Q50 enumeration: every query this beat ran, every zero it recorded with its bound, and the papers it read and did not use
also called Q50 bounded absences · PRC1.1-MYC enumeration
A record of exactly what was searched, what came back empty, and what was deliberately left out - so that someone repeating this work next year repeats the decisions and not just the searches.
The same thing, for a scientist
The audit trail for the Q50 beat, held to brief rule 67 (a zero gets a date, the exact query string, the tool, and a positive control through the identical code path) and to the cycle-48 bounded-rejection standard (record what was read and not used). Seven counted absences, each with its positive control; four bounded rejections; three corrections to premises, two of them to this beat's own dispatch brief. **The headline numbers:** `\bBENC\b` appears in **0** of 1,510 pre-existing node files, confirming the coordinator's pre-dispatch correction; `\bH2AK119ub` in **15** with no entry of its own; `\bTRIM27\b` in **1**; `PRT4165` in **0**. In the literature, the entire published intersection of PRC1.1 subunit symbols and menin-inhibitor terms is **one paper**, and the entire published intersection of RING1B/RNF2 with MYC and enhancer is **two records**, one of which is the inv(16) study and the other a mouse embryonic-stem-cell paper about the aryl hydrocarbon receptor. **The most consequential methodological finding is that brief rule 67 does not protect a counted absence about a noncoding element**, because the instrument works perfectly while the name list is incomplete - written up as `concept-a-noncoding-element-has-no-symbol-and-three-names`.
Counted absences, with bounds
All run 2026-09-20 through NCBI E-utilities esearch db=pubmed, querytranslation read back on each. Positive control means a query of identical construction that returns results.
| # | claim | query | count | on-topic | positive control |
|---|---|---|---|---|---|
| 1 | No paper titles a study on a menin inhibitor and MYC | (revumenib OR "menin inhibitor" OR "menin inhibitors" OR VTP-50469 OR SNDX-5613 OR ziftomenib)[tiab] AND MYC[ti] | 1 | 0 | same clause with MYC[tiab] returns 13 |
| 2 | The whole published PRC1.1 x menin-inhibitor literature is one paper | (RING1B OR RNF2 OR PCGF1 OR BCOR OR KDM2B)[tiab] AND (revumenib OR "menin inhibitor" OR "menin inhibitors" OR SNDX-5613 OR VTP-50469)[tiab] | 1 | 1 | each clause alone returns hundreds |
| 3 | Nobody has measured RING1B/RNF2 at MYC enhancers outside inv(16) | (RING1B OR RNF2)[tiab] AND MYC[tiab] AND enhancer[tiab] | 2 | 1 | the query returns the inv(16) paper - it can return a one |
| 4 | RING1B/RNF2 has almost no KMT2A literature | (RING1B OR RNF2)[tiab] AND (MLL OR KMT2A)[tiab] | 5 | 2 | title-checked; complex form run per rule 64 |
| 5 | No BENC data exist for infant or lymphoblastic leukaemia | BENC[tiab] AND (infant OR "acute lymphoblastic")[tiab] | 1 | 1 (cell lines) | the query returns a record |
| 6 | 'BDME' retrieves nothing about this element | BDME[tiab] | 14 | 0 | the query returns 14 records, all unrelated |
| 7 | The spelled-out enhancer name is unreachable | "BRD4-dependent MYC enhancer"[tiab] OR "BRD4-mediated MYC enhancer"[tiab] | 0 | 0 | "blood enhancer cluster"[tiab] returns 3 - the phrase-search instrument works |
All seven are bounded by their symbol and phrase lists, not by the literature. Rule 64 applies throughout: a paper framing a result at the level of 'Polycomb', 'PRC1' or 'the menin-MLL interaction' without these tokens is invisible to every query above.
Graph counts, with method
Word-boundary regex over all 1,510 node JSON files existing before this beat, run 2026-09-20. The method matters: the dispatch brief for this beat records that a substring search for benc suggested 79 entries and the word-boundary count is zero.
| token | entries | note |
|---|---|---|
\bBENC\b | 0 | and blood enhancer cluster also 0 |
\bH2AK119ub | 15 | no entry of its own until mark-h2ak119ub |
PRC1\.1 | 56 | the beat's brief said 56; confirmed |
\bRING1B\b | 7 | the brief said 7; confirmed |
\bRING1A\b | 6 | |
\bRNF2\b | 6 | |
\bUSP7\b | 3 | none of them an entry about USP7 |
\bTRIM27\b | 1 | in protein-prc1-1-complex only, in passing |
PRT4165 | 0 | the only PRC1 catalytic chemistry that exists |
XL177A | 0 | |
29958106 (the inv(16) paper) | 2 | cited as a counter-evidence note, never as a mechanism |
41634341 (the 2026 PRC1.1 paper) | 14 | |
transcriptional memory | 15 | all tracing to 41634341, all in the inducible sense |
Bounded rejections - read, judged off-beat, recorded so the decision is not repeated blind
Per the cycle-48 standard: papers a reader would reasonably expect to be cited here and are not.
