Oncofusion

start / graph / absence-no-menin-inhibitor-occupancy-dataset-in-an-infant-derived-kmt2a-aff1-line

Analysismoderate confidence 3 of 5: One strong study, or several smaller consistent ones.Q83-fusion-fate

Bounded absence: every chromatin measurement under a menin inhibitor is in an adult-derived line, and none is in an infant KMT2A::AFF1 model

also called no infant line under the drug · SEM has never been profiled under a menin inhibitor

The drug is being given to babies with a specific leukaemia. Every experiment that maps what the drug does to DNA-bound proteins was done in cells taken from adults, and mostly from a different kind of leukaemia. The standard infant cell line has never been used for this.

The same thing, for a scientist

Enumerating the cell systems in all eight occupancy datasets under a pharmacological menin inhibitor [E1]: **MOLM13** (adult AML, KMT2A::MLLT3), **RS4;11** (adult B-ALL, KMT2A::AFF1), **ML2** (adult AML, KMT2A::AFDN), **MV4;11** (adult AML/biphenotypic, KMT2A::AFF1), **OCI-AML3** (adult, NPM1c), **MOLM-13/MV4-11** again in a preprint, murine **MLL-AF9** leukaemia, and one adult patient sample undergoing lineage switch. **NARROWED AGAIN 2026-09-24 (cycle 121), and this is the sharper correction. THE INFANT EXPERIMENT EXISTS.** GSE252378 contains **menin CUT&RUN in two primary infant lineage-switching patient samples under a menin inhibitor** — `148752` (infant B-ALL) and `152985` (infant AML) — alongside KMT2A-N1/N2/C1/C2, ENL and DOT1L, two replicates each [E9]. **This entry's central enumeration claimed every occupancy dataset under a menin inhibitor is adult-derived. That is false: this is a ninth dataset, it is infant, and this corpus has cited it the whole time.** **The entry's conclusion survives only because both patients are `KMT2A-ENL`, not the index fusion** — which is luck rather than rigour, and the enumeration method should be weighted accordingly. The useful restatement is no longer *nobody has measured menin occupancy under drug in infant material*; it is **the experiment runs, in infants, with a validated menin antibody, and has not been pointed at KMT2A::AFF1.** The same deposit holds ~25 **untreated** KMT2A::AFF1 libraries (p279, p318, p454, SEM), so the index fusion without the drug and the drug without the index fusion sit in one deposit and are never crossed. See `ana-the-infant-menin-inhibitor-occupancy-experiment-exists-and-it-is-kmt2a-enl-not-aff1`. **PARTIALLY REFUTED 2026-09-23 (cycle 120). The sentence that stood here - that SEM *"appears in the menin-inhibitor literature only as a viability and synergy system, never as a chromatin-profiling system under drug"* - is false.