is necessary and not sufficient, and transcription of KMT2A is the switch | Hypothesis | 2 | 3/5 |
| The eleven-line panel is nine patients, seven of them myeloid, and none an infant | Explainer | 3 | 0/5 |
| The ELL/EAF activation module (ELL2, EAF1, EAF2) — a general elongation stimulator, not a KMT2A-fusion dependency | Protein | 4 | 4/5 |
| The ELLbow: AFF4 301-351 wrapped over the ELL2 occludin domain at 2.0 A, Kd 86 nM - and no structure of ELL itself, the partner in t(11;19) | Interface | 3 | 4/5 |
| The endocrine cell's resting state is an actively maintained G1 restraint, and menin is what maintains it | Cell state | 4 | 4/5 |
| The endogenous MLL-AF4 localisation experiment was unattributable, not negative: an anti-AF4 polyclonal in a t(4;11) cell images mostly wild-type AF4 | Mechanism | 2 | 3/5 |
| The endosteal niche — the bone surface, where leukaemia-initiating cells were imaged homing and dividing symmetrically | Explainer | 7 | 3/5 |
| The ENL AHD to AFF1 contact: asserted throughout this graph, structurally unsolved, and represented only by an AF9 chimera measured at KD 0.17 nM | Interface | 3 | 4/5 |
| The ENL YEATS acetyl-reader inside KMT2A::MLLT1: what it reads, what it does, and why both control arms carry it | Mechanism | 5 | 4/5 |
| The entire experimental model space for SET::NUP214 is two cell lines, neither of them in DepMap, with no mouse model found - so every mechanism in this beat is n = 1 or n = 2 | Risk | 5 | 4/5 |
| The epigenetics coverage test inspects data{} KEY NAMES and never a field's value, so 71 entries that state a histone mark INSIDE a data field score zero - and four more are missed by one character | Analysis | 2 | 4/5 |
| The epitope that the whole shared-epitope argument turns on is not documented anywhere this beat could reach: three vendor routes for Bethyl A300-086A returned HTTP 404, so 'MLL1 N-terminus, retained in the fusion' rests on the depositors' own target label and on general fusion architecture, not on an immunogen range | Analysis | 1 | 4/5 |
| The EU paediatric investigation plan: an obligation, not an incentive - and the deferral is the loophole | Explainer | 8 | 3/5 |
| The eviction quartiles are defined in the 'MLLAF9 Control' FLAG culture and the H3K79me2 they stratify is measured in the 'NTvKO Control' and 'NTvKO PCGF1 KO' cultures - zero shared libraries - so the commonest way a stratified analysis fools itself is structurally unavailable here | Explainer | 3 | 4/5 |
| The excess overlap survives a structure-respecting null in both beats - permutation p = 0.0005 in all six cells - but every published excess figure shrinks 2.4- to 4-fold | Analysis | 2 | 4/5 |
| The experiment nobody has done: an epitope tag knocked into the endogenous KMT2A fusion allele in a patient-derived line | Explainer | 4 | 3/5 |
| The experiment that closes the LEDGF hole: doxycycline-inducible PSIP1 knockdown switched on AFTER a human KMT2A::AFF1 xenograft is established | Experiment | 4 | 1/5 |
| The experiment that refutes cycle 55's headline was already public: VTP-50469 collapses MEIS1 32-fold in the same line where MI-2-2 left it untouched - and HOXA9 was never actually measured by either dataset | Analysis | 3 | 4/5 |
| The experiment that separates lineage from ontogeny: one KMT2A fusion, two cell-of-origin contexts, three metabolic perturbations, and a limiting-dilution readout alongside the viability one | Experiment | 4 | 1/5 |
| The experiment the public data cannot supply: H3K9me1/2/3 and CTCF at the KMT2A exon-11 anchor in a cord-blood CD34+ progenitor, with and without KDM3B depletion | Experiment | 2 | 3/5 |
| The experiment this beat could not do: an epitope-tagged KMT2A::AFF1 ChIP with a Drosophila spike-in, in a human infant-derived B-lineage line, at three replicates and two menin-inhibitor exposures - the design that would turn a within-sample ranking into an absolute occupancy measurement | Experiment | 2 | 3/5 |
| The experiment this beat could not do: G9a, HP1a, KAP1 and H3K9me3 at the KMT2A promoter and exon-11 anchor in a KMT2A-rearranged B-lineage cell and a CD34+ progenitor, WITH an input arm, an IgG arm and a same-cell CTCF arm | Experiment | 2 | 3/5 |
| The experiment this deposit is one arm short of: MEN1 ChIP after fusion degradation with a PSIP1-depletion arm, a spike-in, replicates, and timepoints past three hours - four additions to an existing protocol that would settle why menin stays | Experiment | 2 | 3/5 |
| The experiment: cross-tabulate MLLT1 breakpoint class against age, lineage and outcome in the Frankfurt archive, then confirm reciprocal status by RNA in whoever has it | Experiment | 5 | 3/5 |
| The FA core complex does not move together, and that is the strongest argument against reading this as a Fanconi-pathway dependency at all | Mechanism | 5 | 3/5 |
| The falsifier that decides the beat, run: 65.6% of the fusion's own top sites overlap a CpG island and 1 of the 52 sites it formally 'gains' under a menin inhibitor does - 1.35-fold over a class-matched null, Fisher p = 0.53 - so the gained set does not carry the signature of CXXC-driven binding and the redistribution model is refuted on its own predicted substrate | Analysis | 2 | 4/5 |
| The Fanconi core complex is 2nd of 719 complexes for KMT2A-selectivity - but coherence does not explain it, and the explanation this entry was built on is dead | Analysis | 9 | 0/5 |
| The Fanconi signal is in both lineage halves, survives the correlation-proof null, and is still there when lineage is held constant | Analysis | 3 | 3/5 |
| The Fanconi signal is real, and it sits in the ubiquitination module | Analysis | 2 | 0/5 |
| The federated sweep this graph prescribes for the missing index-fusion interactor cannot be run: PSICQUIC free text returns ZERO for `mll_af9`, an entity that provably exists and returns 32 records under its accession - so every provider's zero in that sweep is uninterpretable | Analysis | 4 | 5/5 |
| The fetal state is PERMISSIVE for lymphoid KMT2A-fusion transformation and PROTECTIVE against myeloid - which is why LIN28B has opposite signs in the two literatures | Hypothesis | 5 | 1/5 |
| The first measurement of any histone mark outside the top 0.1% of fusion sites: by ratio the drug's mark response is confined to the peaks as pre-registered, while in ABSOLUTE share the movement at the decile below is 5 to 33 times larger - though that is partly guaranteed by the stratum being 100x bigger. H3K79me2 falls at the peaks (0.8065) and is not measurably changed at D1, and H3K4me3 and H3K79me2 both break the floor at the lowest decile | Analysis | 1 | 3/5 |
| The first published complete remission of NUP98-rearranged AML on a menin inhibitor (icovamenib/BMF-219, n=1) | Patient story | 2 | 3/5 |
| The first replicated share ratio this corpus has ever had: two title-declared replicates of ONE murine culture span 0.2623 on the same quantity - 4.5x the 0.0584 between-culture spread this corpus uses as its indifference threshold - and they disagree in SIGN about whether the PCGF1 knockout blunts the DOT1L-inhibitor response | Analysis | 2 | 3/5 |
| The first same-condition H3K79me2 noise floor measured anywhere in this thread: 11.17% at D1 and 26.44% at the TOP 0.1% stratum, against 45.72% and 62.63% for H2AK119ub in the same arm, the same condition and the same pairing shape - 4.1x tighter. A mark floor transferred from H2AK119ub does not describe H3K79me2. | Analysis | 1 | 2/5 |
| The five verdicts in one place, plus what this beat read and did not use | Analysis | 9 | 3/5 |
| The fludarabine prodrug chain - three molecules called by one name, and the one that is measured is neither the one given nor the one that works | Mechanism | 2 | 4/5 |
| The focal half: H3K79 hypermethylation at the HOXA cluster and MEIS1 - but which cluster member differs between CALM-AF10 and MLL-AF10 | Mechanism | 8 | 4/5 |
| The founding WRAD negative was never run on a fusion protein | Explainer | 4 | 5/5 |
| The four AFF4 two-hybrid partners are three rows of one screen, not three experiments - and in that same screen GOLGA2 has 249 partners while AFF4 has five | Analysis | 4 | 4/5 |
| The four eviction quartiles are not equivalent stretches of genome: all three GSE260742 input tracks give a monotone increasing share across Q1 to Q4 at Spearman -1.000, 1.15 / 1.17 / 1.13-fold - small, real, in the same direction as the H3K79me2 gradient, and it cancels exactly in a within-genotype drug/vehicle ratio | Analysis | 3 | 3/5 |
| The four-way ordering given a second cell line: menin, DOT1L and the MLL1-N channel reproduce between KMT2A::AFF1 and KMT2A::MLLT3 to within 0.04 of a share ratio, and H3K79me2 - the one channel the ordering was built around - diverges by 0.21 to 0.30 and changes places with MLL1-N | Analysis | 1 | 4/5 |
| The fusion begins at AFF1 residue 347 and the cyclin T1-binding sequence ends at 308, so KMT2A::AFF1 is the one AFF-family protein that cannot enter the reservoir | Mechanism | 4 | 4/5 |
| The fusion junction itself as a small-molecule target: a candid verdict | Target | 3 | 3/5 |
| The fusion may reach the H2B ubiquitin mark through MOF-MSL rather than through RNF20/RNF40 — the one configuration in which this layer could be selective | Hypothesis | 3 | 1/5 |
| The fusion-biased peak at the AFF1 locus fires in 23 of 27 samples across all six partners, so it is not the fusion visiting its own partner | Analysis | 2 | 3/5 |
| The fusion-oncoprotein TurboID experiment this graph proposes has already been published - for PML::RARA, RUNX1::RUNX1T1, CBFB::MYH11, NUP98::HOXA9 and SET::NUP214, and not for any KMT2A fusion | Analysis | 3 | 4/5 |
| The fusion-specific score's per-promoter reliability inside one patient is r = 0.183, and the median correlation between two DIFFERENT patients is 0.196 - so the ordering question cannot be resolved at promoter resolution, and the corpus's 0.82-0.97 figures cannot be carried to this readout | Analysis | 2 | 4/5 |
| The G1 state in KMT2A-rearranged leukaemia — where CDK6 does a job that is not about the cell cycle at all | Cell state | 3 | 4/5 |
| The gain question is answerable today for free: GSE127508 contains MLL1n ChIP-seq in a fusion-only line, plus and minus VTP-50469, and nobody has called peaks on the treated sample | Analysis | 3 | 3/5 |
| The gap instrument's 'not mentioned anywhere in the corpus' reads only ids, titles and aliases - it was wrong about 9 of 9 this cycle | Analysis | 1 | 5/5 |
| The genome build of GSE127507 is hg19, verified from the chromosome extents written inside each of the nine downloaded .tdf files - 9 bp from hg19 and 2,818,723 bp from hg38 on chr1, in every file - and independently from the deposited TSS table's own coordinates | Analysis | 2 | 5/5 |
| The GEO sweep that q110 named as free and did not run: SUV39H1 chromatin occupancy HAS been measured in two human cell types, six samples, hg38 bigWigs already deposited - so the writer half of the H3K9me3 absence is measured-not-analysed, not never-measured | Analysis | 5 | 4/5 |
| The GMP-like peak class is fusion-enriched in exactly one of GSE252378's 27 KMT2A-rearranged samples - p318, the sample it was derived from - once the null is matched on how coverable those promoters generically are | Analysis | 3 | 3/5 |
| The GMP-like promoter class carries no N-over-C excess in 25 of GSE252378's 27 samples: whatever occupies it is seen equally by the fusion-side and the wild-type-side antibody | Analysis | 2 | 3/5 |
| The GMP-like state is being used as a therapeutic anchor in two independent arguments, and its chromatin definition rests on one post-lineage-switch sample that also defined it | Risk | 2 | 3/5 |
| The GMP-over-B-lineage occupancy contrast tracks the sample's own lineage - and institution, which is the identical split in this deposit - and not its HOXA status | Analysis | 2 | 3/5 |
| The grading rule applied to twenty citations, and ORCID tested as a clustering key and rejected: zero coverage before 2010 | Analysis | 3 | 0/5 |
| The grading rule: confidence grades the claim, not the source - so one paper carrying several grades is correct, and only a three-step spread is worth reading | Explainer | 2 | 0/5 |
| The graph's universal 'every KMT2A fusion loses the SET domain' is a silent, propagating error class | Risk | 4 | 4/5 |
| The GSE149183 per-gene columns are RAW, not spike-in scaled: every one of 1,040,292 values in both files sits exactly on a 0.04 grid, which no per-library scale factor survives - so two entries in this graph called an unscaled number absolute, and the true collapse is 37-91x, not 5.8x | Analysis | 2 | 5/5 |
| The GSE260742 H2AK119ub pair that shares a processing state - rep2 against rep3, both bare `.tdf` - is not an unconfounded replicate pair: rep3 was submitted 2024-10-01 and rep2 2024-03-03, through a different file-naming pipeline. No pairing in this deposit isolates replicate variance alone. | Analysis | 1 | 4/5 |
| The H2BK34ub HOXA9/MEIS1 result is HeLa: the full text contains the word leukaemia zero times | Analysis | 3 | 4/5 |
| The H3K27me3 absence this graph keeps asserting is narrower than stated: the measurement exists, in the genetic arm of the paper the graph cites for the phenocopy | Analysis | 3 | 4/5 |
| The H3K27me3 and H3K4me3 NTvKO arms - twelve files nobody had ever binned, listed as second priority - carry the largest effect in this cycle (H3K27me3 2.0007 at the most-evicted quartile, collapsing to 1.0134 in the PCGF1 knockout) and the free internal control that rules out a library artefact (H3K4me3 runs the opposite way, Spearman -1.000) | Analysis | 2 | 3/5 |
| The H3K79me2 eviction gradient against a DMSO-decile-matched null drawn from outside the fusion's sites at the same quartile sizes: the null is flat at 1.030-1.057, none of 20 draws reached the observed span of 0.6005, and the residual retains Spearman -1.000 - but the restricted-population trap is real and the baseline IS graded 2.2-fold | Analysis | 3 | 3/5 |
| The H3K79me2 eviction gradient is not a ratio of sums dominated by a few bins: the MEDIAN per-bin log2 share ratio is itself monotone at Spearman -1.000, the fraction of bins individually below 1 falls 89.3% to 24.7%, the bootstrap span interval is [-0.651, -0.545], and no single bin moves the span by more than 0.0057 | Analysis | 3 | 3/5 |
| The H3K9 machinery's address at KMT2A is the PROMOTER, not the exon-11 breakpoint anchor: G9a, HP1a and KAP1 all read the top decile of active promoters there in MCF-7 and KAP1's peak replicates a K562 peak to 267 bp, while five proteins across five cell types are ORDINARY or absent at the anchor - so every H3K9-directed intervention this graph has discussed is aimed 52 kb from where the machinery is | Hypothesis | 3 | 3/5 |
| The H3K9me1/2-CTCF brake: a KDM3B-G9a balance keeps the KMT2A breakpoint cluster region methyl-poor and CTCF-bound, and losing either end makes the locus amplify and rearrange - in epithelium, in primary cord-blood progenitors and in mice | Mechanism | 7 | 3/5 |
| The H3K9me3 null that appears to exonerate prophylactic G9a inhibition was measured in retinal pigment epithelium, at 1 kb resolution, with n = 2 - and the warning it appears to lift lives in a leukaemic blast | Risk | 2 | 3/5 |