- PMID 24316986 (Ko CI et al., Stem Cell Res 2014, Pluripotency factors and Polycomb Group proteins repress aryl hydrocarbon receptor expression in murine embryonic stem cells). One of only two hits for RING1B/RNF2 with MYC and enhancer. Read: it is a mouse embryonic-stem-cell study of AhR regulation with no leukaemia and no MYC-enhancer content; the co-occurrence is incidental. Cited once, as the other half of a counted absence, never as evidence. Would change my mind: a leukaemia follow-up from the same axis.
- PMID 33849069 (bimodal regulation of PRC2 by USP7 in tumorigenesis) and PMID 37196079 (USP7 represses lineage differentiation genes in mouse ES cells). Both on the USP7-Polycomb axis and both PRC2- or ES-cell-centred; dropped because this beat's USP7 entry is deliberately scoped to ncPRC1 in a malignant haematopoietic context and adding PRC2-side USP7 biology would blur the PRC1/PRC2 distinction that
mark-h2ak119ubexists to sharpen. Would change my mind: a PRC2-side USP7 result in KMT2A-rearranged cells. - PMID 21125401 (EZH2/RING1/BMI1 overexpression in MDS) was used but graded
weak, and the reasoning is recorded here as well as ingene-ring1: it is a transcript-level association against a non-clonal-cytopenia comparator, confounded by blast fraction, with no KMT2A subgroup. It is the only RING1-specific haematological result located and it carries almost no weight. - PMID 40361117 (RYBP promotes HIV-1 latency through promoting H2AK119ub) and the wider RYBP literature. Not used: a different variant PRC1 flavour in a virological setting. But it flags a real gap outside this beat's folder -
gene-rnf2listsgene-rybpamong its complex partners and no such node exists, which is reported rather than fixed.
A laboratory whose work was considered and not cited: the Hendzel group's PRC1/DNA-damage programme, from which PRT4165 comes. Their axis is genome stability rather than transcriptional repression; the compound is used here and the DNA-repair biology is deliberately out of scope, though it is the reason the compound's cellular phenotypes are ambiguous.
Corrections to premises, including two in this beat's own brief
1. The brief's premise that PMID 41634341 is unwritten here is wrong. The dispatch brief presents the 2026 PRC1.1 paper as the beat's opening finding. It is already written up in mechanism-dot1l-prc1-antagonism (Q41, histone-marks folder), cited in 14 entries, and protein-prc1-1-complex already enumerates PRC1.1 subunit by subunit with 13 evidence items. The genuinely unwritten territory was elsewhere - the mark, the enhancer, and the inv(16) analogy - and this beat redirected accordingly. The brief's own standing instruction covers this: the literature wins and the agent says so.
2. The brief's premise that RING1B is named in 'only 7' entries is correct but incomplete as a gap statement. The gap is not the count; it is that gene-ring1 - a different gene - did not exist, and that the substring RING1 does not distinguish them.
3. The brief's BENC correction is confirmed. Word-boundary count zero, as stated. This beat re-ran it independently rather than quoting it, per the brief's own instruction that an inventory must be checked against disk rather than quoted from a document.