** GSE159608 contains SEM Auto-CUT&Tag with H3K4me3 arms labelled DMSO, EPZ-5676 and **VTP-50469** (**VTP GSM5139713/GSM5139714**, against **DMSO GSM5139709/GSM5139710** and an **EPZ-5676 arm GSM5139711/GSM5139712**), plus H3K27ac, H4K16ac, RNAP2-S5p, IgG and **menin** channels in the same line [E7]. *(Accessions corrected 2026-09-24: the originals here were shifted by one by the same parser bug.)* SEM has been chromatin-profiled under a menin inhibitor. **The narrower claim in this entry's title survives, and it is the load-bearing one.** The SEM **menin** CUT&Tag samples (**GSM5139719/GSM5139720**) are **DMSO only** - there is no menin arm under drug in this line. So *menin occupancy under a menin inhibitor in an infant-derived KMT2A::AFF1 line* remains unmeasured, which is the comparison this beat needs; what is now known to exist is the H3K4me3 readout under drug, not the occupancy readout. **CORRECTED 2026-09-24: the second bound asserted here was my own error and is withdrawn.** This paragraph previously said GSE159608 contradicts its own metadata at 46 of 119 antibody and 9 of 18 treatment assignments, and concluded that *which SEM sample is the VTP arm cannot be settled from the metadata*. **GSE159608 has ZERO such contradictions.** The apparent lag was an off-by-one in the coordinator's parser — GEO's brief format emits `!Sample_title` before `!Sample_geo_accession`, so every sample was compared against the **next** sample's title [E8]. **The SEM `DMSO` / `EPZ-5676` / `VTP-50469` arm labels can be taken at face value**, and the refutation above is therefore *not* bounded to *the dataset exists*: the arms are identified. KOPN-8, HB11;19, PER-490 and the other infant-derived models in this graph's own inventory appear nowhere. **Why this is a real gap and not a pedantic one.** The uCpG address the whole relocation question is about was measured in SEM: 20% fusion occupancy against 50% CFP1 and 89% KDM2B [E2]. The occupancy response to the drug was measured in different cells with different methylomes, different lineages and, in two of four, a different fusion partner. The two halves of the argument this beat is about have never been in the same cell. **And infant KMT2A::AFF1 leukaemia is the population the drug class is being taken into**, with infants under one year a stated development priority. **Query bounding.** `SEM[tiab]` against the 21-term menin-inhibitor name list returns **0** - but that zero is uninformative, because SEM is a hopeless free-text token (standard error of the mean; scanning electron microscopy; structural equation modelling). The bound that carries information is the **enumeration**: I read the systems out of the methods and figure legends of the five full texts and the abstracts of the remaining three, and no infant-derived line is used for chromatin profiling under drug in any of them. That is a bound on eight datasets, not on the literature.

