Oncofusion

start / graph / gene-cdk13

Proteinmoderate confidence 3 of 5: One strong study, or several smaller consistent ones.Q35-ptefb-reservoir

CDK13 - rank 171 of 17,728, equally deep in both lineage halves, and essentially unstudied in leukaemia

also called CDK13 · CDC2L5 · CHED · CDC2L · KIAA1791 · cyclin-dependent kinase 13

CDK13 is another kinase that helps RNA polymerase keep moving. In the public CRISPR screens, KMT2A-rearranged leukaemia cells need it noticeably more than other leukaemia cells do, and unusually the effect is the same size in the lymphoid and myeloid halves - yet almost nobody has studied it in leukaemia at all.

The same thing, for a scientist

CDK13 (UniProt Q14004, 1,512 aa, 7p14.1; previous symbol CDC2L5) pairs with cyclin K alongside CDK12 [E1]. It is here because of a result rather than a hypothesis. On this project's genome-scale scan CDK13 ranks **171st of 17,728** on index-minus-comparator difference (-0.238), and on the lineage split the two halves of the KMT2A-rearranged arm agree closely: **-0.471 myeloid and -0.492 lymphoid against -0.278 in other leukaemia lines and -0.142 across all 1,208 lines** [E2]. Lineage consistency is the property this project demands of a selectivity claim and that CEBPA and SPI1 failed; CDK13 has it, at a magnitude roughly a third of MEN1's. It is expressed in all seven panel lines (median 19.6 nTPM) [E3]. Against that, the literature is close to empty: an alias-aware PubMed search returns four leukaemia records, none of which studies CDK13 as a dependency or a target, and a KMT2A-specific search returns one incidental developmental-genetics record [E4][E5]. **This is a data-driven lead with no literature behind it, and this entry does not claim more than that.**

Go deeper
The number, and the three ways it could still be wrong
armCDK9CDK13MEN1 (reference)
KMT2A-r, myeloid (n=6)-1.826-0.471-1.270
KMT2A-r, lymphoid (n=4)-1.555-0.492-1.268
other leukaemia lines-1.580-0.278-0.416
all 1,208 lines-1.536-0.142-0.363
scan rank (of 17,728)1,1361711

CDK13's shape is MEN1's shape at a third of the amplitude: both halves of the index arm deeper than the comparator, and equally deep as each other. CDK9's shape is the opposite - a very deep number that is deep everywhere 2.

Three ways this could still be wrong, stated before anyone gets attached to it:

  1. n = 6 and n = 4. Ten index lines is not a cohort. The agreement between the halves is reassuring but it is an agreement between two small means.
  2. The comparator arm. -0.278 in other leukaemia lines against -0.142 across all lines means CDK13 is already a leukaemia-leaning dependency before KMT2A status is considered; some of the difference may be leukaemia rather than KMT2A.
  3. Co-dependency with CDK12 and cyclin K. If cyclin K is limiting, a CDK13 knockout may act partly by changing how much cyclin K is available to CDK12, which is a different mechanism from CDK13 doing anything itself.

And one point against: CDK13 lies at 7p14.1, and a myelomonocytic leukaemia cell line has been reported in which CDC2L5 is among the genes lost in a dic(4;7) deletion 6. A gene a leukaemia can delete is an awkward fit for a gene a leukaemia needs. That observation is a single cell line and the authors frame the deletion as haploinsufficiency across many genes, but it belongs in the record.

The literature, bounded

Run on 2026-09-20 with the retired symbol included, because this project has measured a tenfold under-count from searching current symbols alone:

queryrecordsafter title-check
(CDK13[tiab] OR CDC2L5[tiab] OR CHED[tiab] OR KIAA1791[tiab]) AND (leukemia OR leukaemia OR AML)[tiab]40 studies of CDK13 as a dependency or target
(CDK13 OR CDC2L5) AND (MLL OR KMT2A)10 - a developmental-disorder de novo mutation survey

The four are: a dual HDAC/CDK medicinal-chemistry paper in which CDK13 is one of six inhibited targets 5; a case report of leukaemia in a child with CDK13-related disorder, which the authors themselves call probably coincidental; a 2000 Chinese-language expression study of CHED in myelodysplastic syndrome; and the JIH-3 cell-line report where CDC2L5 appears in a list of deleted genes 6. None is a functional study of CDK13 in leukaemia. The alias CHED and the alias CDC2L are both short and word-like, so every hit was title-checked rather than counted, per this project's precision rule 4.

