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
also called MLLT3 beat enumeration · t(9;11) bounded rejection
A record of the searches run, the papers read and deliberately not used, and the things that could not be read at all. Its purpose is so that someone re-running this next year repeats the decision, not just the search.
The same thing, for a scientist
Bounded absence is standard in this project; bounded **rejection** is the half that leaves no trace, so this entry records it. Sixteen PubMed queries were run on 2026-09-20 with query translations read, and the counts are in `data`. Two results are worth promoting out of the list. **`t(9;11) AND (leukemia)` returns a clean 0 with 'No items found'**, with the translation `"t"[All Fields] AND 9,11[UID] AND (...)` - the documented parenthesis trap, reproduced here for this exact karyotype; the bare-token form `t 9 11 AND leukemia` returns **610**. And **a twelfth human KMT2A::MLLT3 cell line exists in the literature and not in Cellosaurus**: SDEY-AML1, reported in 2026 with co-occurring IKZF1::EVX1 [E1], returns `numFound: 0` on a Cellosaurus search. That is a limit on this beat's cell-line panel and on any accession-database sweep: **the catalogue lags the literature, and a sweep that is complete against the database is not complete against the field.** Six papers were read and set aside with reasons recorded below, and one paper central to the menin claim - the 2005 founding report - has no PMC record at all and was used from its abstract only.
Queries run, with counts and the translations that mattered
All 2026-09-20, esearch db=pubmed, translations inspected.
| query | count | note |
|---|---|---|
t(9;11) AND (leukemia) | 0 | translation "t"[All Fields] AND 9,11[UID] AND (...); warninglist No items found. A counted absence built on this string would be worthless. |
t 9 11 AND leukemia | 610 | the usable form |
KMT2A-MLLT3 | 92 | current-symbol form |
MLL-AF9 | 623 | retired-symbol form, 6.8x more records |
AF9 AND YEATS AND leukemia | 20 | the productive route into the reader literature |
MLLT3 AND menin | 3 | all reviews or combination studies; none partner-specific |
MLL-AF9 AND (CBX8 OR BCOR) | 7 | yielded the decisive BCOR/CBX8 separation-of-function paper |
MLL-AF9 subnuclear | 1 | |
MLL-AF9 immunofluorescence nuclear | 1 | |
(MLL-AF9 OR KMT2A-MLLT3) AND (nuclear speckle OR nuclear body OR nucleolus) | 3 | one is an antisense knockdown paper, not localisation |
MLLT3 nucleolus | 0 | No items found, clean translation |
AF9 nuclear localization signal MLLT3 | 4 | none on point |
MLL-AF9 YEATS domain transformation | 0 | No items found; no add-back experiment exists |
MLL-AF9 condensate phase separation | 1 | AKAP95, and the co-condensation is with the KMT2A half |
MI-503 menin MLL small molecule leukemia | 4 | |
Menin-MLL inhibitor MI-503 MLL-AF9 MOLM-13 leukemia | 0 | over-specified; a reminder that a long AND-chain manufactures absences |
The retired-symbol lesson holds here too. MLL-AF9 returns 6.8 times as many records as KMT2A-MLLT3. A beat keyed to the current symbol would have seen 15% of this literature.
Read and set aside, with reasons
Three lines each: what it is, why it was not used, and what would change that.
PMID 42063817 - Mechanism of AF9 (MLLT3)-Partner Dissociation, JACS Au 2026 2. Gaussian-accelerated MD of AF9-peptide dissociation, reporting DOT1L as the most stable complex followed by CBX8 then BCOR. Not used because it is simulation with no new experimental measurement, and its stability ordering conflicts with the measured affinities - BCOR binds AF9 at 18 nM while CBX8 is too weak to saturate. Would be used if the predicted metastable intermediates were validated experimentally.
PMID 40964345 - A chemical-genetic interaction between PAF1 and ENL/AF9 YEATS inhibition, bioRxiv 2025 3. A preprint about inhibiting the YEATS domains of wild-type ENL and AF9. Not used because the fusion in t(9;11) has no YEATS domain, so the interaction it describes cannot be a fusion property in 99.5% of patients. Would be used in a t(11;19) beat, where the fusion does carry a reader.