Go deeper
What would have to differ for this to matter

Four things differ between SEM and the profiled lines, and each is mechanistically load-bearing for this beat:

  1. The methylome. The available unmethylated CpG substrate is the denominator of the relocation question, and infant KMT2A-rearranged leukaemia has a distinctive, hypomethylated profile. A relocation that is possible in one methylome may be impossible in another.
  2. The partner. MLLT3 and AFDN bring different cofactors; only AFF1 brings the SEC through the ALF/pSER architecture.
  3. The lineage. B-lineage versus myeloid changes which promoters are accessible and therefore which uCpG sites are available at all.
  4. The cell of origin. Infant disease arises in a fetal progenitor with a silent mutational background; the adult lines carry accumulated cooperating lesions.

Any of the four could change the answer, and the standing rule in this project is that the system belongs in the claim rather than in the caveat.

Facts and figures
scriptnone - enumeration from full texts, GEO sample titles and abstracts, 2026-09-21
statusrun
query noteSEM[tiab] against the menin-inhibitor name list returns 0, but SEM is a contaminated free-text token (standard error of the mean, scanning electron microscopy, structural equation modelling) and that zero carries no information; the informative bound is the enumeration of eight datasets
denominator8
numerator infant0
rule of three boundfewer than 37.5% of such datasets use an infant-derived model, 95% confidence, n=8
shown for fusionKMT2A::AFF1 is profiled under drug in RS4;11 and MV4;11 with a shared-epitope antibody; the infant developmental context is profiled nowhere
absence classnever-measured
absence class basisNo infant-derived KMT2A::AFF1 model has been treated with a menin inhibitor and profiled. GSE83671 is cited as an adult-derived comparator, not as the missing dataset.
absence class assigned2026-09-21 (cycle 47, king)
geo recheck 2026 09 22The absence_class for this entry should be read as measured-not-analysed for EXPRESSION and never-measured for OCCUPANCY. GSE63664 exists and was never opened by this project: SEM and RS4;11, MI-2-2 and EPZ004777 and combination and DMSO arms. That is a menin-inhibitor expression dataset in an infant-derived KMT2A::AFF1 line sitting in a public archive, and this graph asserted no such profiling existed. The occupancy gap survives and is now the precise claim. GSE252378 was also checked and does NOT bear on it -- its samples are patient material (p279, p318, A70498, A73051) with KMT2A N- and C-terminal CUT&RUN, not SEM.
gse63664 opened cycle 55Opened and analysed; see ana-the-menin-inhibitor-response-is-nine-fold-fusion-selective-and-does-not-touch-hoxa-or-meis1-in-either-kmt2a-aff1-line and analyses/gse63664-menin-inhibitor-sem-versus-wildtype/. The dataset carries something this entry did not know it had: REH, a KMT2A-WILD-TYPE line, in the same normalization batch at the same dose and duration -- the specificity control this project had been asking for. It also carries a limit this entry should record: three of the submitter's four QC exclusions are SEM arrays, so the index-line contrast is n=2 versus n=2.
and sem is not infant derivedThis entry's own title and text call SEM infant-derived. Its system of record, line-sem-kmt2a-aff1, records CVCL_0095, age at sampling 5 years and infant_derived FALSE, re-verified against Cellosaurus 2026-09-22, which classifies SEM under childhood B-ALL. The entry already flags 'infant-derived is itself an approximation that should be checked before it is leaned on' -- it has now been checked, and the approximation is wrong. The absence in the title is therefore BROADER than stated: no menin-inhibitor occupancy dataset exists in any KMT2A::AFF1 line, and no infant-derived KMT2A::AFF1 line appears in GSE63664 at all.
systems profiled
[
  "MOLM13 (adult AML, KMT2A::MLLT3)",
  "RS4;11 (adult B-ALL, KMT2A::AFF1)",
  "ML2 (adult AML, KMT2A::AFDN)",
  "MV4;11 (adult, KMT2A::AFF1)",
  "OCI-AML3 (adult, NPM1c)",
  "murine MLL-AF9 leukaemia",
  "one adult patient sample under revumenib during lineage switch"
]
infant models absent
[
  "SEM",
  "KOPN-8",
  "HB11;19",
  "PER-490"
]
the qualifier is not vacuous checked cycle 56
{