| The H3K9me3 this graph argues about at the KMT2A exon-11 anchor is not deposited by SUV39H1: in SU-DIPG13 the mark sits at the 57.8th percentile of class-matched CTCF anchors while the writer reads an EXPLICIT ZERO in the same nuclei, and genome-wide the two barely track each other (Spearman 0.148, 0.078) | Hypothesis | 3 | 1/5 |
| The H3K9me3 writer reaches the KMT2A anchor only through CTCF and only after the break - which would make this graph's CTCF arm and its H3K9 arm one arm, with CTCF upstream, and would make every resting-state H3K9me3 measurement at that element the wrong assay | Hypothesis | 3 | 1/5 |
| The HBO1/MOZ modules are not selective as modules: one paralogue per family carries the signal, and no member clears both a dependency and a pan-essentiality bar | Analysis | 3 | 0/5 |
| The HDAC7 direction conflict is scaffold versus catalysis: removing the protein and blocking its catalysis are opposite interventions, because class IIa HDACs barely have any catalysis | Hypothesis | 3 | 1/5 |
| The histone/ribosomal shape in the read queue is three classes, not one - H2BC21 is distinguishable AND essential at -0.70, so neither existing rejection ground reaches it, and HMGA1 is a harder dependency than MEN1 or KMT2A | Analysis | 3 | 4/5 |
| The HIV field is NOT drugging LEDGF: LEDGINs and ALLINIs bind integrase, and the proof is that they still work in a LEDGF knockout cell | Explainer | 5 | 4/5 |
| The HOX-PBX interface, and its one peptide: HXR9/HTL001 has been tried in eight tumour types and in KMT2A-rearranged leukaemia exactly once | Target | 7 | 2/5 |
| The HOXA-negative, IRX1-negative KMT2A-rearranged blast | Cell state | 2 | 2/5 |
| The HOXA/IRX1 anti-correlation does not reproduce in KMT2A-ENL, the only other partner group that can carry one | Analysis | 2 | 3/5 |
| The HOXA/IRX1 mutual exclusivity is reproduced at the transcript level in 48 KMT2A::AFF1 infant ALL cases (Fisher two-sided p < 1e-6) and is ABSENT in KMT2A::MLLT1 and in KMT2A-germline controls | Analysis | 3 | 3/5 |
| The HP1 paralogue asymmetry is a guide-cross-reactivity artefact until somebody shows it is not - and if it is real, HP1-beta is doing a job the other two cannot, which is the only HP1 question in this graph with a fitness phenotype attached | Hypothesis | 3 | 1/5 |
| The HSPC-like blast fraction — a minority of blasts that transcriptionally resemble haematopoietic stem and progenitor cells, found in the blood of the youngest KMT2A-rearranged patients and predicting drug response and outcome across leukaemia subtypes | Cell state | 5 | 4/5 |
| The HSPC-like blast fraction is the compartment that survives menin inhibition, and its size at diagnosis predicts depth and durability of response | Hypothesis | 3 | 1/5 |
| The HUCA complex (HIRA/UBN1/CABIN1/ASF1a) - four proteins, one job: put H3.3 into chromatin without waiting for S phase | Protein | 6 | 4/5 |
| The human CXXC/CpG-reading family is exactly twelve proteins, and TET2 is not one of them | Analysis | 7 | 5/5 |
| The Human Protein Atlas lists AFF1 as mitochondrial and nucleoplasmic at only 'Approved' reliability, with mitochondria as the single-cell-variable compartment, against nucleoplasm for KMT2A, menin and most of the pathway - a localisation lead that needs an orthogonal check | Analysis | 2 | 3/5 |
| The hypoxic, glycolytic state — the one state that appears independently in leukaemia-initiating cells, in measurable residual disease, and in KMT2A-rearranged B-ALL as a class | Cell state | 4 | 3/5 |
| The IKK complex — the unit the eviction experiment actually resolves, because the chemistry that produced the result cannot see the subunits | Protein | 3 | 4/5 |
| The immunophenotype beat's own ledger: what was enumerated, what was written, what was dropped and why, and what could not be read | Analysis | 4 | 4/5 |
| The imports that were never necessary: H3K79 methylation in KMT2A::AFF1 has its own literature, and this graph barely cites it | Analysis | 5 | 3/5 |
| The index fusion DISCARDS the SIAH degron: the junction is at AFF1 residue 347, the degron is at human 282-304, and three entries had it the other way because they measured a murine motif against an exon-numbering junction | Analysis | 4 | 4/5 |
| The index fusion's 3' partner has ONE observed binary interaction in IntAct and forty-two residues of solved structure - every SEC contact attributed to AFF1 is an AFF4 result wearing AFF1's name | Analysis | 6 | 4/5 |
| The infant breakpoint mutilates the reciprocal protein's first PHD finger - so 'the reciprocal product' is at least two different proteins | Explainer | 5 | 3/5 |
| The infant menin-inhibitor occupancy experiment has been done and deposited - menin, KMT2A and ENL CUT&RUN under revumenib in ONE infant patient sampled before and after a lineage switch, not two patients - but it is KMT2A-ENL, so the index-fusion absence survives, and the same deposit holds untreated KMT2A::AFF1 libraries this corpus cites once | Analysis | 1 | 4/5 |
| The innate-immune-rewired state — LAMP-5 is a direct fusion target that routes signalling away from interferon and toward NF-kB, and the cell depends on that routing | Cell state | 2 | 3/5 |
| The IntAct interactome gap is closed - all 135 'unwritten' interactors are mentioned and 60% carry an explicit decision - while 95 of the 110 partners unique to the INDEX fusion have never been mentioned at all | Analysis | 3 | 4/5 |
| The interactome coverage figure is computed on 651 of the 1,015 IntAct rows available - 64% - and the gap is worst for menin and LEDGF, the two baits the menin-interface hypothesis rests on | Analysis | 4 | 4/5 |
| The interactome instrument is migrated to IntAct REST: 277 partners, 118 written, 42.6% - the denominator grew by 60 and coverage fell 3.5 points, which is the instrument getting honest | Analysis | 4 | 4/5 |
| The interactome tail is orderable after all, just not by evidence: 62 of the 96 unwritten partners are already DISCUSSED somewhere in this corpus and need only promoting to entries, while 34 have never been read at all. Two cycles looked for a priority order in evidence strength and found none, because the ordering that exists is over how much work is left, not over how good the evidence is | Analysis | 1 | 5/5 |
| The Interfant-06 backbone, phase by phase: what the protocol every infant reference in this graph points at actually does | Explainer | 6 | 4/5 |
| The interferon state is not baseline in this disease — it is something a menin inhibitor creates, through endogenous retrovirus induction and MHC class II | Cell state | 2 | 3/5 |
| The IRX1 address requires the AFF1 partner; the menin interface explains the shared HOXA address and not this one | Hypothesis | 2 | 2/5 |
| The IRX2 / IRX2-DT geometry re-derived from three annotations: 215 bp and 89.2% under RefSeq, 437 bp and 78.2% under Ensembl, and the verdict does not move | Analysis | 5 | 4/5 |
| The junction-peptide absence was a claim about mass-spectrometry datasets bounded by a PubMed abstract search: PRIDE holds three human MLL-AF4 proteomics projects, so measured-not-searched is now named rather than asserted | Analysis | 2 | 4/5 |
| The K1130/K1133 numbering is HUMAN, stated in the paper's own words, and the immunising peptide proves it a second time without relying on that sentence | Analysis | 2 | 5/5 |
| The KDM6 contradiction resolved one step: GSK-J4 inhibits UTX too, so it should ANTAGONISE a menin inhibitor - and nobody has combined them | Analysis | 3 | 3/5 |
| The KMT2-family beat's own ledger: every query run, every gene dropped, every paper read and not used | Analysis | 4 | 3/5 |
| The KMT2A breakpoint cluster region in base positions: three incompatible definitions reconciled to one GRCh38 table, with the DCAL frame's three bp identities re-derived and the GRCh37 lift measured per interval | Non-coding | 2 | 5/5 |
| The KMT2A breakpoint cluster region: an 8.3 kb stretch built to break | Breakpoint | 5 | 3/5 |
| The KMT2A C-terminal site class gives VTP-50469/DMSO = 1.13 - an apparent GAIN of H3K4me3 - and its IgG negative control sits at 2.4-2.6, so the class is background and the number must not be reported as a result | Analysis | 1 | 4/5 |
| The KMT2A exon-11 anchor is not uniquely TARGETED by the KDM3B-G9a axis - it is unusually SENSITIVE to an H3K9me1 rise that happens almost everywhere, and the sensitivity is a property of the element | Hypothesis | 2 | 3/5 |
| The KMT2A exon-11 CTCF anchor carries a CBX3 peak and a BRCA1 peak in three of the very ENCODE experiments Q35 called empty - the peaks are in ENCODE's own pre-IDR files, present in both replicates, and deleted by the IDR threshold at global IDR 0.227 and 0.059 | Analysis | 4 | 4/5 |
| The KMT2A exon-11 CTCF anchor, placed in its population: baseline strength 4.92x (91.7th percentile of 12,443 RPE anchors), KDM3B-depletion ratio 0.396x, rank 58 of 1,625 strength-matched anchors - a strong, strongly-responding anchor at the edge of a continuum, not an outlier | Non-coding | 2 | 4/5 |
| The KMT2A exon-11 CTCF/cohesin summit, measured: GRCh38 chr11:118,488,694 (CTCF) and chr11:118,488,677 (RAD21), 17 bp apart, both inside canonical exon 11 | Non-coding | 2 | 4/5 |
| The KMT2A locus sits inside a 179-318 kb H3K9me2-domain-free block in human CD34+ bone-marrow progenitors - the 7th, 11th and 37th longest such block on chr11 in three ChIPs - and the same block is present in granulocytes, K562 and most primary AML | Non-coding | 2 | 3/5 |
| The KMT2A N-terminal antibody reports wild-type plus fusion and the C-terminal antibody reports wild-type alone - which makes an N-versus-C difference a fusion-specific readout with no tag and no engineering | Explainer | 3 | 4/5 |
| The KMT2A transactivation domain on the CBP KIX domain: a cooperative allosteric site at 2842-2858, solved three times, and thrown away by every breakpoint | Interface | 4 | 4/5 |
| The KMT2A-fusion causal chain: six links, one measured ordering, and two arms that are parallel rather than sequential | Mechanism | 22 | 4/5 |
| The KMT2A-N signal at the AFF1 locus is bimodal, neither mode is on AFF1's TSS, and the flank test I ran first said the opposite | Analysis | 2 | 3/5 |
| The KMT2A-r AML patient table numbers MLLT10 on isoform P55197-1, not the canonical sequence: S674 is S658 and S705 is S689 | Analysis | 3 | 4/5 |
| The KMT2A-r DNA methylation signature — focal hypermethylation, no global hypomethylation, and a hypomethylating agent that did not help | Mechanism | 9 | 4/5 |
| The KMT2A-rearranged DepMap arm is not MTAP-deleted, and the gene that looked like the test cannot answer it | Analysis | 3 | 3/5 |
| The KMT2A::AFF1 oncoprotein-target promoter set is a fusion-level property, and patient identity adds nothing measurable on top of it | Hypothesis | 2 | 1/5 |
| The KMT2A::MLLT1 chimeric protein: exactly what survives the join on each side, in residue numbers | Protein | 5 | 4/5 |
| The KMT2A::MLLT1 mechanism sweep: what was searched, what was read and not used, and the three retrieval traps that would have produced confident wrong answers | Analysis | 4 | 4/5 |
| The KMT2A::MLLT3 chimeric protein: what survives the join on each side, in residue numbers - and the four AF9 modules that do not | Protein | 5 | 4/5 |
| The KOCL series (CVCL_3993, CVCL_6867, CVCL_3994, CVCL_3995) — four Japanese infant KMT2A::AFF1 lines, all under one year | Explainer | 3 | 3/5 |
| The label says monitor bone growth in children. Not one paper has asked what menin does in a growth plate | Explainer | 2 | 4/5 |
| The LEDGF hole, measured: every published LEDGF-removal experiment removes it BEFORE or AT transformation, and none treats an established leukaemia in an animal | Analysis | 7 | 4/5 |
| The LEDGF IBD–KMT2A grip: the second half of the clamp, and nobody is drugging it | Interface | 7 | 4/5 |
| The LEDGF PWWP–H3K36me nucleosome contact: how the fusion learns its address | Interface | 4 | 4/5 |
| The length-matched control I demanded of myself: 42% of the abstract-to-full-text rise is reproduced by an unrelated same-field paper, so the specificity I claimed for it was roughly half what I reported | Analysis | 2 | 4/5 |
| The leukaemia term hid the answer for DPY30 — a rule-77 demonstration with clean rule-67 controls | Analysis | 2 | 4/5 |
| The leukaemia that changed lineage in eleven days and changed back when the drug stopped: KMT2A::AFF4 infant ALL on blinatumomab | Patient story | 1 | 3/5 |
| The leukocyte artefact runs the opposite way to the one I pre-registered: it makes a haematopoietic antigen look dangerous by loading spleen and lymph node, and the fix is to read which tissue carries the signal rather than how big the ratio is | Explainer | 1 | 4/5 |
| The lineage confound, tested: the FA signal is in both halves, the B-lineage half is stronger, and it survives holding lineage constant | Risk | 2 | 3/5 |
| The lineage confound: partner predicts whether the leukaemia is myeloid or lymphoid before it predicts anything else | Explainer | 3 | 3/5 |
| The lineage-switched AML state of infant KMT2A::AFF1, described by chromatin rather than by flow cytometry - fusion retained on PAX5 and MEIS1, lost from EBF1 and HOXA, myeloid promoters gained by DOT1L and ENL | Cell state | 2 | 3/5 |
| The lipid-dependent state — ACSL4 and polyunsaturated fatty acid utilisation in KMT2A-rearranged AML, against ELOVL1 and saturated elongation in KMT2A::AFF1 infant ALL | Cell state | 3 | 3/5 |
| The little elongation complex (ELL + ICE1 + ICE2 + ZC3H8) — the other place ELL works, and why ELL's pan-essentiality is probably not about the fusion | Protein | 2 | 3/5 |
| The lncRNA-DOT1L-LAMP5 axis was measured on H3K79 in MOLM-13 alone: eight human samples, one fusion, no index-fusion arm | Analysis | 3 | 4/5 |
| The lost SET domain, and the verdict: the fusion is a gain-of-function neomorph, not a KMT2A loss-of-function | Mechanism | 6 | 4/5 |
| The LSD1–GFI1 SNAG interface — a second worked example of drugging an undruggable repressor through its partner | Interface | 3 | 3/5 |
| The lymphoid look of the core does not survive an activity-matched null inside the same 332, and the pre-registered power check says 17 genes cannot carry the statistic anyway | Analysis | 2 | 4/5 |
| The lymphoid-restricted DAXX dependency survives three nulls and two comparator restrictions - and ATRX, MEN1 and DOT1L do not survive the same test in the same lines | Analysis | 6 | 3/5 |
| The marrow oxygen gradient — low everywhere, lowest at the sinusoids, and in this leukaemia low oxygen helps the drug rather than the cell | Explainer | 3 | 3/5 |
| The MCF-7 arm, and the clause that saved it: SUV39H1 at the exon-11 anchor reaches the 96.3rd percentile of 56,171 same-cell-type CTCF anchors in one replicate - but all six non-anchor KMT2A intervals are elevated too (medians 73-87), so the pre-registered FIRES clause does not fire, the verdict is NEITHER, and four replicates of one antibody in one cell line span 51.8 to 96.3 at the same 147 bp | Analysis | 3 | 2/5 |
| The measurement everybody said was missing exists: in SEM cells KMT2A::AFF1 occupies 20% of unmethylated CpG sites, CXXC1 50% and KDM2B 89%, and only the fusion tracks menin (r2 = 0.96) | Analysis | 2 | 4/5 |