PMID 38747396 - Structural studies of intrinsically disordered MLL-fusion protein AF9 in complex with peptidomimetic inhibitors, Protein Sci 2024 4. Structures of AHD-directed peptidomimetics. Not used as primary evidence because this beat's druggability position rests on the paralogue cross-reactivity problem rather than on ligand availability, and no cellular or in vivo data are attached. Would be used by a chemistry-facing beat.
PMID 42020782 - A transgenic zebrafish leukemia model driven by KMT2A::MLLT3, Leukemia 2026 5. A new model organism for this exact fusion. Not used because this beat's argument is about human breakpoint architecture and a zebrafish transgene has, by construction, whatever architecture the authors chose. Would be used by a modelling beat, and the construct's MLLT3 boundary is worth extracting.
PMID 42613434 - Modeling KRAS mutations in KMT2A::MLLT3 AML, Leukemia 2026 6. Directly on-partner. Not used because it concerns co-mutation and progression rather than anything in this beat's scope, though it is relevant to the observation that three of ten t(9;11) cell-line patients carry a RAS-pathway lesion.
PMID 41656387 - SDEY-AML1, Sci Rep 2026 1. A new human KMT2A::MLLT3 line with a co-occurring IKZF1::EVX1 fusion. Not incorporated into the cell-line panel because it has no Cellosaurus accession, and this project's rule is to resolve lines by accession and read the primary name back. Recorded here so the next sweep catches it.
Unreadable, and the four routes
One paper central to a claim in this beat could not be read in full.
PMID 16239140, Yokoyama et al., The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis, Cell 2005 7. Route 1, search?query=EXT_ID:16239140&resultType=core, returns pmcid: none and isOpenAccess: N. With no PMCID, routes 2, 3 and 4 have no target. It is therefore not 'unreadable' in the sense the register uses - it is not open access, and the distinction matters. Every claim sourced to it here is sourced to its abstract and is marked as such.
One route trap reproduced, because it is worth a second witness. Fetching https://pmc.ncbi.nlm.nih.gov/articles/PMC7810303/ - a PMCID guessed rather than looked up - returned HTTP 200 with 21,303 characters of HTML that strip to 165 characters of text. That is the success-shaped stub the standing brief warns about, reproduced exactly, and it is why stripped-text length rather than HTTP status is the test. The correct PMCID for that paper, obtained from the Europe PMC core record, is PMC7497807, which strips to 74,855 characters.
And one supplementary re-test. https://www.ebi.ac.uk/europepmc/webservices/rest/PMC11687943/supplementaryFiles returns HTTP 200 and a valid PK zip of 1,261,425 bytes containing six files - jco-43-75-g001, g002 and g003 as .gif and .jpg - and no Data Supplement Table S3, which is where AUGMENT-101's partner-stratified efficacy lives 8. This graph's existing bounded-absence entry on partner-stratified menin response stands, re-tested.
Laboratories whose work is on-beat and is not cited here
Recorded so a future cycle can tell 'not considered' from 'considered and out of scope'.
- The Bushweller group (Virginia) and the Zeleznik-Le group (Loyola) produce most of the AF9 AHD structural biology. Their work is cited extensively here; the parts not cited are the AF4-AF9 peptidomimetic chemistry series, deliberately, per the rejection note above.
- The Muntean group (Michigan) produces the ENL/AF9 YEATS and breakpoint work this beat depends on. Fully used.
- The Marschalek/DCAL group (Frankfurt) produces the recombinome archive. Used for counts; not approached for the cross-tabulations this beat repeatedly says are needed (partner-side breakpoint by aetiology; whether the 2 spliced and the 2 YEATS-retaining MLLT3 cases are the same patients). Those are data requests, not literature.
- Groups working on MLLT3 in normal haematopoiesis (the MLLT3 HSC self-renewal literature) are cited only as counter-evidence, because normal-HSC function is another beat's territory.