| script | no script - queries run interactively through NCBI E-utilities esearch/efetch and the UniProt REST API; every query string is recorded verbatim in this entry |
|---|---|
| status | run |
| date | 2026-09-20 |
| methodological finding | brief rule 67's positive control does not protect a counted absence about a noncoding element, because the instrument works while the NAME LIST is incomplete - see concept-a-noncoding-element-has-no-symbol-and-three-names |
| result summary | Seven bounded absences, four bounded rejections, three premise corrections, two self-caught DOI errors. The beat's substantive output is the mark (mark-h2ak119ub), the enhancer (noncoding-benc-myc-enhancer-cluster), the inv(16) analogy and its hypothesis/experiment pair, and one new class of identifier trap. |
inputs
[ "NCBI E-utilities esearch db=pubmed (querytranslation read back on every query)", "NCBI E-utilities efetch db=pubmed rettype=abstract retmode=xml (titles via itertext, DOIs from ./PubmedData/ArticleIdList only)", "Europe PMC core records for PMCID resolution", "PMC HTML route for full text (tags stripped before entities unescaped)", "UniProt REST gene_exact queries with gene_primary and length in fields", "word-boundary regex over 1,510 pre-existing node JSON files" ]
counted absences — the numbers behind the chart
[
{
"id": 1,
"claim": "no paper titles a study on a menin inhibitor and MYC",
"query": "(revumenib OR \"menin inhibitor\" OR \"menin inhibitors\" OR VTP-50469 OR SNDX-5613 OR ziftomenib)[tiab] AND MYC[ti]",
"count": 1,
"on_topic": 0,
"positive_control": "same clause with MYC[tiab] returns 13"
},
{
"id": 2,
"claim": "the entire published PRC1.1 x menin-inhibitor literature is one paper",
"query": "(RING1B OR RNF2 OR PCGF1 OR BCOR OR KDM2B)[tiab] AND (revumenib OR \"menin inhibitor\" OR \"menin inhibitors\" OR SNDX-5613 OR VTP-50469)[tiab]",
"count": 1,
"on_topic": 1,
"positive_control": "each clause alone returns hundreds"
},
{
"id": 3,
"claim": "no RING1B/RNF2 measurement at MYC enhancers outside inv(16)",
"query": "(RING1B OR RNF2)[tiab] AND MYC[tiab] AND enhancer[tiab]",
"count": 2,
"on_topic": 1,
"positive_control": "the query returns the inv(16) paper"
},
{
"id": 4,
"claim": "RING1B/RNF2 has almost no KMT2A literature",
"query": "(RING1B OR RNF2)[tiab] AND (MLL OR KMT2A)[tiab]",
"count": 5,
"on_topic": 2,
"positive_control": "returns records; title-checked"
},
{
"id": 5,
"claim": "no BENC data for infant or lymphoblastic leukaemia",
"query": "BENC[tiab] AND (infant OR \"acute lymphoblastic\")[tiab]",
"count": 1,
"on_topic": 1,
"note": "the one record is cell lines, framed by its authors as acquired in vitro"
},
{
"id": 6,
"claim": "'BDME' retrieves nothing about this element",
"query": "BDME[tiab]",
"count": 14,
"on_topic": 0,
"note": "Boswellia dalzielii methanol extract, bipolar disorder manic episode, breast duct microendoscopy, bis-demethoxycurcumin, zinc transport in wheat"
},
{
"id": 7,
"claim": "the spelled-out enhancer name is unreachable",
"query": "\"BRD4-dependent MYC enhancer\"[tiab] OR \"BRD4-mediated MYC enhancer\"[tiab]",
"count": 0,
"on_topic": 0,
"positive_control": "\"blood enhancer cluster\"[tiab] returns 3 - phrase search works"
}
]graph word boundary counts over 1510 pre existing files — the numbers behind the chart
{
"BENC": 0,
"blood enhancer cluster": 0,
"H2AK119ub": 15,
"PRC1.1": 56,
"RING1B": 7,
"RING1A": 6,
"RNF2": 6,
"USP7": 3,
"TRIM27": 1,
"PRT4165": 0,
"XL177A": 0,
"PMID 29958106": 2,
"PMID 41634341": 14,
"transcriptional memory": 15
}premise corrections
[ "the dispatch brief presents PMID 41634341 as this beat's opening finding; it is already written up in mechanism-dot1l-prc1-antagonism and cited in 14 entries, and protein-prc1-1-complex already enumerates PRC1.1 subunit by subunit", "the brief's RING1B count of 7 is correct; the gap it points at is not the count but the absence of gene-ring1 and the substring collision between RING1 and RING1B", "the brief's BENC correction is confirmed by independent re-measurement rather than quoted" ]
identifier errors caught in this beat
[ "DOI for PMID 24316986 written as 10.1016/j.scr.2013.11.006 by inference; the fetched record gives 10.1016/j.scr.2013.11.007 - corrected before hand-back", "DOI for PMID 16172399 written as 10.1073/pnas.0501785102 by inference; the fetched record gives 10.1073/pnas.0502330102 - corrected before hand-back" ]
- Every absence recorded here is bounded by a symbol or phrase list and none is a statement about the literature. Quoting any of these counts without its bound would reproduce exactly the error this entry exists to prevent.
- The bounded rejections are judgements made from abstracts, not full texts, and a rejection recorded confidently reads the same as one made carefully.
- The methodological finding about noncoding elements undermines existing absence claims in this graph without repairing them, which creates work rather than closing it.