| The measurement q148 called the one thing that could overturn its headline: scored as ~20 kb intervals instead of 2 kb promoters, the authors' GMP-like class is enriched in 0 of 24 untreated non-circular samples, while the two control classes reach 19 and 10 - so the promoter window was not the limitation | Analysis | 1 | 4/5 |
| The measurement that settles the CTCF dispute: degron-grade CTCF removal versus cohesin removal, with DNA breaks AND rearrangement outcome read out at the same 1 kb of KMT2A in the same cells, reported as rearrangements per break | Experiment | 5 | 1/5 |
| The measurement that would separate a fusion-partner effect from a lineage effect does not exist: GSE127507 deposits H3K79me2 for RS4;11 and MOLM13 and for ML-2 it deposits DOT1L, MENIN, MLL1n and an input and no H3K79me2 at all | Analysis | 1 | 4/5 |
| The Mediator/BET deposition is 48 of 48 mouse MLL-AF9/NrasG12D samples: resolving the KMT2A status behind the MED23 verdict | Analysis | 3 | 5/5 |
| The MEN1 age-penetrance curve: 7% by age 10, 52% by 20, 87% by 30 | Epidemiology | 2 | 5/5 |
| The menin acidic shelf, Glu366-Asp370-Val371: the counter-charge that MBM2 binds, resolved in 3U88 after all - and the one patch where the drug pocket, the SvID and the gamma-H2A.X motif all touch | Interface | 4 | 4/5 |
| The menin arm and the CTCF arm are not two stories: menin/SETD2/H3K36me3/LEDGF licenses CtIP short-range resection and CTCF/H3K9me/HP1-gamma licenses BRCA1/BARD1-EXO1/DNA2 long-range resection, which are the two consecutive halves of ONE reaction - so a menin inhibitor and an H3K9-axis inhibitor are acting on the same pathway at different steps | Hypothesis | 5 | 1/5 |
| The menin gap survives matching on menin's own signal, but only two deciles of the two strata overlap | Analysis | 3 | 3/5 |
| The menin inhibitor in this head-to-head is at 50 nM and all three DOT1L inhibitors are at 100 nM - the comparison is dose-biased AGAINST the menin inhibitor - and compound 10's target engagement at exactly 100 nM is demonstrated inside the same series by a spike-in-normalised H3K79me2 collapse of 5.6-fold by day 3 | Analysis | 2 | 4/5 |
| The menin inhibitor removes three-quarters of the fusion from its own promoters, replicated in two batches | Analysis | 4 | 4/5 |
| The menin inhibitor's effect on H3K79me2 is a REDISTRIBUTION within the fusion's own site set, not a loss from it: the share falls 41.4% at the quartile the fusion is most evicted from and RISES 18.7% at the quartile it is least evicted from, in murine MLL-AF9 | Mechanism | 3 | 3/5 |
| The menin interface cannot be what decides where KMT2A::AFF1 sits: within one patient the fusion's target promoters were almost entirely replaced while the menin-binding motif was unchanged | Mechanism | 3 | 2/5 |
| The menin interface is a requirement of 5'-KMT2A fusions in haematopoiesis, not of KMT2A rearrangement as such - and a solid tumour has been quietly proving it for six years | Hypothesis | 5 | 3/5 |
| The menin interface is identical in all 27 of these patients and the amount of chromatin their oncoproteins occupy differs by up to two orders of magnitude - so the interface can be a permission for binding but cannot be what sets how much binding happens | Mechanism | 3 | 3/5 |
| The menin side of the LEDGF clamp: residues 91-105 and 209-212, on the opposite face of menin from the drug pocket and 26-38 A from every other surface in this beat | Interface | 2 | 4/5 |
| The menin small-molecule pocket as a coordinated surface: four clinical-stage compounds, 21-26 contact residues each, and bleximenib sitting on a different part of it from the other three | Interface | 3 | 5/5 |
| The menin that matters in an infant KMT2A-rearranged leukaemia is the menin on the fusion, and the N-minus-C antibody difference can measure it in any patient sample without a tag | Hypothesis | 3 | 1/5 |
| The menin-dependence test I proposed in the cycle-146 log cannot fire by construction - and what the one pair CAN answer is that 85% of gene-body occupancy is menin-dependent while histone clusters preferentially survive | Analysis | 4 | 3/5 |
| The menin-FANCD2 bridge is dead: it was tested in 2008, the mutation spectra differ, and there is no genetic interaction | Mechanism | 6 | 4/5 |
| The menin-gamma-H2A.X motif, menin Val371-Gln400: necessary, sufficient as a peptide, and the nine residues at its centre have never been seen in any of the 69 menin structures | Interface | 4 | 3/5 |
| The menin-inhibitor class splits at Val371: three of four clinical compounds contact the first residue of the gamma-H2A.X motif and bleximenib does not, so DNA-repair effects should separate from KMT2A-displacement effects within the class | Hypothesis | 3 | 1/5 |
| The menin-inhibitor plus PARP-inhibitor experiment is genuinely unrun, but its rationale should be DNA repair, not HOXA9 - and the evidence comes from a disease where menin is a tumour suppressor | Analysis | 2 | 3/5 |
| The menin-inhibitor-resistant state has its own address: SMARCA4, BRD4 and CREBBP, with no MEN1 mutation anywhere | Resistance | 3 | 3/5 |
| The menin–KMT2A grip (MBM1), the interface the drugs actually block | Interface | 4 | 5/5 |
| The menin, ENL and DOT1L replicates of the drug-exposed relapse sample agree with each other at Spearman 0.11 to 0.25, below the floor this project set in the previous cycle, so no quantitative claim from that arm survives | Analysis | 3 | 4/5 |
| The menin/H3K79 partition this graph leans on was measured in MURINE MLL-AF9 - resolved from GEO, because the abstract does not say | Analysis | 2 | 4/5 |
| The menin/Polycomb split between NLRC5 and CIITA does not extend to their pathways, and the MHC locus is structurally invisible to the method that found it | Analysis | 2 | 4/5 |
| The methylome co-mutation table, recomputed: IDH2 up at p = 0.0004 and not p < 0.0001, IDH1 and DNMT3A flat, and the abstract disagrees with its own Table 2 | Analysis | 2 | 4/5 |
| The MHC was never invisible - the resolver was wrong - and once the classical chains are joined the class I machinery is bivalent, not unmarked | Analysis | 3 | 3/5 |
| The mid-occupancy floor was computed by three consecutive beats, stored in two committed results files for every contrast, and read as data by none of them - because it was introduced as a normaliser, so no criterion was ever written about it and no verdict ever mentioned it | Explainer | 1 | 4/5 |
| The missing measurement: is MHC class I bivalent, does a menin inhibitor raise it, and does raising it cost NK control - in a KMT2A-rearranged cell, for the first time | Experiment | 3 | 1/5 |
| The missing reagent is a spike-in, not a better statistic: a spike-in-normalised H3K4me3, H3K79me2 and H3K27me3 ChIP-seq at 72 h of a clinical menin inhibitor in a KMT2A-rearranged human line, which is the only design that can tell a genuine genome-wide mark redistribution from the compositional shadow of a peak-localised change | Experiment | 2 | 3/5 |
| The missing reagent: a KMT2A-fusion or wild-type-KMT2A proximity bait in a KMT2A-rearranged leukaemia line - IntAct has curated no KMT2A-bait interaction experiment since April 2015 and no PSIP1-bait since October 2012 | Experiment | 2 | 3/5 |
| The MLL-fusion interactome recovers corepressor SCAFFOLDS and not their HDAC1/2 catalytic core: NuRD splits 5/7 remodelling arm versus 0/7 deacetylase arm (Fisher p = 0.021), and HDAC1, HDAC2, RBBP4 and RBBP7 are absent from all seven baits | Analysis | 4 | 3/5 |
| The MLL-protected Hoxa9 CpG sites bind the CXXC domain 4- to 9-fold tighter than the unprotected ones, in one ITC series at fixed everything else | Interface | 2 | 3/5 |
| The MLL-side twin of the 1998 anti-AF4 result: in 1997 the same punctate nuclear pattern was seen with and without an 11q23 translocation, and the authors said so | Mechanism | 3 | 4/5 |
| The MLL3/4-UTX switch fails to throw — menin inhibition kills by turning something ON, and cells that cannot turn it on survive | Resistance | 6 | 3/5 |
| The monocytic confound is worse than recorded: two of the six rearranged lines are one patient, and the four-line control group contains a HOXA-driven fusion and two NPM1c/myelomonocytic lines | Analysis | 8 | 4/5 |
| The most faithful mouse models of t(11;19) are reciprocal-positive by design, and the commonest ones carry no reciprocal allele at all - and nobody has compared them | Explainer | 7 | 3/5 |
| The mouse fusion fraction is 0.73 and the human proxy fusion fraction is 0.21-0.24 - a three-fold gap in the direction a retroviral over-expression model predicts, so the one place the masking factor can be calibrated against a tag is the one place its value does not transfer | Analysis | 1 | 3/5 |
| The MRD target a centre can run decides which infants are intensified, and the two targets disagree in the direction that matters | Risk | 5 | 3/5 |
| The MRN asymmetry adjudicated: RAD50 -0.114 sits with NBN -0.047 and not with MRE11 -0.542, so it is not one subunit against two - and yet MRE11 and RAD50 covary across 1,208 cell lines at r = 0.554, the same as BRCA1 against BARD1, against a background of zero | Analysis | 4 | 4/5 |
| The MT/BCB domain, Q03164 1147-1244: the CXXC fold plus a 41-residue basic tail nobody has measured on its own | Interface | 3 | 4/5 |
| The MTAP-deleted, MTA-high state - a genotype-imposed metabolic state that this project's KMT2A-rearranged arm turns out NOT to have, and that its own screen could never have detected directly | Cell state | 6 | 4/5 |
| The murine MLL1 ChIP that sits beside a FLAG-tagged fusion in GSE260742 uses Bethyl A300-086A - the identical antibody to the human MLL1n track in GSE127507 - which no GEO record in either series would tell you, and which is what makes a masking calibration against a tag possible at all | Analysis | 1 | 4/5 |
| The murine-coordinate sweep is a NEGATIVE result - zero new defects in 3,086 entries - and its actual yield was a fourth entry that had the degron right before Q191 did | Analysis | 3 | 4/5 |
| The MYC contradiction can be advanced but not closed: the enhancer is independently validated, the SWI/SNF route is not, and the two papers never measured the same thing | Mechanism | 5 | 3/5 |
| The myeloid/lymphoid metabolic split in KMT2A-rearranged leukaemia is set by CELL OF ORIGIN (fetal versus adult), not by lineage or by the fusion partner | Hypothesis | 5 | 1/5 |
| The N-over-C oncoprotein score is not fusion-specific by construction, because taspase1 cleaves wild-type KMT2A into an N320 and a C180 fragment that need not occupy the same chromatin - so a fusion-negative cell has a real N/C signal | Hypothesis | 2 | 1/5 |
| The N320-C180 clamp is the only KMT2A module whose disruption has ever been shown to change subnuclear localisation - and the fusion is the disruption | Mechanism | 4 | 3/5 |
| The named-but-unwritten queue is keyed on gene symbols, so CD15 is invisible to it at 23 entries | Analysis | 2 | 4/5 |
| The named-but-unwritten queue's top two entries were a web API and a survival endpoint, and MYC was the real answer all along | Analysis | 1 | 4/5 |
| The national scale: about 24 infants a year in England and Wales, about 12 in Australia | Epidemiology | 4 | 3/5 |
| The near-silent genome of infant KMT2A-r ALL — 1.3 non-silent mutations, and why that is bad news as well as good | Mechanism | 9 | 5/5 |
| The necessary lesion in ZNF384-rearranged leukaemia is LOSS of the ZNF384 C-terminus, not GAIN of a fusion partner | Hypothesis | 5 | 1/5 |
| The neonatal window — the state in which an MLL fusion can transform, bounded at both ends | Cell state | 6 | 3/5 |
| The NF-kB story in KMT2A-rearranged leukaemia is a myeloid story, and the lymphoid half is not a weaker version of it — it is a different subject | Mechanism | 4 | 4/5 |
| The NK cell - the effector arm of haploidentical transplant, the one this disease is documented to evade, and the cell CLEC12A was named on | Cell type | 7 | 3/5 |
| The non-chromatin half: CALM-AF10 breaks the cell's iron intake and the cells are chelator-sensitive in vitro - but iron restriction did not extend survival in vivo (corrected 2026-09-21) | Mechanism | 4 | 3/5 |
| The non-synchronisable state: five KMT2A-rearranged lines refuse mimosine, double thymidine and nocodazole, and the fusion protein does not fluctuate through the cycle | Cell state | 3 | 3/5 |
| The noncoding dependency screen five hypotheses in this graph are waiting on - and the KMT2A-rearranged screen that already exists and bounds it | Experiment | 4 | 3/5 |
| The nuclear lamina and lamina-associated domains - evidence grade for KMT2A: weak and indirect, not none | Mechanism | 5 | 2/5 |
| The nuclear pore and NUP98 fusions — a fusion that takes a pore protein's disordered repeats off the pore and builds nuclear droplets with them | Mechanism | 4 | 4/5 |
| The nucleolus — the one compartment with direct published images of a KMT2A fusion inside it | Mechanism | 3 | 3/5 |
| The null the claim needed: the KMT2A BCR ranks 72 of 18,082 chromosome-11 bins for its H3K9me1 response - top 0.40% - while the same locus ranks 3,877th for H3K9me3 and 10,276th for H3K9me2 | Analysis | 1 | 4/5 |
| The NuRD complex - two separable modules, three paralogue choices that change what it does, and a graph that carried its ATPase and its shared core but never the scaffolds that make it NuRD | Protein | 8 | 3/5 |
| The obvious result was that VTP-50469 cuts H3K4me3 at HOXA9 three-fold in SEM. The pre-registered housekeeping control says GAPDH, RPL13A and TUBB fell just as far, so the obvious result was the normalisation | Analysis | 2 | 4/5 |
| The occupancy rule this project has used since q145 calls a tenth of ALL promoters occupied, and no entry using it records that | Analysis | 2 | 4/5 |
| The off-target surface, measured rather than feared: KDM3B depletion moves CTCF occupancy at 84.6% of 12,443 RPE anchors and halves it at 1,436 - so an H3K9-axis drug given to prevent one rearrangement is remodelling loop architecture genome-wide, and preferentially at the strongest anchors | Risk | 3 | 3/5 |
| The oncoprotein-target site count for sample 148752 is 46, 345 or 745 depending on the interval set and the universe, and the corpus has been quoting one of the three with no label | Analysis | 2 | 4/5 |
| The one experiment that separates fusion partner from lineage: an H3K79me2 ChIP under a menin inhibitor in ML-2 or any KMT2A::AFDN line, alongside the MLL1n and MENIN samples that already exist for that line and can be re-binned for free | Experiment | 2 | 3/5 |
| The one experiment that settles this beat: dose-matched menin and DOT1L arms in RS4;11 with H3K4me3 ChIP at PHGDH, plus 13C-serine flux - and it answers the cycle-58 question at the same time | Experiment | 3 | 3/5 |
| The one experiment that would close the SUV39H1 arm of this graph's H3K9 argument: CST #8729S CUT&RUN in a CD34+ progenitor and in SEM or RS4;11, with an IgG arm and a SUV39H1-degron arm that neither existing deposit has - because after this cycle the enzyme has been measured in exactly two human cell types and neither is a blood cell | Experiment | 3 | 4/5 |
| The one experiment that would close this beat: MEN1 and DOT1L ChIP in RS4;11 (KMT2A::AFF1) under DMSO, a menin inhibitor and a target-engaging DOT1L inhibitor, with Drosophila spike-in and two replicates per arm - about 24 libraries, and the depositing lab already runs every component of it | Experiment | 3 | 3/5 |