Two subnuclear addresses, and the PNC is not a transformation marker (Q87, 2026-09-21)

Subcellular. Nucleus. UniProt Q14004's only location term is 'Nucleus speckle' on ECO:0000269 PubMed:16721827, and that citation is genuinely about the fact. HPA v25.1 IF, reliability Supported: nuclear speckles main, Golgi and cytosol additional.

Subnuclear, and there are two. (1) Nuclear speckles - the bulk pool, RS-domain-dependent. (2) The perinucleolar compartment - CDK13 co-localises with PTB there all through the cell cycle and raises PNC prevalence when overexpressed, while its own cyclins and substrates do not accumulate there. The two are different structures and an experiment has to say which it is scoring.

The correction that travels with the PNC. Its founding literature calls it a cancer-cell structure. It is also present in naive human embryonic stem cells, marked by alpha-satellite RNA (PMID 41730687), and naive hESCs are not transformed. So PNC prevalence is not a clean malignancy readout, and this entry does not assert that it is. gene-ptbp1 carries the same correction; the two entries agree.

A premise in the dispatch brief was wrong. The brief said a 2026 paper identifies CDK13 as a PNC component with PMID 26886422 as 'the older one'. There is exactly one paper linking CDK13 and the PNC in titles and abstracts, and it IS 26886422 - PLoS One, 2016. No 2026 CDK13 PNC paper exists in that index.

Shown for fusion. No, in the strong sense - nobody has looked in any fusion.