- How many existing counted absences in this graph concern noncoding objects and are scoped to a single name? An audit would size the exposure created by the finding in concept-a-noncoding-element-has-no-symbol-and-three-names.
- Should the graph's absence-checking scripts be extended to flag any absence claim whose subject is an enhancer, lncRNA locus or CpG island as requiring a name list in its caveat?
- Two DOIs were written by inference in this beat and both were wrong. Would a pre-commit check that every DOI in a new file was fetched in the same session - rather than only comparing it to PubMed afterwards - catch the class earlier?
- E1strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
The single paper constituting the entire published intersection of PRC1.1 subunit symbols and menin-inhibitor terms on PubMed as of 2026-09-20: loss of PRC1.1 subunits such as PCGF1 or BCOR leads to menin-inhibitor resistance by epigenetic reactivation of non-canonical menin targets including MYC.
Epigenetic regulation of noncanonical menin targets modulates menin inhibitor response in acute myeloid leukemia. · Zhou X, Zhang L, Aryal S, Veasey V, Tajik A, Restelli C, et al. · Blood 2024What this evidence cannot show
The absence bound is symbol- and phrase-limited: five subunit symbols and five drug terms. A paper writing 'non-canonical PRC1' or 'Polycomb' without a subunit symbol, or naming a menin inhibitor by a compound code not on the list, would be invisible. Rule 64's complex form was run and returns records framed at complex level that these queries miss.
Evidence that argues against this (1)
- A second 2026 paper reaches the same axis from the DOT1L side and names PRC1.1 as the mediator of the response to BOTH menin and DOT1L inhibitors - so the intersection at concept level is larger than the intersection at symbol level, and a reader should not conclude from the count of one that only one laboratory works on this. Neville D et al. 2026
- E2strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
The only published report of a RING1B measurement at MYC enhancers in any fusion-oncoprotein leukaemia, and the positive control demonstrating the counted-absence query can return a result: in inv(16) AML, RING1B replaces BRG1 at three MYC distal enhancers under fusion-interface inhibition.
CBFbeta-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia · Pulikkan JA, Hegde M, Ahmad HM, Belaghzal H, Illendula A, Yu J, O'Hagan K, Ou J, Muller-Tidow C, Wolfe SA, Zhu LJ, Dekker J, Bushweller JH, Castilla LH · Cell 2018What this evidence cannot show
Read in full from PMC6211564 on 2026-09-20 via the PMC HTML route (tags stripped before entities unescaped, per brief rule 61). Its role here is dual - it is the substantive analogy and it is the positive control that makes absence #3 a measurement rather than a broken query.
Evidence that argues against this (1)
- The absence it bounds is narrower than it looks: the element in question has three names and only one of them is searchable, so a RING1B measurement described at 'BDME' or by coordinate would not appear in the query that this paper validates. The positive control proves the instrument works and does not prove the name list is complete. Bahr C et al. 2018
- E3moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
Bounded rejection, recorded so the decision is auditable: the only other record returned by the RING1B/RNF2 x MYC x enhancer query is a mouse embryonic-stem-cell study of aryl hydrocarbon receptor repression by pluripotency factors and Polycomb Group proteins, with no leukaemia and no MYC-enhancer content; the co-occurrence of the search terms is incidental.
Pluripotency factors and Polycomb Group proteins repress aryl hydrocarbon receptor expression in murine embryonic stem cells. · Ko CI, Wang Q, Fan Y, Xia Y, Puga A · Stem Cell Res 2014What this evidence cannot show
Judged off-beat from title and abstract only; the full text was not read. It is recorded as a bounded rejection rather than dismissed silently, per the cycle-48 standard. Title, authors and DOI taken from the fetched PubMed record on 2026-09-20 - the DOI initially written into this beat's analogy entry from inference was wrong by one digit and was corrected against the fetched record.
Evidence that argues against this (1)
- Polycomb biology in embryonic stem cells has repeatedly turned out to inform leukaemia - the PRC1-flavour taxonomy this graph uses was established in ES cells - so an ES-cell rejection is a judgement about this beat's scope and not a claim that the work is irrelevant. What would change it: a demonstration that the same regulatory logic operates at a MYC enhancer in a haematopoietic cell. Rossi A et al. 2016
the beat's methodological finding: rule 67's positive control does not protect an absence about a noncoding element
the count that motivated the entry: named in 15 entries, written in none
word-boundary count zero over 1,510 pre-existing node files, re-measured independently of the brief
the whole published PRC1.1 x menin-inhibitor symbol intersection is one paper
named once in the graph before this beat, in the PRC1.1 roster, with no entry of its own
PRT4165 and XL177A each named in zero pre-existing entries