| The one experiment that would separate the H3K9me1/2 rearrangement brake from H3K9me3 was run, deposited as eight public samples, and reported nowhere in the paper | Analysis | 3 | 4/5 |
| The only absolute-scale H3K79me2 deposit this project has contains no IgG or no-primary library, so the 1-31% residual measured after DOT1L inhibition cannot be separated from antibody background - the single cheapest missing control in the dataset | Analysis | 2 | 5/5 |
| The only cellular proposal for how the SEC gets P-TEFb out of the reservoir is a condensate, and the two assays it rests on cannot tell that model from its rival | Mechanism | 4 | 3/5 |
| The only deposited H3K79me2 kinetic series for a menin inhibitor is non-monotone - a minimum at 16 h and a recovery at 24 h that survives common support and two rank statistics - and its 24 h point shows MORE redistribution than the 48 h main-arm sample, so the 48 h/72 h asymmetry in cycle 82's F stands and F keeps the words lower bound | Analysis | 2 | 3/5 |
| The only second mark with a drug arm in SEM is H3K27ac, and its replicates agree at r = 0.21-0.29 against H3K4me3's 0.78-0.83 - so GSE159608's SEM EPZ-5676 experiment has one usable readout, not two | Analysis | 1 | 4/5 |
| The only two trials stopped on a stated risk-benefit judgement are GSK2879552 (LSD1) studies in AML, while iadademstat, another LSD1 inhibitor, ran a KMT2A-rearranged-enriched expansion with an acceptable safety profile - so the stop looks molecule-specific, and its reason is unread | Analysis | 3 | 3/5 |
| The order in which the complex leaves fusion-occupied promoters, all fifteen channels on one scale | Analysis | 3 | 3/5 |
| The order in which the fusion's programme collapses is a property of the partner, not of KMT2A - so there is no single causal chain | Hypothesis | 5 | 1/5 |
| The other arm of the crosstalk: H2Bub licenses H3K4 methylation through ASH2L and relieves a built-in COMPASS autoinhibition — and MLL3 does not respond at all | Mechanism | 3 | 4/5 |
| The other half of the break: what is actually known about the AFF1 breakpoint region, and the negative-control gene nobody cites | Mechanism | 5 | 3/5 |
| The other half of the islet story: losing menin also costs the beta cell its identity and raises glucagon | Risk | 2 | 3/5 |
| The OXPHOS-dependent state — established in KMT2A-rearranged AML, and inverted in KMT2A-rearranged B-ALL where OXPHOS inhibition makes leukaemia-initiating cells appear | Cell state | 4 | 3/5 |
| The PAF complex species is mouse - and its only deposited series is Hoxa9-ER, not an MLL fusion at all | Analysis | 3 | 4/5 |
| The panobinostat H2Bub result is SEM and KOPN8 against a REH comparator: three human lines, two KMT2A partners, one non-KMT2A control | Analysis | 3 | 5/5 |
| The paper's four comparison loci, marks read against FISH calls: the H3K9 mark response agrees with the cytogenetic response at two loci and contradicts it at two - the mark is neither necessary nor sufficient | Analysis | 2 | 3/5 |
| The paralogue split survives the expression control and the ALAS2 control does not: ING4 is transcribed MORE than ING5 and is not required at all | Analysis | 2 | 0/5 |
| The paralogue that covers for LEDGF: HRP-2 carries the only other IBD in the human proteome, substitutes for LEDGF in HIV integration, and the double knockout is embryonic lethal | Mechanism | 5 | 4/5 |
| The parathyroid does not need the rest of the body: deleting menin only there causes neoplasia and hypercalcaemia | Mechanism | 3 | 4/5 |
| The partner-matched control arm is not 241 versus 219 - it is 153 versus 101, and in that subset the two groups make an identical fusion protein | Analysis | 7 | 3/5 |
| The partner, not the site, is what could make a retained KMT2A modification fusion-specific - the AML1-ETO mechanism asked of KMT2A::AFF1 | Hypothesis | 3 | 1/5 |
| The partner's deubiquitinase domain is what lets a PHD-retaining KMT2A fusion survive and transform | Hypothesis | 3 | 1/5 |
| The PBX requirement in KMT2A-rearranged leukaemia is a family property, and every experiment that shaped this graph's view of it removed one paralogue at a time | Hypothesis | 4 | 1/5 |
| The PBX3-MEIS1 dimer, not HOXA9, is the unit that reproduces the MLL-fusion transcriptome - and it turns the HOXA cluster on from underneath | Mechanism | 4 | 3/5 |
| The per-library 'cannot be occupied' floor spans 0.00x to 4.01x an average promoter, and one core gene's AFF1-exclusivity rests entirely on it | Analysis | 1 | 4/5 |
| The perivascular and sinusoidal niche — where the functional evidence actually sits, and where the marrow is genuinely hypoxic | Explainer | 6 | 4/5 |
| The permutation cycle 155 asked for: the two-instrument exclusive intersection is four genes not one, 34 of the 42 could never have been in it, and the surviving IRX1 claim gives p=0.092 against a patient-level null | Analysis | 3 | 4/5 |
| The phase-2 go/no-go register: the numbers we agree to before we look | Explainer | 8 | 3/5 |
| The phosphatase side: SET binds both wild-type KMT2A and the fusion, and inhibiting it changes four kinases at once | Mechanism | 1 | 3/5 |
| The pivotal menin-inhibitor paper reports that the drug does NOT globally displace MLL1 or the fusion from chromatin - menin goes, the fusion largely stays | Mechanism | 3 | 4/5 |
| The plasma membrane - the one compartment this graph targets with drugs and had never written down | Mechanism | 3 | 4/5 |
| The platform argument's best evidence: one drug, two genotypes, one interface | Explainer | 2 | 4/5 |
| The pluripotent stem-cell route has failed from both ends, and the failures are informative | Explainer | 3 | 4/5 |
| The positive control this corpus has never had: degrading MLL::AF9 clears its own tag from 93-97% of its strongest chromatin sites within 3 hours, and two INDEPENDENT sequencing batches agree to within 4.6 points - the first technical noise floor ever measured for a ChIP eviction comparison in this project | Analysis | 2 | 4/5 |
| THE POSITIVE RESULT: the writer G9a, the reader HP1a and the scaffold KAP1 all sit on the KMT2A PROMOTER in MCF-7 at the 87.6th-98.9th percentile of 2,000 ACTIVE promoters - surviving the control that says an active promoter is ChIP-hot for everything - while none of the three is above the 75th percentile at the exon-11 anchor 52 kb away | Analysis | 4 | 3/5 |
| The PPTC childhood PDX panel — 90 leukaemia models, an MLL-ALL group, and no published partner or age breakdown | Explainer | 3 | 4/5 |
| The PRC2 dependency profile, lineage-split and expression-controlled - and the first time this project's paralogue rule came back positive | Analysis | 3 | 3/5 |
| The pre-registered magnitude test failed because the statistic was bounded by construction - top-decile share spreads only 1.1-1.4x between samples and cannot express what the published oncoprotein score says varies | Analysis | 2 | 4/5 |
| The pre-registered three-branch test of 'the HOXA-negative blast's oncoprotein is on the GMP programme' returns NEITHER/UNINFORMATIVE, on four independent gates | Analysis | 3 | 3/5 |
| The predictable clinical error this beat exists to prevent: a menin inhibitor given for a KMT2A-rearranged sarcoma because of the gene name | Risk | 4 | 3/5 |
| The premise that GSE260742 'carries a ChIP-Rx spike-in' does not survive reading the deposit: zero of 158 sample records mention a spike-in, the only ChIP-Rx experiment in the paper is an H2AK119ub panel that is not identifiable among the deposited samples, and 152 of 158 samples ship only an unnormalised igvtools .tdf | Analysis | 3 | 5/5 |
| The prescribed GEO lookup returns zero for every paper this project has ever resolved, including the one it was written from | Analysis | 3 | 5/5 |
| The prevention window: the break happens in a fetus, and we know when it CLOSES but not when it opens | Explainer | 4 | 3/5 |
| The prey-only interactome is 36.3% written, not 0% - the census, by identity, of all 212 human prey-only partners of the six core proteins | Analysis | 3 | 4/5 |
| The primed chromatin state — what is actually established, and why the word 'bivalent' should be used carefully here | Cell state | 6 | 3/5 |
| The pro-B arrest state — what a KMT2A::AFF1 blast is actually doing while it sits there | Cell state | 8 | 4/5 |
| The promoter table's second blind spot is not annotation drift at 1.8% - it is one row per symbol at 14.7%, and the case that motivated the question is not displaced at all | Analysis | 3 | 4/5 |
| The protein nobody can attribute by antibody is the one mass spectrometry finds most easily | Explainer | 3 | 3/5 |
| The protocol and era confound: the partner datasets span 1983 to 2016 and outcome moved under them | Explainer | 3 | 4/5 |
| The PTM-database route runs: K1130 and K1133 acetylation are independently re-observed in deposited mass spectrometry, K1133 in the CBP/p300 acetylome itself - and K1130 is also a ubiquitination site nobody has mentioned | Analysis | 4 | 4/5 |
| The published peak classes do transfer from 20 kb peaks to 2 kb promoters - the GMP-over-B-lineage ratio swings 8.56-fold across the pair that defined them - but only in the between-sample direction the classes were built in | Analysis | 3 | 4/5 |
| The quiet genome, audited - the famous 1.3 mutations is a count of point mutations in the dominant clone, and all three of those words do work | Mechanism | 5 | 4/5 |
| The rare paediatric disease priority review voucher: a $150-200m bearer bond, lapsed for 14 months, now live to 2029 | Explainer | 12 | 4/5 |
| The rarest thing in the deposit, measured: across 59,821 CTCF anchors in the SAME nuclei, SUV39H1 occupancy and H3K9me3 correlate at Spearman 0.148 and 0.078 - and a quarter to two-fifths of the enzyme's own strongest sites carry no more of its mark than the median anchor | Analysis | 3 | 3/5 |
| The RAS-mutant subclone is where the leukaemia goes, not what it is - a dissemination modifier that a marrow aspirate systematically under-counts | Hypothesis | 5 | 1/5 |
| The reciprocal ChIP: is chromatin-bound XPO1 present in a KMT2A-rearranged cell, and does a menin inhibitor move it? | Experiment | 3 | 1/5 |
| The reciprocal fusion (AFF1::KMT2A and friends): a second oncoprotein that opens chromatin for the first | Mechanism | 6 | 3/5 |
| The reciprocal MLLT1::KMT2A transcript was reported in the paper that discovered KMT2A, and nobody has gone back to it in thirty-four years | Explainer | 5 | 3/5 |
| The reciprocal-antibody ratio splits the six-gene AFF1-exclusive class in two: H3C15 and SPAG7 sit at or below background, the three most enriched are the three the authors' caller says are not exclusive, and IRX1 is the only member that is both | Analysis | 2 | 3/5 |
| The referral-denominator audit: 97 frequency claims, 63 qualified, and one real defect where the ledger predicted seven | Analysis | 1 | 3/5 |
| The relapse-initiating persister state — present at diagnosis, identifiable before a single dose is given, and defined by basal glucocorticoid-response activation plus small size plus quiescence | Cell state | 3 | 4/5 |
| The reopening watchlist read for the first time: 0 of 10 candidate papers meet their condition, 8 of 10 watched decisions returned nothing, and not one of the ten titles names the gene it was retrieved for | Analysis | 1 | 3/5 |
| The replication protein A heterotrimer (RPA1/RPA2/RPA3) - the ssDNA clamp that every resection and replication-stress claim in this corpus silently depends on, and which had no entry until cycle 160 | Protein | 7 | 5/5 |
| The residual fraction this graph says is absent from the entire literature, measured: FLAG-MLLAF9 enrichment at its own top 1,228 sites falls from 15.9x the genome median to 3.0x under VTP50469 - about 18% residual - and 12.8% of those sites stay in the top 0.1% | Analysis | 3 | 3/5 |
| The residue-type numbering check passed a site that is in the wrong place | Analysis | 2 | 0/5 |
| The resolution floor: every deposited H3K9 track in GSE210480 is 1,000 bp binned, so the 147 bp exon-11 question cannot be answered from the processed files - and the planned analysis that asked for 500 bp windows was asking for something that is not there | Analysis | 2 | 5/5 |
| The REST-wide direction audit Q104 asked for: scaffold-as-bait rows DO exist in the 36% of the record PSICQUIC hides - KMT2A is a bait in 96 of 376 rows across 18 publications and PSIP1 in 11 of 114 across 4, but the most recent is 2015 and 2012, and none of the thirteen never-discussed partners comes from one | Analysis | 4 | 4/5 |
| The resting-state H3K9me2 depletion over KMT2A DOES replicate in a human CD34+ haematopoietic progenitor - measured in 3 of 3 progenitor ChIPs, where the locus sits in the 7th, 11th and 37th longest H3K9me2-free gap on chr11 - but it is not a progenitor property: granulocytes, K562 and 6 of 10 primary AML samples show the same gap | Analysis | 3 | 3/5 |
| The result that runs the wrong way: in Psip1-null cells Hoxa and Hoxd expression goes UP, because Psip1 also recruits Bmi1 and Ctbp1 | Mechanism | 4 | 3/5 |
| The retained AF9 surface in residue detail: one disordered 70-mer, three DOT1L sites, two of them high-affinity and simultaneously occupiable | Interface | 2 | 4/5 |
| The reversibility question: months of partial occupancy against a syndrome built from decades of loss | Risk | 7 | 1/5 |
| The RNA layer and the menin interface are separable: IGF2BP3 depletion sensitises MLL-AF4 leukaemia to menin inhibition and outperformed it alone | Mechanism | 4 | 3/5 |
| The RNA layer scored for KMT2A-selectivity across 79 genes, lineage-split — PTBP1 is the only menin-shaped hit, and the IGF2BP family shows no co-dependency | Analysis | 7 | 3/5 |
| The rule-64 complex-form query that the RPA2 decline flagged as unrun has now been run, and it finds a published damage-state RPA occupancy measurement AT the KMT2A breakpoint cluster region - so two of this corpus's absence entries carry ids that are broader than the claims inside them | Analysis | 4 | 4/5 |
| The same baseline-matched test that kills the target effect under EPZ5676 fires hard under compound 10 - at d6 and d9, in both cell lines, 4 of 4 contrasts (p = 0.0012 to <0.0001) - and in MOLM13 HOXA9 holds 24.5% of its H3K79me2 where the genome median holds 4.5% | Analysis | 3 | 3/5 |
| The same drug target, pursued for benefit: menin inhibition is a diabetes strategy in the literature | Explainer | 5 | 4/5 |
| The same occupancy rule passes 0.61% of gene bodies and 10.75% of promoters, so IRX1 at 3 of 27 is 18x its gene-scale expectation where at promoter scale it was below it | Analysis | 2 | 4/5 |
| The same pocket suppresses JUND: menin inhibition's unmeasured endocrine liability in infants | Risk | 4 | 3/5 |
| The same reader domain, mutated instead of fused, causes a childhood kidney tumour | Analogy | 3 | 0/5 |
| The same-condition H2AK119ub noise floor in GSE260742 spans twentyfold across the deposit's three experimental arms - D1 |R-1| of 1.89% in the PCGF1-KO clone, 10.49% in the non-targeting control and 37.04% in the MLLAF9 Control arm - at one mark, one lab, one pairing shape and one external stratifier. A single same-condition floor for this deposit does not exist. | Analysis | 1 | 3/5 |