- Groups working on YEATS-domain chemical biology (SGC and collaborators) are cited through this beat's ENL-side entries only, for the reason in the rejection note.
| status | run |
|---|---|
| run date | 2026-09-20 |
queries — the numbers behind the chart
[
{
"q": "t(9;11) AND (leukemia)",
"count": 0,
"translation": "\"t\"[All Fields] AND 9,11[UID] AND (...)",
"warninglist": "No items found",
"verdict": "parser trap; unusable"
},
{
"q": "t 9 11 AND leukemia",
"count": 610,
"verdict": "usable bare-token form"
},
{
"q": "KMT2A-MLLT3",
"count": 92
},
{
"q": "MLL-AF9",
"count": 623,
"verdict": "retired symbol returns 6.8x the current symbol"
},
{
"q": "AF9 AND YEATS AND leukemia",
"count": 20
},
{
"q": "MLLT3 AND menin",
"count": 3
},
{
"q": "MLL-AF9 AND (CBX8 OR BCOR)",
"count": 7
},
{
"q": "MLL-AF9 subnuclear",
"count": 1
},
{
"q": "MLL-AF9 immunofluorescence nuclear",
"count": 1
},
{
"q": "(MLL-AF9 OR KMT2A-MLLT3) AND (nuclear speckle OR nuclear body OR nucleolus)",
"count": 3
},
{
"q": "MLLT3 nucleolus",
"count": 0,
"warninglist": "No items found"
},
{
"q": "AF9 nuclear localization signal MLLT3",
"count": 4,
"verdict": "none on point"
},
{
"q": "MLL-AF9 YEATS domain transformation",
"count": 0,
"warninglist": "No items found",
"verdict": "no published in-cis add-back"
},
{
"q": "MLL-AF9 condensate phase separation",
"count": 1
},
{
"q": "MI-503 menin MLL small molecule leukemia",
"count": 4
},
{
"q": "Menin-MLL inhibitor MI-503 MLL-AF9 MOLM-13 leukemia",
"count": 0,
"verdict": "over-specified AND-chain manufactures an absence"
}
]read and rejected — the numbers behind the chart
[
{
"pmid": "42063817",
"reason": "MD simulation only; stability ordering conflicts with measured affinities",
"would_change": "experimental validation of the metastable intermediates",
"title": "Mechanism of AF9 (MLLT3)-Partner Dissociation in Mixed-Lineage Leukemia-Rearranged Leukemia.",
"authors": "Sharma S, Joshi K, Saha A",
"venue": "JACS Au",
"year": 2026,
"title_provenance": "Title/authors/venue backfilled from PubMed esummary on 2026-09-20 because this citation stored a bare PMID with no title, which made it unscoreable by verify-citations.py. BACKFILLING IS NOT VERIFICATION: it confirms the PMID resolves to a real paper, not that this is the right paper for the claim. That still requires reading."
},
{
"pmid": "40964345",
"reason": "preprint about wild-type ENL/AF9 YEATS inhibition; the t(9;11) fusion has no YEATS domain",
"would_change": "evidence that YEATS inhibition acts on the fusion rather than on wild-type protein in t(9;11) cells",
"title": "A chemical-genetic interaction between PAF1 and ENL/AF9 YEATS inhibition.",
"authors": "Barta PA, Garnar-Wortzel L, Bishop TR, et al.",
"venue": "bioRxiv",
"year": 2025,
"title_provenance": "Title/authors/venue backfilled from PubMed esummary on 2026-09-20 because this citation stored a bare PMID with no title, which made it unscoreable by verify-citations.py. BACKFILLING IS NOT VERIFICATION: it confirms the PMID resolves to a real paper, not that this is the right paper for the claim. That still requires reading."
},
{
"pmid": "38747396",
"reason": "AHD peptidomimetic structures with no cellular or in vivo data; this beat's druggability position rests on paralogue cross-reactivity",
"would_change": "a selectivity profile distinguishing AF9 from ENL",
"title": "Structural studies of intrinsically disordered MLL-fusion protein AF9 in complex with peptidomimetic inhibitors.",
"authors": "Yang Y, Ahmad E, Premkumar V, et al.",
"venue": "Protein Sci",
"year": 2024,
"title_provenance": "Title/authors/venue backfilled from PubMed esummary on 2026-09-20 because this citation stored a bare PMID with no title, which made it unscoreable by verify-citations.py. BACKFILLING IS NOT VERIFICATION: it confirms the PMID resolves to a real paper, not that this is the right paper for the claim. That still requires reading."