Facts and figures
uniprotQ14004
length AA1512
gene symbolCDK13
cytoband7p14.1
uniprot verifiedQ14004 = CDK13_HUMAN, primary gene name CDK13 (synonyms CDC2L, CDC2L5, CHED, KIAA1791), 1,512 aa, Homo sapiens; UniProt REST fetched and read back 2026-09-20
cyclin partnercyclin K (CCNK), shared with CDK12
breakpoint sidenot applicable - no documented KMT2A contact
subnuclear localizationNUCLEAR SPECKLES (bulk pool, RS-domain-dependent, PMID 16721827, corroborated by HPA v25.1 IF at reliability Supported) AND THE PERINUCLEOLAR COMPARTMENT (CDK13 is a PNC constituent, co-localises with PTB all through the cell cycle, and increases PNC prevalence when overexpressed, PMID 26886422). The PNC is NOT simply a marker of the transformed state - it is present in naive human embryonic stem cells (PMID 41730687) - and this entry is written to agree with gene-ptbp1, which carries the same correction.
cell statePROLIFERATIVE / TRANSFORMED, but stated with the correction above attached. CDK13's PNC residence is the only state-like localisation fact available, and the PNC's status as a malignancy readout is contested by its presence in naive hESCs. The defensible statement is that CDK13 occupies a compartment whose prevalence tracks with something about cell state, and that what that something is has not been settled.
shown for fusionNO - nobody has looked in any fusion. Measured 2026-09-21: (CDK13[tiab] OR CDC2L5[tiab] OR CHED[tiab]) AND the eight-term fusion clause AND the ten-term localisation clause returns 0 records. Neither CDK13's speckle pool nor its PNC pool has been imaged in a KMT2A-rearranged cell, and PNC prevalence has never been scored in one.
expression hpa celline nTPM
RS4;115.000RS4;11: 5SEM14.2SEM: 14.2NOMO-116.4NOMO-1: 16.4MOLM-1319.6MOLM-13: 19.6median19.6median: 19.6MV4-1123.7MV4-11: 23.7OCI-AML-224.5OCI-AML-2: 24.5THP-132.0THP-1: 32
essentiality
{
  "chronos_mean": -0.1421,
  "n_lines": 1208,
  "chronos_mean_kmt2ar_myeloid": -0.4712,
  "n_myeloid": 6,
  "chronos_mean_kmt2ar_lymphoid": -0.4922,
  "n_lymphoid": 4,
  "chronos_mean_other_leukemia": -0.2781,
  "scan_rank": 171,
  "scan_n_genes": 17728,
  "difference": -0.2383,
  "interpretation": "lineage-consistent KMT2A-rearranged-leaning dependency at a third of MEN1's amplitude; n=10 index lines"
}
expression hpa celline nTPM — the numbers behind the chart
{
  "SEM": 14.2,
  "RS4;11": 5,
  "MV4-11": 23.7,
  "THP-1": 32,
  "NOMO-1": 16.4,
  "MOLM-13": 19.6,
  "OCI-AML-2": 24.5,
  "median": 19.6
}
leukaemia literature
{
  "queries_run": [
    "(CDK13[tiab] OR CDC2L5[tiab] OR CHED[tiab] OR KIAA1791[tiab]) AND (leukemia[tiab] OR leukaemia[tiab] OR AML[tiab])",
    "(CDK13 OR CDC2L5) AND (MLL OR KMT2A)"
  ],
  "records": [
    4,
    1
  ],
  "functional_studies_after_title_check": 0,
  "date": "2026-09-20",
  "note": "PubMed dropped KIAA1791 from the query translation; CHED and CDC2L are word-like aliases so every hit was title-checked"
}
related entries
[
  "gene-cdk12",
  "gene-cdk9",
  "hyp-cdk13-is-the-lineage-consistent-transcriptional-cdk-dependency"
]
depmap kmt2a selectivity
{
  "chronos_mean_kmt2a_rearranged": -0.5052,
  "chronos_mean_other_leukaemia": -0.2669,
  "difference": -0.2383,
  "pan_essentiality_all_lines": -0.1421,
  "selectivity_rank": 171,
  "rank_denominator": 17728,
  "provenance": "Joined 2026-09-21 from analyses/depmap-kmt2a-selective-scan-full (generated 2026-09-19T10:12:06Z), the project's own genome-wide scan over 11 KMT2A-rearranged and 43 other leukaemia DepMap lines. NOT re-fetched and NOT independent of that scan: every caveat it carries applies here, including that the KMT2A-rearranged arm is a small number of lines drawn from nine individuals, that the rank denominator is 17,728 genes, and that a difference is not a dependency. Added because only 26 of 308 gene entries carried this number, which made any KMT2A-selectivity question answerable for 8% of the corpus.",
  "how_to_read": "A negative difference means MORE required in KMT2A-rearranged lines than in other leukaemia lines. A rank near 17,728 is ANTI-selective. Neither is evidence of a fusion-driven dependency on its own: check pan_essentiality_all_lines before calling anything selective, and note that a paralogue-redundant gene can score near zero for reasons that have nothing to do with this disease - see ana-the-paralogue-redundancy-excuse-is-not-tested-and-my-proxy-decided-the-answer."
}
localization
{
  "subcellular": "NUCLEUS. UniProt Q14004 carries a single location term, 'Nucleus speckle', on ECO:0000269 PubMed:16721827 - and unusually for this graph, the cited paper really is about the fact (rule 91): it states that CDC2L5 'is located in the nucleoplasm, at a higher concentration in speckles', and maps the requirement to the N-terminal RS domain. HPA v25.1 IF, reliability Supported, agrees and is more specific: main location Nuclear speckles, with Golgi apparatus and Cytosol as additional locations.",
  "subnuclear": "TWO subnuclear addresses, and they are not the same structure. (1) NUCLEAR SPECKLES - enriched over a nucleoplasmic background, RS-domain-dependent (PMID 16721827), corroborated independently by HPA immunofluorescence. (2) THE PERINUCLEOLAR COMPARTMENT (PNC) - CDK13 is enriched in the PNC and co-localises with the PNC component PTB throughout the cell cycle, while cyclins K and L and CDK13's candidate substrates do NOT accumulate there; CDK13 overexpression increases PNC prevalence (PMID 26886422). Two compartments for one protein is not a contradiction - the speckle pool is the bulk pool and the PNC pool is a small perinucleolar structure that speckle-resolution imaging does not separate - but any experiment here has to say which one it is scoring.",
  "the_pnc_is_not_simply_a_transformed-state_marker": "The PNC literature describes it as 'forming predominantly in cancer cells' with prevalence correlating with metastatic capacity (PMID 26886422), and it is tempting to read CDK13's PNC residence as a transformation marker. DO NOT. The PNC has since been shown in NAIVE HUMAN EMBRYONIC STEM CELLS, marked by alpha-satellite RNA and repressing rRNA expression (PMID 41730687) - naive hESCs are not transformed. So the PNC is better read as a property of a permissive nucleolar/chromatin-associated-RNA configuration than of malignancy, and this graph's gene-ptbp1 entry already carries the same correction. The two entries agree by construction.",
  "how_shown": "immunofluorescence of tagged and endogenous protein with deletion mapping of the RS domain (PMID 16721827); immunofluorescence co-localisation with PTB across the cell cycle plus an overexpression prevalence assay (PMID 26886422); HPA antibody IF",
  "tissue_of_evidence": "HeLa-class and other transformed human lines for both compartments. NOTHING haematopoietic has been imaged, which matters because CDK13 is 171st of 17,728 on this project's own KMT2A-selectivity scan with agreeing myeloid and lymphoid halves.",
  "node": "localization-nuclear-speckles-kmt2a-r"
}
cell type
{
  "haematopoietic_answer": "NONE MEASURED. No CDK13 localisation or PNC experiment has been done in any haematopoietic cell. What this graph has instead is a dependency number: CDK13 is expressed in all seven KMT2A-rearranged panel lines (median 19.6 nTPM, already recorded in this entry) and ranks 171st of 17,728 on the index-minus-comparator difference with myeloid and lymphoid halves agreeing. Expression and dependency are not localisation.",
  "cells_actually_imaged": "HeLa and other transformed human lines (PNC and speckle work); no blood cell of any kind."
}
How this could bite us back
  • CDK13 is a transcriptional CDK, so the general essential-function objection to CDK9 applies to it too - it is depleting in other leukaemia lines as well and mildly depleting across all lines.
  • Cyclin K is shared with CDK12, whose loss suppresses BRCA1 and the Fanconi genes; an inhibitor with any CDK12 cross-reactivity carries an induced DNA-repair defect.
  • No selective CDK13 chemical probe with published leukaemia data exists. Every compound that hits CDK13 in the literature also hits CDK9 and often HDACs, so a clinical test of this idea does not currently have a tool.
Still open
  1. Does CDK13 knockdown reduce KMT2A fusion target-gene output in a KMT2A::AFF1 line, and does it do so more than CDK12 knockdown?
  2. Is the CDK13 dependency mediated by competition for cyclin K with CDK12, or by CDK13 itself?
  3. Does the dependency hold in KMT2A::AFF1 B-ALL patient-derived xenografts, where the lineage confound is removed by construction?
Every source behind this entry (9)
  1. E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.paper