| The score's amplitude correlates with sequencing depth at Spearman -0.474 (p = 0.012) - a real and significant depth dependence that cleared the pre-registered voiding threshold of 0.6 only because the threshold was set loosely | Analysis | 2 | 4/5 |
| The screen this beat was dispatched to run 'because it has never been run' was published in Haematologica in 2022, used the same instrument, and is cited in this graph already - in an entry filed under innate immunity | Analysis | 6 | 4/5 |
| The SEC-family target sets, reconstructed as a full three-way Venn: 27.5% of the family's transcriptional output is invisible to AFF4 depletion — and the two 'distinct' sibling sets overlap 8-20x more than chance | Analysis | 3 | 3/5 |
| The second handle on the retained fragment is CK2-dependent, not 14-3-3-dependent | Hypothesis | 3 | 3/5 |
| The second ring — smaller KMT2A-fusion mechanism labs, and where the literature actually points | Group | 8 | 3/5 |
| The selection control, run at last: two biologically identical vehicle-treated input libraries produce a MONOTONE decile gradient from 0.9040 to 1.2349 - wider than the real FLAG gradient cycle 103 called a finding - when the strata are cut on the pair itself, and are flat within 0.73% and non-monotone when the strata are cut externally. Monotonicity across deciles is therefore NOT evidence against a coverage artefact. Cycle 103 is safe because it cut externally | Analysis | 3 | 4/5 |
| The separation MARGIN, not the recurrence count, is the statistic that identifies a partner-specific promoter | Hypothesis | 2 | 1/5 |
| The serine arm replicates in a third KMT2A::AFF1 line from an independent laboratory - PHGDH -2.77, PSAT1 -2.17, GPT2 -2.34, ASNS -1.16 - but the ISR output genes do not, and it survives PCGF1 and BCOR knockout | Analysis | 3 | 3/5 |
| The serine/one-carbon arm is NOT a pure ATF4 output: it is menin-selective where the ISR arm is compound-independent (median margin -0.55 vs -0.02, p=0.011), and it is ABSENT in KMT2A::MLLT3 AML where the ISR arm is present | Analysis | 5 | 3/5 |
| The serine/one-carbon programme has a SECOND, chromatin-proximal menin input that is not ATF4 - which is why PHGDH is menin-selective where CHAC1 is not, and why the arm is absent in KMT2A::MLLT3 | Hypothesis | 3 | 1/5 |
| The shared reader sits in a complex whose only well-defined normal job is parent-of-origin silencing — and the published safety package for YEATS inhibition is entirely haematopoietic | Risk | 5 | 1/5 |
| The shared-epitope masking calibration, run against a FLAG tag and then refuted by its own control: the MLL1 antibody reports 2.23-fold more retained signal than the tag at the fusion's own sites, but MLL1-dominated non-fusion sites fall HARDER than the fusion does (0.1069 against 0.1793), so no mixture of fusion and wild-type MLL1 can produce the observed 0.3995 | Analysis | 1 | 4/5 |
| The six open read-queue members split three rejected and three earning entries - and the flattest dependency in the set, ASB7, turns out to be a negative regulator of H3K9me3 via SUV39H1 degradation | Analysis | 3 | 4/5 |
| The six unwritten DOT1L partners are not six findings - they are nine spokes of ONE GFP-DOT1L pulldown, and the source paper already graded them | Analysis | 8 | 4/5 |
| The size correction that dissolved KMT2A's proximity promiscuity should run the OTHER WAY for PSIP1: at 530 aa, recovery by 9 of 50 BioID2 baits may be MORE than its length predicts, which would make PSIP1 rather than KMT2A the promiscuous prey in this project's core pair | Hypothesis | 3 | 1/5 |
| The soluble-nucleoplasm versus chromatin-bound axis - the one localisation readout that keeps a size dimension, and nobody has run it on a KMT2A fusion | Mechanism | 7 | 4/5 |
| The specificity control that should have clinched this beat inverts instead: the C-terminal MLL1 epitope the fusion does NOT contain loses MORE than the N-terminal epitope it does contain (68.8% vs 78.4% retained), and because the deposit records different cell-line names for these four samples than for every other one, the arm is reported as uninterpretable rather than interpreted | Analysis | 2 | 2/5 |
| The spike-in ruler this thread has been blocked on for eight cycles is deposited as a 2 MB text file, and it includes RS4;11 - the index fusion: under DOT1L inhibition the fly fraction rises 4.9x to 23.4x against matched DMSO, so H3K79me2 collapses GLOBALLY by roughly that factor, and a within-sample share would have shown almost none of it | Analysis | 1 | 4/5 |
| The standing duplicate-check exits 126 and returns nothing at 3,000 files; it caused no duplicate ids, but the audit it should have been doing found two superseded entries that never name their successor - one of them a live safety verdict | Analysis | 5 | 4/5 |
| The standing priority asks for localization on every interactor; the graph has it on 14% of genes and 24% of its most central ones, and DOT1L has none at all | Analysis | 2 | 5/5 |
| The standing worry about same-source counter-evidence, read at n=50: 84% are the author's own caveat or a point of logic, 16% could have cited independent literature, and none of fifty is unsupported | Analysis | 1 | 4/5 |
| The state under menin inhibition — differentiation in AML, rapid death in ALL, and a GMP-like exit in the cells that switch lineage instead | Cell state | 5 | 4/5 |
| The stem-like self-renewal state — a limited stem-cell module grafted onto a committed cell | Cell state | 4 | 4/5 |
| The stratification passes its own positive control: the fusion tag separates the two strata 62-fold | Analysis | 3 | 4/5 |
| The stricter null, and it partly reverses the last one (run) | Analysis | 1 | 3/5 |
| The strongest published case that condensates are load-bearing in KMT2A-fusion leukemia — and it is AKAP95, not AFF1 | Mechanism | 5 | 3/5 |
| The super elongation complex, sampled from the RNA side: ELL, ENL, CDK9 and cyclin T1 are all in the proximity record - ELL2, EAF1/2, AF9 and AF10 are at zero | Analysis | 2 | 4/5 |
| The SvID, menin 360-445: a truncation boundary the field reads as a domain, whose functional residues D418 and W436 are 10-20 A from every menin drug - but whose first ten residues ARE the drug pocket | Interface | 4 | 3/5 |
| The SWI/SNF dependency in KMT2A-rearranged leukaemia belongs to ncBAF, not to canonical BAF - and the drug in the clinic is aimed at the wrong module | Hypothesis | 8 | 1/5 |
| The taspase-1 N/C antibody control separates fusion-occupied from wild-type KMT2A promoters in every primary infant sample, and it is the C-terminal arm that does the work while being the less reproducible arm | Analysis | 2 | 4/5 |
| The ten reported menin-inhibitor escape substitutions are each one nucleotide change from the MEN1 sequence - which the sources could not have shown otherwise - so the useful outputs are a 25-variant validation panel and a burden threshold, not the headline | Analysis | 4 | 3/5 |
| The test bed nobody names: KMT2A rearrangement can be induced and counted in primary human CD34+ and fetal liver stem cells, and it happens without any drug at all | Experiment | 7 | 3/5 |
| The third category: modules lost from the fusion protein but supplied in trans by the wild-type KMT2A allele | Mechanism | 4 | 4/5 |
| The third job: LEDGF sits on transcribed gene bodies with splicing factors and changes exon choice in half the genes that have alternative isoforms | Mechanism | 4 | 3/5 |
| The third resolution trap in three cycles: an ENRICHED-domain BED has a median domain of 13-17 kb and a per-SAMPLE bin size, so 'the GAPDH promoter is inside an H3K9me3 domain' is true in the file and means nothing about the promoter | Explainer | 2 | 5/5 |
| The third silent-failure class, audited after being named in four king logs: exactly one of seven bigWig analyses is raw-coverage, the single incommensurable pair is already labelled three times, and the cross-pipeline ratio comparison was bounded at the point of measurement | Analysis | 1 | 3/5 |
| The three AT-hooks (aa 169-180, 217-227, 301-309) as a localisation determinant — and the correction that MLL's hooks read DNA *structure*, not AT-richness | Mechanism | 8 | 3/5 |
| The tissue selectivity of MEN1 syndrome is not in MEN1: menin is expressed evenly everywhere and MLL, p27 and p18 are the endocrine-predominant ones | Explainer | 2 | 3/5 |
| The trans-histone crosstalk H2Bub → DOT1L → H3K79me: modulatory for me1, effectively required for me2/me3 | Mechanism | 9 | 5/5 |
| The transcriptional CDK with a real KMT2A-rearranged selectivity signal is CDK13, not CDK9 - and nobody has looked | Hypothesis | 4 | 1/5 |
| The transfer rule: which MLL-AF9 results can be carried into t(11;19) and t(4;11), and which are statements about a protein missing a reading module | Explainer | 6 | 4/5 |
| The twelve partners with no entry are three times LESS spoke-expanded than the interactome they came from - 23.1% spoke-only against a 70.6% null, Fisher p = 0.00068 | Analysis | 3 | 4/5 |
| The two beats' opposite answers are produced by the calling rule, not by the promoter universe: three universes give one answer, two rules give two | Analysis | 2 | 4/5 |
| The two co-IPs that settle whether menin's SUV39H1 window and its gamma-H2A.X motif are one surface: swap each laboratory's construct into the other's assay | Experiment | 2 | 3/5 |
| The two founding conditional Mll knockouts were published back to back and they do not agree: fatal marrow failure in three weeks, or grossly normal blood | Explainer | 2 | 5/5 |
| The two instruments' opposite verdicts decompose: the CALLER explains the 16-fold magnitude gap and the UNIVERSE explains the patient-level survival - and inside the shared universe the only gene both call AFF1-exclusive is IRX1 | Analysis | 2 | 4/5 |
| The two silent-failure classes found in cycle 59 did not propagate through the corpus - 13 candidates, all legitimate on reading, and the audit corrected itself twice before it found anything | Analysis | 1 | 3/5 |
| The two t(4;11) products split AFF1 exactly at the P-TEFb-binding module, and the elongation half goes to the reciprocal | Mechanism | 5 | 3/5 |
| The two TARGET B-ALL studies in cBioPortal are 868 of the same patients assayed twice, so joining them DOES answer the question I had just written off as unanswerable: all four ARID1A-mutant B-ALL patients are definitively KMT2A-negative, three of them with truncating calls. The answer is zero of three - and at a 2.7% KMT2A-positive rate an empty overlap has probability 0.92, so it is an upper bound and not a finding | Analysis | 1 | 3/5 |
| The two VTP-50469 H3K4me3 libraries hold 3.3% and 3.8% of their reads in the DMSO-defined peak set against 8.9% for DMSO and 9.4% for EPZ-5676 - one global fact that explains every raw locus difference in the SEM menin-inhibitor arm, and that cannot be resolved into drug effect or library quality | Analysis | 2 | 4/5 |
| The unbiased half of the token audit: 0 of 15 never-measured tokens are wrong, the entries my filters could NOT see are the best-scoped ones, and two scoping fields already existed that I had claimed to add | Analysis | 1 | 3/5 |
| The unbounded oncoprotein score spans 1.73-12.32 log2 units within a sample - it is not the compressed statistic q142 was stuck with - and the pre-registered magnitude verdict is STILL void, because the score's amplitude is no larger than the disagreement between two antibodies against the same end of KMT2A | Analysis | 2 | 4/5 |
| The universe-overlap gate this thread inherited from cycle 107 divides by a track and multiplies by the stratifier, so it also measures whether both libraries are as deep as the stratifier - a property of the stratifier, not of the pair. It aborted 13 of 16 comparisons here, and cycle 107's own pair passed it by 0.25 percentage points while losing more bins to the stratifier than any pair it refused. | Explainer | 1 | 4/5 |
| The unnamed AML lines are NB4 and THP-1 - and NB4 is not KMT2A-rearranged at all | Analysis | 3 | 3/5 |
| The unnamed Cre is Mb1-Cre, which acts at the pro-B stage: the one resolution in this beat that lands on the right cell | Analysis | 3 | 5/5 |
| The unnamed KMT2A-rearranged B-ALL line is SEM, and the deposition says KMT2A::AFF1 in a genotype field | Analysis | 3 | 5/5 |
| The unnamed osteolineage Cre is Prx1-Cre, which is not osteoblast-restricted - and that changes what the negative result means | Analysis | 3 | 4/5 |
| The unstated-system worklist: 26 sources carry a caveat of this class, 18 now resolve, and 13 of 16 new resolutions are imports | Analysis | 3 | 5/5 |
| The washout data cannot say whether the serine/ASNS collapse is durable - the washout control never recovers, ASNS is undetectable in the line, and the housekeeping drifts in opposite directions in the two matrices | Analysis | 2 | 3/5 |
| The white cell count at diagnosis in infants, and why the reported medians disagree by fivefold | Explainer | 6 | 4/5 |
| The whole bone-mineral axis moves on revumenib: phosphate in 51%, alkaline phosphatase in 33%, calcium in 15% | Risk | 2 | 3/5 |
| The whole deposit is hg38 even where the filename does not say so, and the guard that checked it was worth running | Analysis | 3 | 4/5 |
| The whole protein-coding genome: menin is still first, and a metabolic pathway appears (run) | Analysis | 2 | 3/5 |
| The whole-peak-set overlap metric cannot tell a MEN1 ChIP from a DOT1L ChIP in the same untreated cells (Jaccard 0.357, inside the 0.310-0.487 range of all 45 sample pairs) - so on the same data it scores cycle 83's threat as SURVIVING while the pre-specified locus set scores it as FALLING | Analysis | 2 | 4/5 |
| The within-donor null: MEN1 sits at the 99.4th percentile of variation between two sublines of ONE child, and at the 98.9th between donors - menin dependence is not heterogeneous between patients so much as unstable in this background | Analysis | 3 | 4/5 |
| The working attribution reagent in this literature is not an antibody, it is the gel - and that single fact predicts which claim classes survive | Explainer | 4 | 4/5 |
| The WRAD degron absence survives, and the reason is worth more than the verdict: a 3.7 nM chemical degron of WDR5 with 2-hour kinetics already exists IN MV4;11, and it still cannot see the fusion | Analysis | 3 | 4/5 |
| The YEATS asymmetry is breakage geography, not selection: the reader's fate is decided by where topoisomerase II cuts, before any leukaemia exists | Hypothesis | 4 | 1/5 |
| The ZNF384 family is not the inverse of KMT2A::AFF1 - it is the SAME grammar written in the opposite gene order, and three of the four claims in the inverse framing are false | Analysis | 7 | 4/5 |
| The ZNF384-fusion immunophenotype - weak CD10 with aberrant CD13/CD33 - and the one marker that separates it from KMT2A-rearranged disease runs the OPPOSITE way to expectation | Mechanism | 5 | 4/5 |
| There is no selective PRC1 catalytic inhibitor - the entire chemistry is one 2013 tool compound and its analogues, and it hits both paralogues by design | Target | 4 | 4/5 |
| Thiotepa - the third agent that reaches the central nervous system completely, and whose alkylating metabolites are excreted through the skin into a nappy | Drug | 5 | 3/5 |