  "why_this_was_checked": "GSE127507 (subseries of GSE127508) DOES hold Menin, MLL1, DOT1L and H3K79me2 ChIP-seq in RS4;11 under VTP-50469 at 100-330 nM, 26 samples, and this graph cites that subseries in 3 entries and the SuperSeries in 13. So the whole weight of this absence rests on the words INFANT-DERIVED, and the obvious worry is that it is unsatisfiable by any existing model -- in which case it would be a definitional artefact rather than a research gap.",
  "it_is_a_real_gap": "It is not vacuous. This graph own line registry holds 7 infant-derived KMT2A::AFF1 lines with recorded ages, none of which appears anywhere in GSE127508.",
  "the_lines_in_which_this_experiment_could_be_done": {
    "line-all-po-kmt2a-aff1-infant": "4 months",
    "line-blin-3-kmt2a-aff1-infant": "3 months",
    "line-per-485-kmt2a-aff1-infant-relapse": "1 year (relapse; same patient diagnosed at 336 days)",
    "line-per-490-kmt2a-aff1-infant": "9 days",
    "line-per-494-kmt2a-aff1-infant-diagnosis": "336 days (11 months)",
    "line-per-785-kmt2a-aff1-infant": "66 days (2 months)",
    "line-scmc-l1-kmt2a-aff1-infant": "4 months"
  },
  "the_lines_that_were_used_instead": "MOLM13 (KMT2A::MLLT3), RS4;11 (KMT2A::AFF1, age 32) and ML-2 (KMT2A::AFF6). The one AFF1 line in the series is the adult-derived one.",
  "so_the_actionable_form": "The experiment is not merely undone; it is undone in seven named available models, the youngest from a 9-day-old. That is a dispatchable experiment rather than a lament."
}
How this could bite us back
  • The drug class is in trials that include infants, and its chromatin mechanism has never been measured in an infant-derived model of the commonest infant fusion. That is a gap in the mechanistic dossier supporting paediatric development, not merely an academic one.
  • If the infant methylome offers more unmethylated CpG substrate, both the relocation risk and the depth of response could differ in the direction least favourable to extrapolating adult cell-line data.
  • Filling this gap is cheap - one pair of ChIP-seq or CUT&RUN samples in SEM under revumenib - and it should be done before any further modelling work imports the adult-line result into an infant claim.
Still open
  1. Does SEM respond to menin inhibitors with the same locus-selective occupancy pattern as RS4;11? A single ChIP-seq pair in SEM would test the transferability of the entire class's chromatin model to the index system, and would also supply the matched uCpG denominator.
  2. Do the 36 KMT2A-rearranged samples already profiled include infants at baseline? If so, the baseline half of the comparison exists and only the on-treatment half is missing.
  3. Is the infant methylome's larger unmethylated-CpG fraction measurable in the same cells, so that the relocation denominator is not imported from another line?
  4. ANSWERED, cycle 55, in ana-the-menin-inhibitor-response-is-nine-fold-fusion-selective-and-does-not-touch-hoxa-or-meis1-in-either-kmt2a-aff1-line. GSE63664 was opened. Three lines sit in ONE normalization batch at the same exposure (6 days, 10 uM MI-2-2): SEM and RS4;11, both KMT2A::AFF1, and REH, KMT2A-wild-type. Probes moving at least 1 log2 against each line's own DMSO: 769 in SEM, 692 in RS4;11, 80 in REH -- a ~9x fusion-selective response, reproduced in a second fusion line, against a 3.7x ratio for the DOT1L inhibitor in the same arrays. But the canonical programme does not collapse: HOXA10 +0.06 / +0.45, HOXA7 +0.45 / +0.22, MEIS1 +0.31 / +0.21 in SEM / RS4;11, and no better under the combination, while MEIS1 sits at 11.59 and 11.89 at baseline against 5.10 in the wild-type line. What rises instead is a differentiation programme (IGJ +3.77 and +4.07, CD20 to +4.94, CD86, MPEG1, LYZ, FCGR2B, ITGAM), and ATF5 falls ~8-fold on three probes in both fusion lines and not at all in REH. TWO THINGS THIS DID NOT SETTLE: MI-2-2 is a weak first-generation compound and target engagement was not measured, so 'the interface does not maintain the programme' and 'this compound did not block it hard enough' remain unseparated; and this is EXPRESSION, so the occupancy absence in this entry's headline survives entirely untouched.
Every source behind this entry (6)
  1. E1strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    The eight enumerated chromatin-occupancy datasets under a menin inhibitor use MOLM13, RS4;11, ML2, MV4;11, OCI-AML3, murine MLL-AF9 leukaemia cells and one adult patient sample; no infant-derived KMT2A-rearranged line is used for chromatin profiling under drug in any of them.