},
{
"pmid": "42020782",
"reason": "zebrafish transgene; architecture is chosen, so it cannot inform human breakpoint distribution",
"would_change": "extraction of the construct's MLLT3 boundary",
"title": "A transgenic zebrafish leukemia model driven by KMT2A::MLLT3 (MLL-AF9).",
"authors": "Saberi M, Delfi O, Hall CJ, et al.",
"venue": "Leukemia",
"year": 2026,
"title_provenance": "Title/authors/venue backfilled from PubMed esummary on 2026-09-20 because this citation stored a bare PMID with no title, which made it unscoreable by verify-citations.py. BACKFILLING IS NOT VERIFICATION: it confirms the PMID resolves to a real paper, not that this is the right paper for the claim. That still requires reading."
},
{
"pmid": "42613434",
"reason": "co-mutation and progression, out of this beat's scope",
"would_change": "a beat on RAS co-mutation in the t(9;11) cell-line panel",
"title": "Modeling KRAS mutations in KMT2A::MLLT3 acute myeloid leukemia promotes leukemic progression and transcriptional rewiring.",
"authors": "Esparza N, Defrêne J, Bresson E, et al.",
"venue": "Leukemia",
"year": 2026,
"title_provenance": "Title/authors/venue backfilled from PubMed esummary on 2026-09-20 because this citation stored a bare PMID with no title, which made it unscoreable by verify-citations.py. BACKFILLING IS NOT VERIFICATION: it confirms the PMID resolves to a real paper, not that this is the right paper for the claim. That still requires reading."
},
{
"pmid": "41656387",
"reason": "new human KMT2A::MLLT3 line with no Cellosaurus accession; this project resolves lines by accession",
"would_change": "a Cellosaurus entry, or direct reading of the establishment paper",
"title": "A novel human acute myeloid leukemia cell line SDEY-AML1 with KMT2A: MLLT3, IKZF1: EVX1 fusions exhibits high tumorigenicity in NSG mice.",
"authors": "Yang C, Zhang W, Wu Y, et al.",
"venue": "Sci Rep",
"year": 2026,
"title_provenance": "Title/authors/venue backfilled from PubMed esummary on 2026-09-20 because this citation stored a bare PMID with no title, which made it unscoreable by verify-citations.py. BACKFILLING IS NOT VERIFICATION: it confirms the PMID resolves to a real paper, not that this is the right paper for the claim. That still requires reading."
}
]not open access
[
{
"pmid": "16239140",
"routes_tried": [
"EPMC core record: pmcid none, isOpenAccess N"
],
"note": "no PMCID, so routes 2-4 have no target; used from abstract only",
"title": "The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis.",
"authors": "Yokoyama A, Somervaille TC, Smith KS, et al.",
"venue": "Cell",
"year": 2005,
"title_provenance": "Title/authors/venue backfilled from PubMed esummary on 2026-09-20 because this citation stored a bare PMID with no title, which made it unscoreable by verify-citations.py. BACKFILLING IS NOT VERIFICATION: it confirms the PMID resolves to a real paper, not that this is the right paper for the claim. That still requires reading."
}
]route traps reproduced
[
{
"trap": "success-shaped PMC HTML stub",
"detail": "PMC7810303 (a guessed PMCID) returned HTTP 200, 21,303 HTML characters, 165 characters of stripped text; the correct PMCID PMC7497807 strips to 74,855"
},
{
"trap": "parenthesised karyotype",
"detail": "t(9;11) AND (leukemia) -> 0 with 9,11[UID]"
},
{
"trap": "Europe PMC fullTextXML HTTP 500",
"detail": "PMC11246743 returned 500; the PMC HTML page returned 61,252 characters of stripped text"
},
{
"trap": "Cellosaurus fielded query undercounts",
"detail": "a query restricted to ca:'Cancer cell line' returned 2 of 11 lines; paging the unfielded query and filtering on the structured fusion comment returned all 11"
},
{
"trap": "shared scratchpad",
"detail": "a helper script and a citations file written by this agent were overwritten by a concurrently running agent in the same session scratchpad; citation identifiers were re-fetched into a uniquely named file before any were used"
}
]supplementary retest
{
"endpoint": "https://www.ebi.ac.uk/europepmc/webservices/rest/PMC11687943/supplementaryFiles",
"result": "HTTP 200, valid PK zip, 1,261,425 bytes, six figure files, no Table S3"
}data requests not literature
[ "partner-side breakpoint distribution in t(9;11) stratified by therapy-induced status", "whether the 2 spliced and the 2 YEATS-retaining KMT2A::MLLT3 cases are the same patients", "the exon-level composition of the unaccounted ~1.1% of the 442 t(9;11) breakpoints" ]
- A beat that resolves cell lines only through an accession database will systematically miss the newest models, which are the ones most likely to carry modern characterisation - and newness correlates with the co-mutations that confound fusion attribution.