    Cyclin K binds CDK12 and CDK13 to form two distinct complexes in human cells, and the DNA damage response gene requirement is specific to cyclin K/CDK12 rather than cyclin K/CDK13.

    The Cyclin K/Cdk12 complex maintains genomic stability via regulation of expression of DNA damage response genes. · Blazek D, Kohoutek J, Bartholomeeusen K, Johansen E, Hulinkova P, Luo Z, Cimermancic P, Ule J, Peterlin BM · Genes Dev 2011
    PMID 22012619DOI
    What this evidence cannot show

    Human cell lines; the CDK13 arm is defined largely by what it does not do in that assay, so CDK13's own programme is not characterised there.

    Evidence that argues against this (1)
    • Later work reports CDK13 cooperating with CDK12 over global Pol II processivity rather than acting on a disjoint gene set, so the clean separation does not hold generally. Bosken CA et al. 2014
  2. E2moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database

    CDK13 ranks 171st of 17,728 on index-minus-comparator difference (-0.238) in this project's genome-scale DepMap scan, and on the lineage split means -0.471 in the six KMT2A-rearranged myeloid lines and -0.492 in the four lymphoid lines against -0.278 in other leukaemia lines and -0.142 across all 1,208 lines.

    What this evidence cannot show

    Six myeloid and four lymphoid lines; ten index lines in total. The comparator arm is itself deeper than the all-lines mean, so part of the difference is leukaemia rather than KMT2A rearrangement. Cyclin K is shared with CDK12 and could mediate the effect. This is a raw effect-size difference, not a z, and no permutation p was computed for CDK13 in the original scan.

    Evidence that argues against this (1)
    • CDK13 sits at 7p14.1 and has been reported among the genes lost in a dicentric 4;7 deletion in a myelomonocytic leukaemia cell line, which is hard to reconcile with a dependency; the deletion is one line and spans many genes, but it is on record. Pan J et al. 2012
  3. E3established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    CDK13 is detected in all seven KMT2A-rearranged panel lines the Human Protein Atlas carries, median 19.6 nTPM, so the dependency is not confounded by expression.

    What this evidence cannot show

    Bulk poly-A cell-line RNA, not protein; seven of the project's eleven-line panel.

    Evidence that argues against this (1)
    • Expression is not the relevant control for a dependency this shallow; what would matter is whether cyclin K is limiting, and that was not measured. Blazek D et al. 2011
  4. E4moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database

    An alias-aware PubMed search on 2026-09-20 returns four leukaemia records for CDK13 and its retired symbols, none of which studies CDK13 as a dependency or therapeutic target; a KMT2A-specific search returns one record, a developmental-disorder de novo mutation survey.