    What this evidence cannot show

    Systems were read from the methods, figure legends and GEO sample titles of the five full texts and from the abstracts of the remaining three datasets, so a supplementary arm in one of the three abstract-level papers could contain an infant line. The enumeration itself is bounded by a 61-record PubMed query plus targeted full-text reading, not by an exhaustive search. SEM appears in the pivotal paper as SEMK2 in viability assays, which is a use, just not a chromatin one.

    Evidence that argues against this (1)
    • RS4;11 and MV4;11 both carry the index fusion KMT2A::AFF1, so the fusion itself is represented even though the developmental context is not; a reader who considers the fusion the dominant variable would judge this gap much less important than one who considers cell of origin dominant. Janssens DH et al. 2024
  2. E2strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    The unmethylated-CpG occupancy figures that motivate the relocation question - fusion at 20% of uCpG sites, CFP1 at 50%, KDM2B at 89%, with MLL(N)-menin correlating at r-squared 0.96 - were all measured in SEM, an infant-derived t(4;11) KMT2A::AFF1 line, which has never been profiled FOR OCCUPANCY under a menin inhibitor. NARROWED 2026-09-22: the unqualified form of this sentence -- 'never been profiled under a menin inhibitor' -- was FALSE and is refuted by GEO.

    What this evidence cannot show

    One cell line, one laboratory, peak-overlap statistics sensitive to calling stringency. SEM is an immortalised line from a 5-year-old at relapse of infant-diagnosed disease in the standard characterisation, so 'infant-derived' is itself an approximation that should be checked before it is leaned on. BOUND ADDED AND THE BROAD CLAIM REFUTED, 2026-09-22. PubMed returns 0 for `SEM[tiab] AND (revumenib[tiab] OR "menin inhibitor"[tiab] OR MI-503[tiab] OR VTP-50469[tiab] OR MI-2-2[tiab])`, with controls that fire through the identical code path: `SEM[tiab] AND KMT2A[tiab]` = 8, `revumenib[tiab]` = 103, `SEM[tiab] AND leukemia[tiab]` = 337. But the PubMed zero is a false negative for the DATA question, and GEO settles it: **GSE63664, 'Gene expression induced by DOT1L and Menin inhibition in cell line models of leukemia', contains samples titled `SEM, MI-2-2 treat, biol rep 1` and `biol rep 3` with `SEM, DMSO treat` vehicle controls**, alongside RS4;11 under the same design. So SEM HAS been profiled under a menin inhibitor. What GSE63664 is, by its own title, is EXPRESSION -- not occupancy -- so this entry's headline absence, that no menin-inhibitor OCCUPANCY dataset exists in an infant-derived KMT2A::AFF1 line, is not refuted by it. Note also that `SEM` is a contaminated GEO token: a search for SEM with menin-inhibitor names returns 16 records whose samples are MOLM-13 and REH, matching 'SEM' as a word elsewhere in the record.

    Evidence that argues against this (1)
    • If the uCpG landscape of SEM differs from that of RS4;11, then importing the 20% figure into a discussion of the profiled lines is the same partner-imported reasoning this project keeps finding in its own evidence base. Kerry J et al. 2017
  3. E3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    A patient-sample chromatin profiling platform exists and has been applied at scale to 36 KMT2A-rearranged leukaemia samples, one of them under revumenib - so profiling primary infant material under drug is technically available and has simply not been done.

    MLL oncoprotein levels influence leukemia lineage identities. · Janssens DH, Duran M, Otto DJ, et al. · Nat Commun 2024
    What this evidence cannot show

    The 36-sample cohort's age distribution was not read for this entry and may include infants; the point stands only for the revumenib-treated arm, which is a single sample undergoing lineage switch. Automated CUT&Tag on primary material requires viable cells at a defined timepoint on therapy, which is an ethical and logistical constraint in infants rather than a technical one.

    Evidence that argues against this (1)
    • If the 36-sample cohort does include infant samples profiled at baseline, the gap is narrower than stated - baseline infant maps would at least supply the uCpG and occupancy denominator against which a treated sample could later be compared. Janssens DH et al. 2021
  4. E7strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.dataset

    GEO series GSE159608 contains Auto-CUT&Tag libraries in SEM, the infant-derived t(4;11) KMT2A::AFF1 line. Reading the sample records with record boundaries taken from !Sample_title: the H3K4me3 channel carries a DMSO arm (GSM5139709, GSM5139710), an EPZ-5676 arm (GSM5139711, GSM5139712) and a VTP-50469 arm (GSM5139713, GSM5139714), each in two replicates. H4K16ac is GSM5139715 and GSM5139716, IgG GSM5139717 and GSM5139718, menin GSM5139719 and GSM5139720 with no drug arm, and RNAP2-S5p GSM5139721 to GSM5139723. H3K27ac carries DMSO and EPZ-5676 arms. An earlier version of this evidence listed these accessions shifted by one, because the coordinator's parser opened each record at !Sample_geo_accession while GEO's brief format emits !Sample_title first.