| Thirteen of q152's seventeen AFF1-only core promoters are absent from the deposit paper's whole target-gene table, and the four that are present are AFF1-exclusive there too | Analysis | 2 | 4/5 |
| This beat pre-registered 'the observed span exceeds the matched-null span by >= 5x' and never said WHICH summary of a 20-draw null: against the maximum it is 3.71x and the criterion fails, against the median it is 30.0x and it passes. The conservative reading was scored and the defect is recorded rather than repaired. | Explainer | 2 | 5/5 |
| This corpus argued from the literature that intersecting fusion peaks with partner peaks cannot attribute occupancy, and eighty cycles later a beat measured that partner antibody sitting at the negative control in primary patient samples - two independent derivations from the same paper, with no edge between them and one wrong premise | Analysis | 2 | 4/5 |
| This cycle's word 'silenced' means two repressive marks up and one active mark down at 2 kb resolution - GSE260742 deposits no RNA-seq, no nascent transcription and no reporter for either NTvKO genotype, so whether the vacated sites stop being transcribed is unmeasured in the experiment that established they are marked for silencing | Analysis | 2 | 4/5 |
| This graph recorded 'nobody has looked at AKAP95 in any KMT2A fusion' one cycle before reading the 2026 paper that did - KMT2A returns 0, MLL returns 2, and every cell-line token returns 0 because cell lines live in figures | Analysis | 3 | 5/5 |
| This graph states 624 falsifiers and records the outcome of 17 - a figure this entry first published as 8, because the detector did not know the corpus's own ALL-CAPS convention for recording one | Analysis | 1 | 3/5 |
| This repo's "the pan-fusion core is 7.4-fold cleaner per unit signal than the singleton tail" divides one control column by a denominator summed over seven baits — on a per-bait denominator the ratio is 1.06 and p goes from 0.074 to 0.91 | Analysis | 2 | 4/5 |
| Thomas Milne (MRC WIMM, Oxford) — MLL-AF4 target biology, enhancer architecture and PROM1/CD133 | Group | 4 | 4/5 |
| THP-1 (CVCL_0006): the default KMT2A::MLLT3 line, from a one-year-old, carrying NRAS G12D and a TP53 frameshift | Explainer | 3 | 4/5 |
| Three addresses, one output: what SET::NUP214 actually does to the menin-interface hypothesis, and why it is a weaker test than CALM-AF10 | Explainer | 3 | 3/5 |
| Three archives, one answer: SUV39H1 has no ENCODE target record under any label (three routes, all empty), ChIP-Atlas's entire hg38 SUV39H1 holding IS the four GSE139196 MCF-7 samples re-indexed, and KMT2A is not among the 26 genes ChIP-Atlas calls SUV39H1 targets | Analysis | 3 | 4/5 |
| Three blots and one drug curve: does the ZMYND11::MBTD1 fusion protein still bind KMT2A, and does a menin inhibitor work in a leukaemia with no KMT2A rearrangement | Experiment | 3 | 1/5 |
| Three CXXC-pathway activities converge on rDNA - KDM2B represses Pol I, KMT2A and SETD1A bind the whole locus, MLL-AF4 is predominantly nucleolar - and no paper contains two of them | Analysis | 6 | 3/5 |
| Three extra tubes: the glucose study that answers the inversion in children | Experiment | 5 | 3/5 |
| Three hours after the fusion is degraded to 2.5-7.1% of its own sites, NOT ONE of the eight complex components profiled beside it falls below 68% retention genome-wide - menin 80.0%, DOT1L 68.7%, CDK9 83.6%, AFF4 92.7%, RNA Pol II 99.6%, pS2 98.3%, pS5 86.8% - so nothing in the complex is held on chromatin by the fusion at genome scale | Analysis | 2 | 3/5 |
| Three measurements the export axis needs and nobody has published: XPO1 occupancy in KMT2A-r, H3K79 under an XPO1 inhibitor, and CRM1 occupancy under a menin inhibitor | Analysis | 4 | 4/5 |
| Three of eight CUT&RUN libraries are too shallow for a zero to mean anything — measured, not assumed | Explainer | 2 | 4/5 |
| Three of menin's nine declined partners are E3 ligase substrate receptors - either menin turnover is ubiquitin-controlled, or substrate receptors are this beat's artefact signature | Hypothesis | 3 | 1/5 |
| Three of seventeen KMT2A-GERMLINE infant ALL cases are IRX1-high, one at 10.37 - so a high IRX1 in an infant leukaemia is not by itself evidence of anything fusion-related | Analysis | 1 | 3/5 |
| Three of the four AFF scaffolds have a named human Mendelian syndrome and the index fusion's partner has none — a 0/4 that is a fact about AFF1 and not about how hard anyone has looked | Analysis | 6 | 3/5 |
| Three pairs of twins who both got leukaemia: the patients who proved the fusion happens before birth | Patient story | 1 | 5/5 |
| Three quarters of KMT2A::AFF1's top partners are shared with other MLL fusions — and the two analyses that said otherwise were both artifacts of how the source table was built | Analysis | 3 | 3/5 |
| Three recurrent breakpoints give three junction peptides - and the one nobody uses needs no missed cleavage at all | Analysis | 2 | 0/5 |
| Three routes to one observation: the CUT&RUN panel that says whether menin eviction, H3K36me3 loss or MLL loss takes LEDGF off the fusion's genes | Experiment | 4 | 1/5 |
| Three unnamed things at once: the DOT1L-PRC1.1 deposition names the fusion, the cell types and both inhibitors with concentrations | Analysis | 3 | 5/5 |
| TIFAB — a 161-residue NF-kB adaptor-layer protein with TWO direct KMT2A-fusion papers, which is more disease-specific evidence than any receptor or TRAF in this beat has | Protein | 6 | 3/5 |
| Tile chr5:2,750,677-2,752,892 at 100 bp from the GSE252378 bigWigs and ask which TSS the p454 signal sits on | Experiment | 2 | 3/5 |
| Titrate PRC1.1 capacity against menin-inhibitor response, and measure H2AK119ub on the same timecourse as H3K79me2 | Experiment | 4 | 3/5 |
| TMPRSS13 (MSPL) - a cell-surface serine protease fused in frame to KMT2A exon 20, the clearest NOT-APPLICABLE epigenetics call of the seven, and a symbol whose approved form has a third of its alias's recall | Gene | 13 | 3/5 |
| TNF — the only NF-kB-activating ligand with real KMT2A::AFF1 B-ALL evidence, and the evidence says the blasts are RESISTANT to it | Protein | 7 | 4/5 |
| TOP1 domain architecture (UniProt P11387) | Protein | 1 | 5/5 |
| TOP2A - the proliferation isoform, the one the drugs are actually measured against, and the only one with a germline association in this disease | Gene | 9 | 3/5 |
| TOP2B - the isoform most etoposide-induced KMT2A breaks depend on, resolved genetically and not resolvable pharmacologically | Gene | 14 | 4/5 |
| TOP3B (O95985) - the only human topoisomerase that works on RNA as well as DNA, delivered to the MYC promoter by an arginine mark, and it has poisons | Gene | 4 | 3/5 |
| TOPBP1 - a real KMT2A contact that no abstract-level query can see, because it is a control panel in a paper about a different protein | Gene | 9 | 2/5 |
| Topoisomerase II cleavage and TOP2 poisons as a source of KMT2A breaks | Mechanism | 5 | 3/5 |
| Total body irradiation and the age-four boundary - the best conditioning in childhood ALL has never been tested in the children who most need a transplant | Explainer | 6 | 4/5 |
| TP53 - named in 84 entries of this graph, absent from the index genome study of the disease, and four different things depending on when you look | Gene | 15 | 4/5 |
| TP53 inactivation and the apoptotic threshold — the drug still switches the program off, and the cell still does not die | Resistance | 4 | 3/5 |
| TP53BP1 (53BP1) - the end-protection factor that decides between the two repair routes, reachable only under the wrong symbol | Gene | 7 | 3/5 |
| TPR / Megator (P12270) - the nuclear-basket nucleoporin that builds heterochromatin exclusion zones, in the pan-MLL-fusion core | Gene | 3 | 2/5 |
| Track the sub-1% cooperating-lesion clones through menin inhibition, because nobody has measured what the drug selects for | Experiment | 3 | 1/5 |
| TRAF2 - a cytoplasmic NF-kB brake reported as an AFF4 two-hybrid hit, 97 partners in the screen that found it, and the live instance of the brief's own accession trap | Protein | 6 | 1/5 |
| Trans-splicing: healthy human cells make cancer-associated fusion transcripts without any chromosome rearrangement | Mechanism | 4 | 3/5 |
| Transcription factories and Pol II clusters - no KMT2A::AFF1 imaging, condensate evidence for SEC and MLL-ENL, and 3D-FISH that actively contradicts the factory story for t(4;11) | Mechanism | 7 | 3/5 |
| Transcription–replication conflict as the candidate reason KMT2A-rearranged cells need the Fanconi pathway — a chain with two measured links and three inferred ones | Mechanism | 12 | 1/5 |
| Treat a KMT2A::AFF1 patient-derived xenograft with an NG2-directed agent and read out the CD34+CD19-CD117+ fraction at nadir - does the reservoir the 2006 flow data predicts actually survive? | Experiment | 4 | 3/5 |
| Treating a subclonal lesion is selection pressure applied to the clone you did not aim at | Risk | 4 | 3/5 |
| Treating the five menin inhibitors as one drug, when a 2026 title says they are not | Risk | 4 | 2/5 |
| Treosulfan - a European conditioning standard for three decades that the FDA first approved in January 2025, for a diagnosis and an age that exclude the infant with KMT2A-rearranged ALL | Drug | 4 | 4/5 |
| TRIB3 / TRB3 (Q96RU7) - a pseudokinase that is the ISR's own brake, falls 3.1 log2 under either inhibitor, and has a published physical link to the MLL complex in the wrong tissue | Gene | 4 | 4/5 |
| TRIM27 - the E3 ligase inside PRC1.1 that USP7 spends its time undoing, and the worst UniProt localisation record this graph has audited | Protein | 9 | 3/5 |
| TRIM28 / KAP1 / TIF1beta (Q13263) - the KRAB-ZFP corepressor scaffold in the pan-MLL-fusion core, with the weakest index-fusion p-value but a leukaemic role in another fusion family | Gene | 3 | 2/5 |
| Trithorax against Polycomb at HOXA: the textbook antagonism, and the two ways this disease breaks it | Mechanism | 6 | 3/5 |
| TRK inhibitors: one drug, seventeen cancers, and a paediatric population that actually got dosed | Explainer | 3 | 4/5 |
| TRRAP — a 3,859-residue DotCom subunit that every cell needs and no KMT2A cell needs more | Protein | 6 | 3/5 |
| Turn menin off for a defined window, then back on: the missing experiment that would bound reversibility | Experiment | 6 | 3/5 |
| Twelve weeks of a menin inhibitor in diabetic mice: more beta cells, lower fasting glucose, and nobody looked for a tumour | Mechanism | 3 | 3/5 |
| Twenty-five of thirty-six analyses that measure this graph were computed against a graph that no longer exists, and seven stamp a date that never moves | Analysis | 2 | 3/5 |
| Twin concordance: near-total for infant KMT2A-rearranged leukaemia, about 5% for childhood ALL overall | Epidemiology | 6 | 4/5 |
| Two classes of KMT2A rearrangement keep the SET domain, and the graph says otherwise | Explainer | 4 | 4/5 |
| Two clones, two antibodies: a four-month-old with refractory KMT2A::AFF1 mixed-phenotype leukaemia treated with blinatumomab and gemtuzumab together | Patient story | 1 | 3/5 |
| Two cohorts, a hundred infants each, and opposite answers on which sex does worse | Explainer | 4 | 0/5 |
| Two constructs that would decide whether menin dependency is about the menin-binding motif or about HOXA level | Experiment | 2 | 1/5 |
| Two coupled traps in one conversion: pybigtools writes only the chromosomes the input actually touched, so a scaffold in your query set raises KeyError on one track and not another - and when the scaffolds were dropped to fix it, 71 of 59,892 anchors (0.12%) turned out to carry enough of the top signal to HALVE a control's numerator | Explainer | 2 | 4/5 |
| Two deposit defects in one beat, both invisible to the check in use: a genome-build verdict read from a file's declared extents names its CONTAINER, and the furthest coordinate carrying signal names its DATA - and a clause that cannot return the other answer has been reported as a passing check in four beats | Explainer | 2 | 4/5 |
| Two drugs, two spatial mechanisms on one mark: catalytic DOT1L inhibition de-concentrates H3K79me2 out of its peaks and into mid-occupancy chromatin, while menin-interface inhibition lowers the mark's share at the peaks AND at mid-occupancy, so its effect is relocation rather than a smaller version of the same change | Mechanism | 1 | 3/5 |
| Two entries record zero chemical matter against the CXXC-DNA interface. There is one: dimethyl fumarate, IC50 about 1 uM, and it is already an approved drug | Analysis | 2 | 3/5 |
| Two groups invoke LIN28B to explain the SAME epidemiological fact in OPPOSITE directions - and neither claim is the one this graph has been repeating | Explainer | 4 | 3/5 |
| Two hypotheses in this graph make the same prediction on every lesion that exists, and the experiment queued to test them picks the one arm where neither speaks | Analysis | 5 | 3/5 |
| Two inhibitors of the same DOT1L active site leave different residual H3K79me2 landscapes, and the difference sits at the KMT2A-fusion target loci - so 'how much H3K79me2 is left' is a compound-specific readout, not a generic measure of DOT1L inhibition | Hypothesis | 3 | 1/5 |
| Two instruments on the same cell line give opposite answers about DOT1L under a menin inhibitor: the depositors' own TSS-window table puts DOT1L at 0.6638 beside menin's 0.2513, and 2 kb genome-wide bins put it at 0.2219 beside menin's 0.1657 - and only the genome-wide instrument can see the 86% of the co-occupied set that is not at a TSS | Analysis | 1 | 4/5 |
| Two KMT2A-rearranged patients share oncoprotein-target promoters at a median Jaccard of 0.132 against an independence expectation of 0.069 - an enrichment of only 1.63x, with 5 of 351 pairs at or below chance | Analysis | 2 | 4/5 |
| Two measurement defects confirmed: a denominator summed over seven baits made the pan-fusion core look 7.5x cleaner than it is (corrected fold 1.06, p 0.91), and my own gap report counts as coverage in the join that measures the gap | Analysis | 2 | 4/5 |
| Two more independent cell types put the KMT2A exon-11 CTCF summit within 12 bp of the coordinate this graph carries: MCF-7 at chr11:118,488,689 (5 bp away) and SK-N-SH at chr11:118,488,682 (12 bp), both score-1000 optimal-IDR peaks - and in the same tracks the anchor ranks only 72.95th of 56,171 MCF-7 anchors, so it is an unambiguous anchor and an ordinary one | Non-coding | 3 | 4/5 |
| Two new contaminated tokens for the registry - p75 (12 of 27 hits are TNF receptor) and AF-10 (an IL-6-responsive B cell line) - and SEM firing a second time, in a different query, one cycle after being written down | Analysis | 3 | 4/5 |
| Two of seven interactome read-queue partners should not get a gene entry, and the reasons are a pseudokinase with no nuclear pool and a membrane-skeleton protein whose two leukaemia hits are a gene-name artefact | Analysis | 7 | 4/5 |
| Two of ten hand-typed genomic intervals in this beat were on the wrong chromosome or a megabase off, and neither produced an error - one would have published the exact opposite of the truth about PAX5 | Analysis | 1 | 5/5 |
| Two of the nineteen non-AFF1 samples are menin-inhibitor treated, so the specificity arm is effectively seventeen - and removing them does not rescue the core | Analysis | 2 | 4/5 |