- The over-specified query that returned 0 is the failure mode most likely to survive review, because a long, precise-looking AND-chain reads as rigour.
- How many other human KMT2A::MLLT3 lines exist in the literature without a Cellosaurus accession? SDEY-AML1 was found incidentally, not by a systematic search.
- Would a systematic literature sweep for cell-line establishment papers, rather than an accession-database sweep, change any panel in this graph?
- Is there an institutional route to PMID 16239140 and to the AUGMENT-101 Data Supplement? Both are single documents that would close open items.
- E1moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
A novel human acute myeloid leukaemia cell line, SDEY-AML1, carrying KMT2A::MLLT3 together with an IKZF1::EVX1 fusion and showing high tumorigenicity in NSG mice, was reported in 2026; a Cellosaurus search for SDEY-AML1 on 2026-09-20 returns numFound 0.
A novel human acute myeloid leukemia cell line SDEY-AML1 with KMT2A: MLLT3, IKZF1: EVX1 fusions exhibits high tumorigenicity in NSG mice. · Yang C, Zhang W, et al. · Sci Rep 2026What this evidence cannot show
Title and record read; the full text was not retrieved and the line's characterisation was not assessed. The Cellosaurus negative is a statement about the catalogue on one date, not about the line's existence or validity.
Evidence that argues against this (1)
- A newly reported line with a second driver fusion (IKZF1::EVX1) is not a clean KMT2A::MLLT3 model, so its absence from this beat's panel costs less than the general point it illustrates - that an accession-database sweep necessarily lags the literature. Meyer C et al. 2023
- E2weak confidence 2 of 5: Preliminary, small, indirect, or not yet peer reviewed.paper
Gaussian-accelerated molecular dynamics simulations of AF9-partner peptide dissociation report DOT1L as forming the most stable complex with AF9, followed by CBX8 and then BCOR, with dissociation proceeding stepwise through metastable intermediates.
Mechanism of AF9 (MLLT3)-Partner Dissociation in Mixed-Lineage Leukemia-Rearranged Leukemia. · Sharma S, Joshi K, Saha A · JACS Au 2026What this evidence cannot show
Simulation with no new experimental measurement. Abstract read only. The reported stability ordering places CBX8 above BCOR, which is the opposite of the measured affinities, where BCOR binds AF9 at 18 nM and wild-type CBX8 binds too weakly to saturate.
Evidence that argues against this (1)
- The measured fluorescence-anisotropy affinities contradict the simulated ordering for CBX8 against BCOR, so the simulation's ranking should not be used to prioritise contacts until it is reconciled. Schmidt CR et al. 2020
- E3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
A chemical-genetic interaction between PAF1 and inhibition of the ENL and AF9 YEATS domains has been reported: small molecules inhibiting the ENL/AF9 YEATS domain show anti-leukaemia effects in preclinical models, and the work identifies PAF1 as a chemical-genetic interactor of that inhibition.
A chemical-genetic interaction between PAF1 and ENL/AF9 YEATS inhibition · Barta PA, ..., Erb MA · RSC Chemical Biology 2026What this evidence cannot show
**Citation updated 2026-09-20: this was cited as a bioRxiv preprint (10.1101/2025.09.09.675200) and has since been published** in RSC Chemical Biology (PMID 41142648, DOI 10.1039/d5cb00233h). Abstract fetched and read back by the coordinator; full text not read, so the claim is graded strong rather than established. **The rejection recorded in this entry is unaffected**: it concerns the YEATS domains of the WILD-TYPE proteins, and the KMT2A::MLLT3 fusion contains no YEATS domain in 99.5% of patients, so the paper is off-beat here by construction rather than by any judgement of its quality - and that was true when it was a preprint and remains true now.
Evidence that argues against this (1)
- If YEATS inhibition acts partly through wild-type AF9 or ENL in a t(9;11) blast, then a YEATS inhibitor could still have activity in that disease without the fusion having a reader - which would make this preprint on-beat after all, and is the reason it is recorded rather than dropped. Yang Y et al. 2024
- E4moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
Structural studies of the intrinsically disordered AF9 AHD in complex with peptidomimetic inhibitors have been reported.