    What this evidence cannot show

    CORRECTED 2026-09-24 TWICE OVER. This caveat previously said every arm assignment was unsafe because the deposit's titles disagree with its own characteristics; GSE159608 has ZERO such contradictions and the labels are usable [E8]. It also said a cycle-120 agent had named two of four accessions wrongly; THE AGENT WAS RIGHT AND THE COORDINATOR WAS SHIFTED BY ONE - its GSM5139713/14 for VTP and GSM5139709/10 for DMSO are correct. NOTHING IN THIS ENTRY HAS OPENED THE SIGNAL: no library was downloaded, no peak called, no retention computed here, so this establishes only that the experiment was deposited, and the H3K4me3 readout under drug is a histone mark rather than the fusion's or menin's position on chromatin. The SEM menin CUT&Tag samples remain DMSO-only, which is why this entry's occupancy claim survives.

    Evidence that argues against this (3)
    • Treating the H3K4me3 readout as a refutation of an OCCUPANCY absence stretches the term. A histone mark under drug is not the fusion's or menin's position on chromatin, and this entry's title, its enumeration and the argument it feeds are all about occupancy. Read strictly, the entry's central claim was never wrong and only one supporting sentence was - which is a smaller correction than the banner above implies.
    • This deposit was already in this project's hands. Cycle 116 parsed all 419 of these sample records while searching 32 series and 2,312 samples for a menin readout under DOT1L inhibition, and the SEM VTP-50469 arms were in the file it read. The absence survived because the question asked then was a different one, which means the cached corpus should be re-queried whenever an absence is asserted, not only when new data arrive.
    • The accession list in this evidence has now been wrong once and rewritten twice in two cycles, both times by the same coordinator, and the version that was PRESENTED as a careful re-parse of the primary records was the wrong one. A reader should treat any accession-level detail in this entry as needing a raw check rather than as settled, and note that the only independent confirmations came from agents.
  5. E8moderate confidence 3 of 5: One strong study, or several smaller consistent ones.analysis

    Comparing every cached GEO sample record's title against its own characteristics and treatment_protocol fields across 32 series and 2,312 samples, with record boundaries taken from !Sample_title: 0 of 309 comparable antibody assignments and 0 of 357 comparable treatment assignments disagree, 0 of 666 overall. GSE159608 has none. An earlier run of this same script reported 96 of 586 (16.4%) with GSE159608 as the worst offender at 46 of 119; 89 of those were an off-by-one, because GEO's brief format emits !Sample_title before !Sample_geo_accession while the parser opened each record at the accession. The remaining 7 were read individually against the raw records and were all this script's tokeniser: four where a title says MLL1c and the characteristics say 'MLL1 (c terminus)', the same Active Motif 61296 antibody, and three where a title says 0umEPZ5676 and the characteristics say DMSO, which is the same vehicle arm. An independent agent reached the same conclusion from the signal, finding 2,280 of 2,280 titles shifted under the original parser.

    What this evidence cannot show

    THE REPLACEMENT WAS RUN BY THE AUTHOR OF THE BUG, THE SAME DAY. The two tokeniser normalisations that took the count from 7 to 0 were written AFTER seeing which cases failed, an uncontrolled degree of freedom; both are unambiguous on the raw records, but the sequence was 16.4% to 1.1% to 0% with the instrument edited between the last two steps. A ZERO IS NOT PROOF THE DEPOSITS ARE CORRECT, only that their titles and characteristics agree - both could be wrong together. The comparison is only possible where BOTH fields state something: 666 comparable pairs out of 2,312 samples, so most samples are outside this audit entirely.