| Two of the seventeen core promoter windows are shared with a neighbouring TSS - PBLD overlaps HNRNPH3 by 38.2% and CCP110 overlaps GDE1 by 7.8% | Analysis | 1 | 4/5 |
| Two of the three top new dependencies are myeloid identity, not KMT2A | Analysis | 1 | 3/5 |
| Two of three KMT2A::EPS15 infant ALL cases carry IRX1 at KMT2A::AFF1 magnitude, while the only KMT2A::EPS15 patient with occupancy data has no oncoprotein at IRX1 at all | Analysis | 2 | 2/5 |
| Two pools of one protein: the chromatin-bound XPO1 that matters here has never been separated biochemically from the soluble export machine | Mechanism | 6 | 3/5 |
| Two processing batches inside one GEO series: the FLAG and KDM2B tracks put 1.7-1.9% of their coverage in ENCODE blacklist regions and the BCOR, RING1B and input tracks put 14-46%, with a single 2 kb bin at chr2:98,666,000 carrying 18.1% of the BCOR SGC0946 track on its own | Analysis | 2 | 5/5 |
| Two published ways a fusion oncoprotein engages BAF - be a subunit, or recruit it with a disordered domain - and KMT2A has never been tested for either | Mechanism | 6 | 4/5 |
| Two quality checkers audited: one was skipping a quarter of its input, the other did not exist and failed its own defining case twice before it worked | Analysis | 3 | 0/5 |
| Two reasons XPO1 is a hard target: every cell needs it, and blocking it switches on a survival pathway | Risk | 5 | 4/5 |
| Two surfaces, two jobs: the AHD picks the scaffold and the YEATS pocket reads the histone — so a YEATS ligand cannot ask which of the three SEC-family complexes it is disabling | Mechanism | 4 | 3/5 |
| Two thirds of the curated interactome of this project's six core proteins is spoke-expanded - and the pairs this graph chose to write are significantly better than the ones it did not | Analysis | 6 | 4/5 |
| Two-thirds of the load-bearing evidence names no lineage, which is why this graph cannot audit its own commonest failure | Analysis | 1 | 3/5 |
| Two-thirds of this graph's core-complex interaction evidence comes from experiments where our protein was not the bait, and LEDGF has one bait-supported partner out of thirty-six | Analysis | 2 | 4/5 |
| Two-window deconvolution: at a typical shared promoter only 1.8% of the signal can be proved to belong to the gene it is filed under, and at IRX2's one near-positive it is 19.7% | Analysis | 2 | 3/5 |
| U-937 (CVCL_0007) - the single line carrying this graph's menin-independence argument, and it is adult, monocytic, historically contaminated, and exists as two variants nobody here distinguishes | Explainer | 2 | 3/5 |
| U2AF1 - the 3' splice-site recognition factor, a speckle protein whose BioID neighbourhood contains LEDGF | Gene | 3 | 2/5 |
| U4 was assumed, so I tested it: full text raises the low claim-to-paper overlap scores with a +0.108 median margin over same-field decoys (42% of the raw rise is document length), and every one of the seven pairs that stays low is a blind spot in my own instrument rather than a misattached citation | Analysis | 3 | 4/5 |
| UBAP2L (Q14157) - a BMI1-interacting protein essential for haematopoietic stem cell activity, in the pan-MLL-fusion core, and a stress-granule nucleator recovered from NUCLEAR lysate | Gene | 3 | 3/5 |
| UBE2A (RAD6A) — the E2 for H2B ubiquitination in one primary account, contradicted by another, and with no KMT2A literature at all | Protein | 5 | 3/5 |
| UBE2T — E2; rank 33 of 8,269 for KMT2A-selective dependency, and no KMT2A literature at all | Protein | 11 | 3/5 |
| UBN1 - the subunit that decides the HIRA complex is carrying H3.3 and not H3.1, by reading a single glycine | Gene | 5 | 3/5 |
| UBTF tandem duplications INVENT an export signal, and that invented signal is what puts the protein on chromatin - the cleanest proof the XPO1 address is real | Mechanism | 2 | 3/5 |
| UNC0642 - the G9a/GLP chemical probe that abolished doxorubicin-induced Kmt2a copy gain in mice, and the one intervention in this beat that has been given to an animal | Drug | 6 | 3/5 |
| Under all three DOT1L inhibitors, DOT1L's fold-enrichment at canonical target loci is HIGHER than DMSO (PBX3 4.85 to 13.92, SENP6 3.37 to 9.68) - either catalytically dead DOT1L is retained or trapped on chromatin, or the reading is an artefact of a 1.35-fold spread in MACS fragment-size estimates, and this deposit cannot tell which | Hypothesis | 3 | 1/5 |
| Under EPZ5676 the canonical KMT2A-fusion targets look like they lose H3K79me2 far more than the genome (p=0.017 and p=0.0004), and against a baseline-matched null the entire effect vanishes (p=0.34 and p=0.22) - eight of the ten are simply top-decile genes | Analysis | 3 | 3/5 |
| Under revumenib the oncoprotein leaves chromatin globally, so 'does IRX1 become a menin-inhibitor escape route' cannot be answered from this deposit | Analysis | 2 | 3/5 |
| Under VTP-50469 in RS4;11, the 209 bins that rise to the top of the MENIN distribution are 3.7-fold CpG-island-enriched over a class-matched null at p = 5.2e-07, while the MLL1-N gained set is not enriched at all - so menin's residue is island-biased and an MLL1-N gain is not | Analysis | 2 | 3/5 |
| UniProt's menin 214-390 FANCD2 region is not a surface: it spans three spatial lobes and 29.9% of menin's solvent-accessible area, so its twenty-residue overlap with the gamma-H2A.X motif is what chance gives you | Analysis | 3 | 4/5 |
| UROS: searched and empty — the scan's rank-15 hit has no leukemia literature, and no entry was written | Analysis | 4 | 3/5 |
| Use centrifugal elutriation, not a chemical block: the one separation method demonstrated to work in KMT2A-rearranged cells, applied to both the cell-cycle question and the small-persister question | Experiment | 2 | 1/5 |
| USP1 does not behave like part of the Fanconi module, and does not track ID1 either | Analysis | 3 | 0/5 |
| USP1: an inhibitor, activity in B-ALL, and zero papers in the disease we care about | Target | 3 | 0/5 |
| USP2 (ubiquitin carboxyl-terminal hydrolase 2) - the ninth commonest KMT2A partner and the only one that is a deubiquitinase | Protein | 8 | 3/5 |
| USP22 — a KMT2A-rearranged dependency that works through MEIS1 protein stability, and is not an interactor of the fusion | Protein | 7 | 3/5 |
| USP7 - the enzyme that holds PRC1.1 together, and the only pharmacological handle on this complex that exists today | Protein | 10 | 3/5 |
| USP8 (UBPY) - the second deubiquitinase KMT2A partner, three patients, same UCH logic | Protein | 9 | 3/5 |
| UTP14A (Q9BVJ6) - an SSU processome component that binds and destabilises p53, in four MLL-fusion interactomes but NOT the index fusion's and below the screen threshold | Gene | 4 | 2/5 |
| UTP18 / WDR50 (Q9Y5J1) - the SSU processome subunit that recruits the exosome helicase MTREX to rRNA fragments; in three MLL-fusion interactomes but not the index fusion's, and separately the subject of a 21-year-old IntAct curation error in this graph | Gene | 5 | 2/5 |
| UTP18 is not a KMT2A partner - it is WDR5, mis-curated into IntAct from the founding paper, and it manufactured the only KMT2A-bait gap in the interactome recount | Analysis | 6 | 4/5 |
| V(D)J recombination: the immune system deliberately cuts its own chromosomes, using a domesticated transposon | Mechanism | 6 | 5/5 |
| Valemetostat - an approved dual EZH1/EZH2 inhibitor that has already worked in an MLL-AF4 xenograft, in a disease nobody has enrolled it in | Drug | 6 | 3/5 |
| Validating the wrong-paper year check against this project's own recorded identifier errors - 16 of 23 would have been flagged, 7 would have passed silently on a shared year, and the figure is biased optimistic because every pair in the set is an error somebody caught | Analysis | 1 | 3/5 |
| VCAM1 - the stromal counter-receptor for VLA-4, and in MLL-fusion AML its UPREGULATION is anti-leukaemic, which is the opposite of the expected sign | Gene | 4 | 3/5 |
| Venetoclax in KMT2A-rearranged leukemia — the apoptotic partner every other drug needs | Drug | 6 | 3/5 |
| Verdict on the WRAD contradiction: the graph is right, its citation class is wrong, and its universal is wrong | Explainer | 5 | 4/5 |
| Verdict: 'eleven cell lines, none infant-derived' is right about the screen and wrong about the material — at least ten infant KMT2A::AFF1 lines exist | Analysis | 4 | 4/5 |
| Verdict: q147's IRX1 headline survives as a measurement and not as an inference - the pre-registered branch is NEITHER, on U5 and on a FALLS condition that fired | Analysis | 3 | 4/5 |
| Verified against the live records rather than inherited: HUDEP-2 and mESC each carry a DMSO and an SGC0946 H3K79me2 sample and no VTP-50469 sample, so K562 remains the only fusion-free line in GSE260742 able to score a menin-inhibitor effect - and cycle 82's request for a second and third fusion-free line cannot be met from this series | Analysis | 1 | 4/5 |
| VIM / vimentin (P08670) - a pan-MLL-fusion prey with a clean negative control, and separately a genuine KMT2A rearrangement partner in sarcoma, which are two different facts | Gene | 3 | 2/5 |
| VIM::KMT2A - the one KMT2A rearrangement that keeps the SET domain and still throws away the menin-binding exon | Fusion | 6 | 4/5 |
| Vimentin domain coordinates (P08670) - so the VIM::KMT2A breakpoint can actually be drawn | Protein | 2 | 5/5 |
| Vincristine - measured to be no different in KMT2A-rearranged disease, and measured to be UNDERDOSED in infants by the very rule meant to protect them | Drug | 5 | 4/5 |
| Volasertib against PLK1: a differential window claimed in infant-type cells, on a target every dividing cell needs | Target | 1 | 0/5 |
| Vorinostat (SAHA) - the only HDAC inhibitor given to newly diagnosed infants with ALL, in a 50-patient trial whose endpoint was tolerability and which reported four treatment-related deaths, all infectious | Drug | 4 | 4/5 |
| VTP-50469 - the preclinical menin-KMT2A interface inhibitor that almost every chromatin experiment in this field actually used, and which had no entry of its own in this graph | Drug | 3 | 4/5 |
| WAC — the adaptor that hands RNF20/RNF40 to RNA polymerase II, and the only member of this axis whose knockdown alone killed MLL-rearranged ALL cells | Protein | 9 | 4/5 |
| WBC 300, age 6 months, MRD 0.01%: three lines drawn by committees, not by biology | Explainer | 7 | 4/5 |
| WBC 300: a stratification convenience, not a biological threshold - and the evidence says so four different ways | Explainer | 8 | 4/5 |
| WBP11 (Q9Y2W2) - a splicing activator in the pan-MLL-fusion core, isolated from its own partners, and a human haploinsufficiency gene | Gene | 4 | 3/5 |
| WDR18 (Q9BV38) - the Rix1/PELP1-TEX10-WDR18 60S maturation subunit, in five MLL-fusion interactomes but NOT the index fusion's, and the block's only member whose nucleolar partitioning is SUMO-controlled | Gene | 5 | 2/5 |
| WDR33 (Q9C0J8) - the subunit that reads AAUAAA, in the pan-MLL-fusion core, and the plant homolog of which physically links 3' processing to H3K4 demethylation | Gene | 5 | 3/5 |
| WDR5 — the partner that is not a partner: it binds the half of KMT2A the fusion throws away | Protein | 11 | 4/5 |
| WDR5 and KMT2A are at the centrosome and the midbody - a non-chromatin address for both, with a patient-cell phenotype | Mechanism | 5 | 3/5 |
| WDR5 and RBBP5: the second arm of the WRAD hub, RBBP5 V375-D376-V377 into the same propeller face, co-crystallised with the MLL1 WIN peptide in one structure | Interface | 7 | 4/5 |
| WDR5 is partitioned, not shared: NSL and SET1/MLL complexes compete for one pool, so perturbing NSL changes how much WDR5 reaches the wild-type KMT2A complex the fusion depends on | Hypothesis | 7 | 1/5 |
| WDR5 maintains a differentiation block — in CEBPA p30 AML, not in KMT2A-rearranged disease, and a title check nearly buried it | Mechanism | 3 | 4/5 |
| WDR5 WIN site and KMT2A Arg3765: measured at 1.7 uM, three co-crystals, and absent from every leukaemic fusion - plus the MLL3 peptide that binds it 51-fold tighter | Interface | 5 | 5/5 |
| WDR5: an established wild-type KMT2A contact, and no fusion contact ever measured | Explainer | 9 | 4/5 |
| We have read a tenth of the recent field, and the gap found a real interactor | Analysis | 4 | 0/5 |
| WEE1 - the one checkpoint target with a KMT2A::AFF1-specific result, and the paper that also found the escape route | Gene | 6 | 3/5 |
| Weight or surface area - the Interfant-06 conditioning week uses both units in eight days, and the one measured correction in the literature went the wrong way | Explainer | 4 | 3/5 |
| What 160 infants a year actually permits: the sample-size arithmetic | Analysis | 4 | 3/5 |
| What a curated interaction row actually claims: spoke expansion, and the ladder from 'was in the same tube' to 'touches' | Explainer | 4 | 5/5 |
| What a menin inhibitor costs: the list price, worked out for an infant | Explainer | 3 | 4/5 |
| What a transplant costs: about $276,000 for the admission alone | Explainer | 2 | 4/5 |
| What an immunophenotype can and cannot tell you about a genotype - the arithmetic of a surrogate marker, worked on NG2 | Explainer | 7 | 4/5 |
| What could refute the menin-interface bet, restated after the provenance audit: three tests, none of which is about menin binding | Hypothesis | 5 | 1/5 |
| What fills the space: RING1B and BCOR arrive at the fusion's sites under BOTH drugs, but the DOT1L inhibitor puts them everywhere on the fusion's territory while the menin inhibitor puts them only in the quartile where the fusion is most completely evicted - and at Meis1 RING1B rises 16-fold | Analysis | 3 | 3/5 |
| What fraction of fusion-positive newborns ever get leukaemia? For ETV6::RUNX1, very few. For KMT2A, nobody knows, and the biology says the answer may be most of them | Epidemiology | 6 | 3/5 |
| What is a fusion gene? | Explainer | 3 | 5/5 |
| What is actually conserved across KMT2A partner classes — forced self-association, with two documented exceptions that break the rule | Mechanism | 6 | 4/5 |
| What is left after the missing arm was read: there is no H3K9me1, me2 or me3 measurement at the KMT2A breakpoint region in ANY haematopoietic cell, and the founding paper's own archive contains none because all 60 of its samples are epithelial | Analysis | 2 | 4/5 |
| What is left of the resection absence after the compute was done: the resting state is now MEASURED and negative in 13 ENCODE datasets, so the whole question collapses onto the DAMAGE state, which is never-measured for all six proteins in every cell type on Earth | Analysis | 2 | 4/5 |
| What is lost: the PHD3/CYP33 switch that lets wild-type KMT2A turn itself off | Mechanism | 5 | 4/5 |
| What it costs to treat a child through frontline leukemia therapy | Explainer | 3 | 3/5 |
| What LEDGF actually does for the fusion: it brings AF4, CDK9, BRD4, P-TEFb and Ser2P Pol II to the target gene, and H4K16ac with them | Mechanism | 3 | 3/5 |
| What maps a DNA break, and the fact that none of the modern instruments has ever been pointed at KMT2A in a blood progenitor | Analysis | 4 | 3/5 |
| What MRD-negative actually means: a quantitative range, a laboratory judgement, and three incompatible definitions | Explainer | 8 | 4/5 |