    What this evidence cannot show

    Bounded by the symbol set actually searched: CDK13, CDC2L5, CHED, KIAA1791 and CDC2L. PubMed dropped KIAA1791 from its query translation, so that alias was effectively not run. CHED and CDC2L are short and word-like, so every hit was title-checked rather than counted. A paper framing the work as 'transcriptional CDKs' without naming CDK13 would not be retrieved.

    Evidence that argues against this (1)
    • This project has documented complex-level and class-level phrasing making individual members unreachable from their symbols; dual CDK9/12/13 inhibitor papers exist and would mostly be retrieved under CDK9. Liu Y et al. 2023
  5. E5moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper

    A dual HDAC/CDK inhibitor series produced a lead compound inhibiting CDK9, CDK12, CDK13, HDAC1, HDAC2 and HDAC3 at low nanomolar concentrations that induced differentiation of leukaemic stem-like cells and inhibited AML proliferation.

    Discovery of novel and bioavailable histone deacetylases and cyclin-dependent kinases dual inhibitor to impair the stemness of leukemia cells. · Liu Y, Wei Y, Wang X, Ma L, Li X, Sun Y, Wu Y, Zhang L, Wang J, Li M, Zhang K, Wei M, et al · Eur J Med Chem 2023
    PMID 36736154DOI
    What this evidence cannot show

    A medicinal-chemistry paper. Six targets are inhibited simultaneously, so nothing in it attributes the cellular effect to CDK13, and no KMT2A-rearranged genotype is specified.

    Evidence that argues against this (1)
    • A compound hitting CDK9 and three HDACs at low nanomolar potency would be expected to have leukaemia activity for reasons that have nothing to do with CDK13, so this is not evidence for CDK13 as a target. Blazek D et al. 2011
  6. E6weak confidence 2 of 5: Preliminary, small, indirect, or not yet peer reviewed.paper

    In the acute myelomonocytic leukaemia cell line JIH-3, a dic(4;7)(p11;p11) deletion removes a 7p region containing CDC2L5 (CDK13) among other genes, and the authors attribute a role in leukaemogenesis to haploinsufficiency across the deleted region.

    Establishment and characterization of a new human acute myelomonocytic leukemia cell line JIH-3. · Pan J, Xue Y, Chen S, Qiu H, Wu C, Jiang H, Wang Q, Zhang J, Bai S, Wu Y, Wang Y, Shen J · Leuk Res 2012
    PMID 22340903DOI
    What this evidence cannot show

    One cell line, one deletion spanning many genes, no functional test of CDK13 itself. This is a plausibility check against the dependency claim, not a refutation of it: a heterozygous deletion is not a knockout, and the line is not KMT2A-rearranged.

    Evidence that argues against this (1)
    • The deletion arose during passage and is described alongside two other structural changes, so attributing anything to CDK13 specifically is unsupported in either direction. Pan J et al. 2012
  7. E7strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    CDK13 is enriched in the nucleoplasm and concentrated further in nuclear speckles, and this localisation requires the N-terminal RS domain. UniProt Q14004's single location term, 'Nucleus speckle', rests on this paper (ECO:0000269 PubMed:16721827), and unlike most of the coded citations audited in rule 91 it is genuinely the paper that made the observation. HPA v25.1 immunofluorescence independently gives Nuclear speckles as the main location at reliability Supported.

    CDC2L5, a Cdk-like kinase with RS domain, interacts with the ASF/SF2-associated protein p32 and affects splicing in vivo. · Even Y, Durieux S, Escande ML, Lozano JC, Peaucellier G, Weil D, et al. · J Cell Biochem 2006
    PMID 16721827DOI
    What this evidence cannot show

    The paper is from 2006, works on CDC2L5 under its former name, and uses overexpressed tagged constructs for the deletion mapping - so the RS-domain requirement is established on a construct rather than on the endogenous protein. The system is a transformed human line, not a haematopoietic cell, and the speckle enrichment is over a nucleoplasmic background rather than an exclusive residence.