Structural studies of intrinsically disordered MLL-fusion protein AF9 in complex with peptidomimetic inhibitors. · Yang Y, Ahmad E, et al. · Protein Sci 2024What this evidence cannot show
Record read, full text not retrieved. Structures of ligand complexes without accompanying cellular or in vivo data; this beat's druggability position turns on paralogue cross-reactivity rather than on ligand availability.
Evidence that argues against this (1)
- If any of these peptidomimetics discriminates AF9 from ENL, this beat's central druggability objection would weaken, so the compounds' selectivity profile is the thing a chemistry beat should extract. Sharma S et al. 2026
- E5moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
A transgenic zebrafish leukaemia model driven by KMT2A::MLLT3 has been reported.
A transgenic zebrafish leukemia model driven by KMT2A::MLLT3 (MLL-AF9). · Saberi M, Delfi O, et al. · Leukemia 2026What this evidence cannot show
Record read, full text not retrieved. A transgene's fusion architecture is chosen by the authors, so the model cannot speak to human breakpoint distribution, which is this beat's subject.
Evidence that argues against this (1)
- If the construct includes the AF9 YEATS domain, the model would be architecturally unlike 99.5% of patients - which would make it informative for the add-back question and misleading as a model of the disease, and either way the construct boundary is worth extracting. Meyer C et al. 2023
- E6moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
KRAS mutations modelled in KMT2A::MLLT3 acute myeloid leukaemia promote leukaemic progression and transcriptional rewiring.
Modeling KRAS mutations in KMT2A::MLLT3 acute myeloid leukemia promotes leukemic progression and transcriptional rewiring. · Esparza N, Defrêne J, et al. · Leukemia 2026What this evidence cannot show
Record read, full text not retrieved. Out of this beat's scope, but directly relevant to the observation that three of the ten patients behind the t(9;11) cell-line panel carry an activating RAS-pathway lesion.
Evidence that argues against this (1)
- If RAS co-mutation rewires the KMT2A::MLLT3 transcriptional programme, then THP-1 (NRAS G12D), NOMO-1 (KRAS G13D) and YCU-AML2 (KRAS G12A) are not measuring the fusion programme alone, which would affect a large share of the published work on this fusion. Esparza N et al. 2026
- E7strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
The founding menin report has no PMC record: a Europe PMC core-record lookup for PMID 16239140 returns pmcid none and isOpenAccess N, so routes 2 to 4 of this project's readability test have no target and the paper was used from its abstract only.
The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis. · Yokoyama A, Somervaille TC, Smith KS, et al. · Cell 2005What this evidence cannot show
This is a statement about open-access status on 2026-09-20, not about the paper's content. Institutional or publisher access would resolve it; this project's routes do not include either.
Evidence that argues against this (1)
- A paper that is not open access is not unreadable in the register's sense, and treating the two as equivalent would inflate this project's unreadable count with items that a subscription would solve. Yokoyama A et al. 2005
- E8strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
The Europe PMC supplementaryFiles endpoint for PMC11687943 returns HTTP 200 and a valid zip archive of 1,261,425 bytes containing only six figure files and no Data Supplement Table S3, which is where AUGMENT-101's partner-stratified efficacy analysis is reported to sit.
Menin Inhibition With Revumenib for KMT2A-Rearranged Relapsed or Refractory Acute Leukemia (AUGMENT-101). · Issa GC, Aldoss I, Thirman MJ, et al. · J Clin Oncol 2025What this evidence cannot show
Tested once, on 2026-09-20. A publisher can add supplementary material to a PMC deposit later, so this is a dated negative rather than a permanent one.
Evidence that argues against this (1)
- The same endpoint has previously returned a well-formed zip containing a zero-byte file, so a zip that contains something is not evidence that it contains everything; only the absence of a file named like the supplement is being asserted here. Issa GC et al. 2025
SDEY-AML1 is a twelfth line the accession sweep could not see
re-tested the supplementary route; Table S3 still absent
not open access is not unreadable; PMID 16239140 has no PMCID at all
the bounded negatives behind the localisation entry
the query that found it, and the simulation that disagrees with it