| What the CTCF-protects paper actually cites: it names Gothe and Atkin in ONE direction-free sentence and declares the direction unresolved, and the two papers that ran the reciprocal experiment are absent from all 81 of its references | Analysis | 9 | 4/5 |
| What the labels measure in a treated child: bone growth, in one sentence, and nothing else endocrine | Explainer | 2 | 5/5 |
| What the paralogues' disease biology says about AFF1: the AFF family shares one SIAH degron — and the index fusion DISCARDS it, because the whole degron lies in the AFF1 leader that the junction at residue 347 throws away | Mechanism | 5 | 3/5 |
| What the Polycomb beat searched, what it counted as absent, what it read and rejected, and the two absences it got wrong before hand-back | Analysis | 4 | 4/5 |
| What the reciprocal product assembles: P-TEFb, an H3K4 methyltransferase, an H3K79 methyltransferase, an arginine methyltransferase and an acetyltransferase | Mechanism | 4 | 3/5 |
| What the treated brain looks like later: neurocognitive late effects after CNS-directed therapy in infancy | Explainer | 5 | 3/5 |
| What this beat looked at and did not write: rejected candidates, with counts for both halves of every search | Analysis | 2 | 4/5 |
| What this beat read and did not use: bounded absences, bounded rejections and one bounded unreadable | Analysis | 4 | 3/5 |
| What this beat searched, read and set aside - including one cell line the accession database has not caught up with, and one query that returns a clean zero | Analysis | 8 | 4/5 |
| What this beat searched, what it rejected, and the two papers it could not read - after a fifth route rescued the third | Analysis | 5 | 3/5 |
| What was searched for a structure and what came back empty: the KMT2A interface layer enumerated by accession pair, with the graph's own unmapped interfaces listed | Analysis | 5 | 4/5 |
| What was searched, what came back empty, and what was read and not used - the P-TEFb reservoir beat's audit trail | Analysis | 6 | 4/5 |
| When a 2 kb promoter call fires at a window shared with another gene, the neighbour fires too 91.3% of the time - against 4.3% for random promoter pairs | Analysis | 2 | 3/5 |
| When a deposit has no recoverable spike-in, two comparisons still work and one does not: a within-sample rank and a within-sample share both cancel the unknown scale factor, a fold change does not - and the share is the one that also has no ceiling | Explainer | 2 | 5/5 |
| When a family shares a complex, the result is family-selective, not member-selective - the protein version of this graph's inhibitor-class rule | Explainer | 7 | 4/5 |
| When a paper will not say what it was done in, ask its data: resolving an unstated experimental system from GEO | Explainer | 4 | 5/5 |
| When infant leukaemia comes back, it comes back early and while treatment is still running | Explainer | 6 | 4/5 |
| When MYC falls after a menin inhibitor, there are three mechanisms it could be, and no published experiment separates them | Mechanism | 5 | 3/5 |
| When one infant's KMT2A::AFF1 B-ALL became an AML, EBF1 lost fusion occupancy and PAX5 kept it - the B-lineage transcription-factor programme is not vacated as a block | Analysis | 2 | 3/5 |
| When one thing goes wrong, do several? In infant KMT2A-rearranged leukaemia the answer is no, and that cuts against the intuition | Explainer | 3 | 4/5 |
| Where does the fusion go when menin inhibition evicts it? Almost nobody has looked - the published readouts are chromatin occupancy, the one protein whose fate was measured properly is menin, and the single human observation of fusion loss is confounded by a lineage switch | Mechanism | 6 | 3/5 |
| Where else in a child is the target switched on? (run) | Analysis | 2 | 4/5 |
| Where else in the body each target is expressed, and the two controls that say the method works | Analysis | 2 | 0/5 |
| Where KMT2A and its fusions sit inside the nucleus — SNL1/SNL2, nuclear speckles and the condensate question | Mechanism | 9 | 3/5 |
| Where KMT2A-rearranged leukemia physically sits — marrow niche, CNS, blood, liver/spleen and skin | Mechanism | 12 | 4/5 |
| Where KMT2A::MLLT1 actually sits: chromatin occupancy is mapped, subnuclear localisation of the endogenous fusion has never been imaged | Mechanism | 8 | 3/5 |
| Where KMT2A::MLLT3 sits in the nucleus: two papers, both overexpression, both from before 2005 - and the fusion carries no AF9 import signal | Mechanism | 5 | 3/5 |
| Where LEDGF/p75 actually is: bound to chromatin through mitosis, in the nuclear interior with H3K36me3 - and never once imaged in a KMT2A-rearranged cell | Mechanism | 5 | 3/5 |
| Where RPA actually is: nucleoplasmic and diffuse until there is single-stranded DNA, then punctate prereplication foci at the G1/S border, damage-induced foci with RAD51, and a PML-body pool - and the subunits differ in how well any of this is measured | Mechanism | 6 | 4/5 |
| Where SET::NUP214 actually is: mobile intranuclear bodies that trap CRM1, dissolve in mitosis and under CRM1 inhibitor, and reassemble on washout | Mechanism | 5 | 4/5 |
| Where t(9;11) actually breaks inside MLLT3: 98.4% downstream of exon 4, and the two patients in 442 who kept the reader | Breakpoint | 4 | 4/5 |
| Where the break falls, and the three incompatible numbering frames that make it easy to get wrong | Breakpoint | 4 | 4/5 |
| Where wild-type PICALM actually is: coated pits, the Golgi, coated vesicles - and a nuclear pool nobody has explained | Mechanism | 4 | 4/5 |
| Which immune-evasion routes are actually documented in KMT2A-rearranged disease, and which are borrowed from AML and assumed - a ranked ledger with the bounded absences that define it | Analysis | 10 | 3/5 |
| Which KMT2A exon carries which interface: exon 1 is the menin-binding motif, exons 5-6 are the CXXC zinc finger (computed, not recalled) | Analysis | 3 | 5/5 |
| Which leukemia co-dependencies survive uncertainty? (run, with p-values) | Analysis | 1 | 3/5 |
| Which marker moves first? A re-analysis of flow files that already exist, to put an order on lineage switch | Experiment | 5 | 1/5 |
| Which MRD timepoint drives which decision in infant ALL, and how good the evidence for each is | Explainer | 6 | 4/5 |
| Which of our phospho-sites are actually seen in patients | Analysis | 4 | 0/5 |
| Which partner, in which patient: KMT2A partner frequencies across six age-lineage strata | Breakpoint | 10 | 4/5 |
| Which repair pathway glues the fusion together: classical NHEJ vs alternative end joining | Mechanism | 4 | 3/5 |
| Which step is rate-limiting, and what compensates when you block it — the bite-back map for the causal chain | Mechanism | 11 | 4/5 |
| Who gets transplanted in infant KMT2A-rearranged ALL, and whether it helps - four criteria, and a literature that points both ways | Explainer | 6 | 3/5 |
| Who holds the data and samples we cannot generate ourselves — an access map | Group | 4 | 3/5 |
| Who the 460 KMT2A::MLLT1 patients actually are: 88% lymphoblastic, 53% infants, and only 47 cases of AML in the whole series | Epidemiology | 3 | 4/5 |
| Why a nucleoporin fusion needs menin-MLL1: the second menin-dependent fusion family, and what it borrows rather than carries | Mechanism | 6 | 3/5 |
| Why BCR::ABL1 became treatable — and what KMT2A::AFF1 does not share with it | Explainer | 9 | 5/5 |
| Why endocrine tumours do not carry KRAS mutations: menin blocks the proliferative arm of RAS | Mechanism | 1 | 3/5 |
| Why KMT2A picks AFF1: spatial proximity, shared transcription hubs, and the unsettled proximity-versus-damage question | Mechanism | 4 | 3/5 |
| Why PML::RARA became curable — and what KMT2A::AFF1 does not share with it | Explainer | 8 | 4/5 |
| Why this one rare leukaemia was thought to decide an argument about a drug used in a commoner one - and why it decides less than the title says (corrected 2026-09-21) | Explainer | 3 | 3/5 |
| Wild-type AF10 is called nuclear on a construct and found in both fractions in tissue - and that disagreement decides whether CALM-AF10's cytoplasmic life is a gain or an inheritance | Mechanism | 4 | 2/5 |
| Wild-type KMT2A is one of the most promiscuously labelled proteins in the proximity record - 25 of 50 baits - and menin is one of the least, at 3 | Analysis | 3 | 3/5 |
| With H3K79me2 added, the eviction-depth panel over one set of 1,228 bins under one drug is H3K27me3 +1.000, H2AK119ub +1.000, H3K4me3 -1.000 and H3K79me2 -1.000 - a clean repressive-up / active-down split that no shared library, blacklist or regression artefact can produce | Analysis | 3 | 3/5 |
| With no eraser, how fast the histone itself is replaced decides how much H3K79 methylation there is - and that sets the clock a DOT1L drug has to beat | Mechanism | 6 | 3/5 |
| WITHDRAWN - "thirteen genuinely absent" was wrong: 14 of the 15 are adjudicated in corpus prose and the fifteenth is not an interactor. Superseded by ana-zero-of-fifteen-again-the-same-worklist-the-same-thirteen-and-the-third-recurrence | Analysis | 1 | 4/5 |
| WITHDRAWN: I identified the promoter-matrix column mean as library coverage and called A73051 depth-confounded; the column mean is the enrichment fraction, A73051 is at the 37th-39th percentile of true depth, and the share-versus-depth correlation is negative | Analysis | 2 | 2/5 |
| Within one arm, swapping the processing-marker confound for a submission-batch confound takes the same-condition H2AK119ub floor from 37.04% to 16.84% at D1 (tighter, 0.45x) and from 37.37% to 61.89% at the TOP 0.1% stratum (worse, 1.66x). The brief's question - tighter, wider, or unchanged - has no single answer, and it is worse exactly where this thread scores its claims. | Analysis | 1 | 3/5 |
| Working the queue deferred for four cycles: the 40 are three different things, and one absence claim the graph had already refuted ten entries away | Analysis | 2 | 0/5 |
| WRAD reaches KMT2A fusions only as a passenger on a recruited wild-type complex | Hypothesis | 7 | 1/5 |
| WT1 - Wilms tumour 1, leukaemia antigen and MRD marker, and the widest-margin promoter in the Q152 AFF1-only core | Gene | 3 | 3/5 |
| WTAP — an oncogenic m6A writer subunit in AML with ZERO records against MLL or KMT2A over six aliases | Gene | 4 | 3/5 |
| XPO1 / exportin-1 (CRM1) - the cell's main nuclear export receptor, and a chromatin-bound transcriptional scaffold | Gene | 12 | 4/5 |
| XPO1 E571K: a change-of-function hot spot in the NES-binding groove - and it does NOT confer resistance to the drugs that bind the same groove | Mechanism | 5 | 4/5 |
| XPO1 mRNA goes UP when you inhibit the protein - the pharmacodynamic marker that made the paediatric trial interpretable, and what it cannot tell you | Mechanism | 3 | 4/5 |
| XPO1 mutation in acute leukaemia, counted with denominators and a positive control: 1 of 739 B-ALL, 0 of 584 paediatric AML, 0 of 1,103 adult AML | Analysis | 2 | 4/5 |
| YAP1 (P46937) - the Hippo pathway's transcriptional co-activator, and a KMT2A fusion partner from a completely different functional class | Gene | 10 | 4/5 |
| YAP1::KMT2A::YAP1 (YKY) - an insertional KMT2A rearrangement that keeps the CXXC zinc finger and throws the menin-binding exon away | Fusion | 6 | 4/5 |
| You can lower LEDGF without a LEDGF ligand: its protein half-life is about 4 hours against a proteome average of 20, so blocking guanine nucleotide or rRNA synthesis takes it out first | Mechanism | 3 | 4/5 |
| YTHDC1 — the nuclear m6A reader in the MLL-METTL3-CTCF axis, with an inhibitor, and no dependency signal in KMT2A-rearranged lines | Gene | 6 | 3/5 |
| YTHDF2 — the cytoplasmic m6A reader that selectively compromises AML cancer stem cells, discordant across the lineage split here | Gene | 4 | 3/5 |
| YWHAG / 14-3-3 gamma (P61981) - the only cross-laboratory reproduced KMT2A proximity partner in the curated record, and UniProt places it nowhere near the nucleus | Gene | 6 | 2/5 |
| YY1 - the enhancer-promoter looping factor that recovers KMT2A in a 109-transcription-factor BioID screen | Gene | 4 | 2/5 |
| ZC3H13 — the m6A writer subunit with the most evenly KMT2A-selective dependency signal in the panel, and almost no literature | Gene | 4 | 2/5 |
| ZC3H18 (Q86VM9) - the CBC-to-exosome bridge in the pan-MLL-fusion core, and the ONLY member of this tranche whose own complex came with it | Gene | 3 | 3/5 |
| ZC3H8 / Fliz1 - the last little-elongation-complex subunit without an entry, discovered in fetal liver haematopoietic progenitors, and a selective BioID2 bait that reaches KMT2A in K562 | Gene | 10 | 2/5 |
| ZEB2 — an EMT transcription factor that turns out to be a leukemia dependency and a guardian of lineage fidelity | Protein | 9 | 3/5 |
| ZEB2 level sets how easily a KMT2A-rearranged blast can change lineage under CD19-directed pressure | Hypothesis | 2 | 1/5 |
| Zero of eight unwritten AFF4/MEN1 partners has an experimentally coded nuclear localisation, and the two that are called nuclear are called it by inference | Analysis | 3 | 3/5 |
| Zero of fifteen, again: the same worklist, the same wrong intermediate answer of thirteen, and the third recurrence of a gap list that cannot see a decision | Analysis | 1 | 4/5 |
| ZFP64 — rank 4 on selectivity, and there is not even a ChEMBL entry for it | Protein | 5 | 3/5 |
| Ziftomenib (KO-539, Komzifti) — once-daily menin inhibitor approved in NPM1-mutant AML | Drug | 4 | 4/5 |
| ZMYND11 (BS69) - an H3.3K36me3 reader that restrains elongation, is itself the 5' partner of a chromatin-hijacking AML fusion driving HOXA/MEIS1/MYB, and whose promoter is the third-strongest MLL1-N bin in RS4;11 | Gene | 9 | 4/5 |
| ZMYND11::MBTD1 AML is menin-inhibitor sensitive despite having no KMT2A rearrangement, because the translocation deletes ZMYND11's MYND domain and with it a physical brake on wild-type KMT2A | Hypothesis | 4 | 1/5 |
| ZMYND11::MBTD1 is the KMT2A-fusion architecture assembled from different parts - and the part it throws away is a direct physical brake on KMT2A itself | Analogy | 9 | 3/5 |
| ZMYND11::MBTD1, t(10;17)(p15;q21) - a chromatin reader welded to the NuA4/TIP60 acetyltransferase, maintaining Hoxa/Meis1/Myb/Myc/Sox4 in AML: the KMT2A-fusion architecture built from different parts | Fusion | 11 | 4/5 |
| ZNF362 - the paralogue that makes the same leukaemia with the same partners, and that explains the six-zinc-finger convention | Gene | 3 | 3/5 |
| ZNF384 - a C2H2 transcription factor that is the invariant 3' half of a whole B-ALL fusion subtype, including AKAP8::ZNF384 | Gene | 3 | 3/5 |
| ZNF384 fusions make lineage-ambiguous leukaemia by acting in a haematopoietic stem cell - and the founding lesion is in the HSC itself, unlike Ph-like B-ALL | Mechanism | 3 | 4/5 |
| ZNF384::TEX41 - the case that breaks the family's architecture: ZNF384 is the 5' partner, the 3' partner is a lncRNA, and the fusion is out of frame | Fusion | 3 | 3/5 |
| ZNF512 (Q96ME7) - the one protein of the nine deferred pan-MLL-fusion preys that is a sequence-specific chromatin factor, and it initiates pericentric heterochromatin | Gene | 3 | 2/5 |
| Zoledronic acid against the osteoclast: a bone-marrow-niche target, but not tested in infant KMT2A-rearranged disease | Target | 3 | 3/5 |
| ZRANB2 - the only bait in any published proximity experiment that reaches AFF1, AFF4, ELL, MLLT1, CCNT1, KMT2A and DOT1L at once | Gene | 5 | 2/5 |