    Evidence that argues against this (1)
    • A single 'nuclear speckle' answer for CDK13 is incomplete in a way that matters for any experiment designed from this entry, because CDK13 is ALSO a constituent of a different compartment - the perinucleolar compartment, where it co-localises with PTB throughout the cell cycle and whose prevalence it increases on overexpression. Crucially, the cyclins K and L that partner CDK13, and its candidate substrates, do NOT accumulate in the PNC, so the PNC pool is not simply the kinase complex being carried along - it is a distinct pool with a distinct composition. An imaging experiment scored at speckle resolution will not resolve it, and an entry recording only the speckle would send someone to the wrong compartment. Even Y et al. 2016
  8. E8moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper

    CDK13 is a component of the perinucleolar compartment: it is enriched in the PNC, co-localises with the PNC component PTB throughout the cell cycle, and its overexpression increases PNC prevalence, while the cyclins K and L and its candidate substrates do not accumulate there.

    PMID 26886422DOI
    What this evidence cannot show

    The evidence is immunofluorescence in transformed human lines, with the prevalence result resting on overexpression, so the causal direction - CDK13 builds the PNC versus CDK13 accumulates in a PNC built by something else - is not settled by this experiment. Nothing haematopoietic; the PNC has never been scored in a leukaemic blast of any genotype. Note also that the graph's premise that a 2026 paper identified CDK13 as a PNC component is WRONG: there is exactly one paper linking the two in titles and abstracts, and it is this 2016 one ("perinucleolar compartment"[tiab] AND CDK13[tiab] = 1, 2026-09-21).

    Evidence that argues against this (1)
    • This paper's own framing - the PNC is 'a subnuclear structure forming predominantly in cancer cells' whose prevalence correlates with metastatic capacity - should NOT be carried into this entry as a statement that the PNC marks the transformed state. It does not: alpha-satellite RNA marks the perinucleolar compartment in NAIVE HUMAN EMBRYONIC STEM CELLS, where it represses ribosomal RNA expression, and naive hESCs are not transformed. That reframes the PNC as a property of a permissive nucleolar and chromatin-associated-RNA configuration rather than of malignancy, which in turn means PNC prevalence is not a clean malignancy readout and any proposed PNC-scoring experiment in KMT2A-rearranged blasts would need a naive-pluripotent-like comparator, not merely a normal-blood one. gene-ptbp1 in this graph carries the identical correction, and these two entries are written to agree. Mittal K et al. 2026
  9. E9moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database

    No CDK13 localisation result exists in any KMT2A-fusion context. Measured 2026-09-21: (CDK13[tiab] OR CDC2L5[tiab] OR CHED[tiab]) AND (KMT2A[tiab] OR MLL[tiab] OR "MLL-AF4"[tiab] OR "MLL-AF9"[tiab] OR "MLL-ENL"[tiab] OR "MLL-AF10"[tiab] OR "t(4;11)"[tiab] OR "t(9;11)"[tiab]) AND (localization[tiab] OR localisation[tiab] OR subnuclear[tiab] OR nuclear[tiab] OR nucleolar[tiab] OR speckle[tiab] OR speckles[tiab] OR "PML bodies"[tiab] OR chromatin-bound[tiab] OR cytoplasmic[tiab]) returns 0 records. Neither the speckle pool nor the PNC pool has been imaged in a KMT2A-rearranged cell, and PNC prevalence has never been scored in one.

    What this evidence cannot show

    Bounded by titles and abstracts only (rule 80); a fractionation panel inside a supplementary figure would be invisible. The alias list was CDK13, CDC2L5 and CHED - CHED is short and word-like and would inflate a bare count, but it cannot inflate a zero. Rule-67 positive control for this query SHAPE: the identical construction, run over all sixteen genes of this tranche on the same day, returned non-zero for seven of them - H2AZ1 1, EED 2, CHAF1B 1, CEBPA 3, TIFAB 1, SAMHD1 1, PROM1 1 - so the instrument can return a one. The querytranslation was read back on every run and confirms the quoted cytogenetic terms expand to "t 4 11"[Title/Abstract] and "t 9 11"[Title/Abstract] and not to a UID filter (rule 95); every term carries its own [tiab] tag rather than sitting inside a parenthesised group (rule 94).

    Evidence that argues against this (1)
    • A zero here understates how reachable this question is, and reporting it as 'unstudied' would be the wrong conclusion to draw. CDK13's PNC residence was established by co-localisation with PTB, and PTB/PTBP1 is this graph's strongest RNA-layer dependency in KMT2A-rearranged lines - so the reagent, the marker and the motivating dependency all already exist, and the missing experiment is one two-colour stain in a KMT2A-rearranged blast rather than a research programme. The absence class is measured-not-searched at worst, not never-measured. Even Y et al. 2016
Connected to