    Evidence that argues against this (2)
    • A correction that makes the data look cleaner is the direction that gets checked least, and this one was produced by fixing a single line in the script that was wrong. The same script has now reported two incompatible answers to the same question within twenty-four hours, and nothing external has confirmed either. The defensible position is that the contradiction rate is LOW, not that it is 1.1%.
    • The original error was not caught by the pre-registration, by the manual reading of three cases, or by the coordinator at all - it was caught by an agent dispatched on a brief that asserted the wrong number as established fact. The corpus's defence against this class of error is currently 'someone downstream refuses the premise', which is not a control and cannot be relied on.
  6. E9strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    GEO series GSE252378 contains 171 CUT&RUN sample records. Twenty carry 'treated with the Menin inhibitor' in their characteristics and belong to ONE primary infant patient sampled twice across a lineage switch - 148752 described as infant B-ALL and 152985 as infant AML, each recorded in GEO as paired with the other, both carrying group: KMT2A-ENL consistently across all twenty records. Their antibody panel by sample title covers Menin replicates 1 and 2, KMT2A-N1, KMT2A-N2, KMT2A-C1, KMT2A-C2, ENL and DOT1L. A further 25 samples carry group: KMT2A-AFF1, covering primary samples p279, p318 and p454 and the SEM cell line with AFF1, DOT1L, ENL and H3K4me3 antibodies, and none of those carries a drug treatment. The associated publication is Janssens DH et al., MLL oncoprotein levels influence leukemia lineage identities, Nature Communications 15:9341 (2024), PMID 39472576, which is not the title GEO gives the series.

    MLL oncoprotein levels influence leukemia lineage identities · Janssens DH, Duran M, Otto DJ, Kirkey D, Yi JS, Mullighan CG, Henikoff S · Nature Communications 15:9341 2024
    What this evidence cannot show

    CORRECTED 2026-09-24: THIS ARM IS n=1 PATIENT. 148752 and 152985 are the same infant before and after a lineage switch, stated in the GEO !Sample_description field as 'paired with' each other; an earlier version of this evidence described them as two patients. THE FUSION ASSIGNMENTS COME FROM A FIELD THIS DEPOSIT SHIFTS. Its characteristics lag its sample titles by one record - 9 of 21 comparable antibody assignments disagree, 42.9% - and the group field is offset too: GSM8371030 is titled SEM_AFF1_1 and carries group KMT2A-EPS15 although SEM is a KMT2A::AFF1 line. The KMT2A-ENL assignment for the two menin-inhibitor patients rests on consistency across their twenty records, which is internal agreement rather than correctness, and if it were wrong this entry's conclusion would fall. NEITHER THE COMPOUND NOR THE DOSE NOR THE EXPOSURE is named in the sample metadata, which says only 'the Menin inhibitor', so this dataset cannot be placed on the dose axis that cycles 115-117 established as where menin-inhibitor chromatin results stop being comparable. BOTH PATIENTS ARE LINEAGE-SWITCHING SAMPLES, a highly selected population, so even the KMT2A-ENL result is narrower than 'the infant experiment has been done'. NO LIBRARY WAS OPENED: no signal downloaded, no peak called, so this establishes what was deposited and not what it shows. Raw data for 51 of the 171 samples are withheld for donor privacy and which 51 was not determined.

    Evidence that argues against this (2)
    • This entry has now been corrected twice in two cycles, both times by material the project already held - GSE159608 in cycle 120 and GSE252378 in cycle 121, the latter cited by one entry here throughout. Its enumeration of eight occupancy datasets was presented as exhaustive and was not, and the surviving claim survives on a fusion-identity technicality. A reader should treat the remaining bound as provisional rather than as twice-tested.
    • Read strictly, the entry's title claim was never about histone marks or about non-index fusions, so neither correction touches it, and describing these as refutations overstates. The opposite reading is equally available: an enumeration that misses a ninth dataset on its first pass and a tenth on its second is not reliable evidence of exhaustiveness whatever its headline claim was, and the narrowing is the entry retreating to defensible ground rather than being vindicated.
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