Menin has never been tested against SET::NUP214 - a bounded absence in three independent registers: literature, cell-line dependency data, and the founding paper's own blots

Bounded absence. Query translations were read back on every zero; PubMed expands `menin` to 'men1 protein human'[Supplementary Concept] OR 'menin'[All Fields] OR 'menin s'[All Fields], so the clause is not a bare string match. Bound: titles, abstracts and MeSH only - not full text, not figures, not supplementary material, not conference abstracts, not preprints. Also note the standing registry trap that MENIN is an author surname, which inflates rather than deflates a count and is therefore not a risk to a zero.

• A zero of exactly this shape, with exactly these controls, was FALSE as a conclusion in this same beat. `SET-NUP214 AND (H3K79 OR "H3-K79" OR "K79" OR "lysine 79")` returns 0 with a clean positive control, and yet PMID 18299449 contains an H3K79 dimethylation ChIP across five HOXA promoters - invisible because the measurement is in a figure and the abstract never names the mark. The menin zeros above are bounded by abstracts, not by papers, and a menin blot in a supplementary figure would not appear in any of them. Van Vlierberghe P et al. 2008

Abstract-level title-check of the single hit, which is the standard this brief requires before recording a count as a result. The classification as incidental rests on the abstract; the full text was not read, so a buried menin-plus-NUP214 statement inside the review cannot be excluded - but a review would not be primary evidence in any case.

• PUBLISHED CONFLICTING RESULT. The query token, not the biology, is what returns one record. The premise this absence is used to support - that a KMT2A-free nucleoporin fusion is outside the menin axis - has been tested directly in the other nucleoporin-fusion family and came out the opposite way: in murine NUP98-HOXA9 and NUP98-JARID1A lines the menin-MLL1 inhibitor VTP50469 is active at an IC50 the authors report as similar to KMT2A-rearranged and NPM1c cells, MLL1 and the NUP98 fusion protein are both evicted from chromatin, and VTP50469 prolongs survival in NUP98-NSD1 and NUP98-JARID1A patient-derived xenografts. So a NUP214-scoped menin query returning 1 bounds the string NUP214 and bounds nothing about whether a nucleoporin fusion can be menin-dependent. Heikamp EB et al. 2022

Fetched 2026-09-20. The DepMap release version is NOT stated in the API response, so the release is unverified - the same limitation this project's existing DepMap analyses record. The absence of LOUCY was checked two ways: by its DepMap id ACH-000104 (resolved from Cellosaurus CVCL_1380) and by cell-line name across all 1,258 screens. The eight T-lymphoblastic MEN1 values are reported here only to show the comparator set exists and is small; they are RAW gene effects over a mixed panel and are NOT a lineage-split selectivity claim, which this fetch is not powered to make.

• METHODOLOGICAL DEFEATER, and it applies to the instrument rather than to the fetch. A pooled CRISPR gene-effect value on MEN1 is a poor readout for menin dependence in this disease, and this beat's own sibling item measures why: MEN1's mean Chronos gene effect across 1,208 lines is -0.36 and it is NOT flagged essential - in a graph whose central hypothesis is a menin dependency that revumenib converts into a 22.8% CR+CRh rate (95% CI 12.7 to 35.8) in centrally confirmed KMT2A-rearranged relapsed/refractory acute leukaemia in the AUGMENT-101 phase 2. A register that fails to register the dependency in the arm where it is clinically demonstrated cannot bound it in the arm where it is untested, so the absence of LOUCY and MEGAL from DepMap is a weaker fact than it reads as. Issa GC et al. 2025

A string search of the flattened full text obtained via the PMC HTML route (PMC2343598, 68,564 characters after tag-strip-then-unescape per rule 61). It bounds this paper only. In 2008 the menin-KMT2A interaction was known but no menin inhibitor existed, so the absence is unsurprising and carries little weight as evidence that the authors considered and rejected the idea.

• THE SOURCE'S OWN SCOPE IS THE OBJECTION, and a later paper says why it matters. The 2008 blot list is evidence about what the authors looked for under their own model, in which CRM1 and DOT1L supplied the mechanism and menin had nowhere to enter. The route by which menin could enter was proposed thirteen years later and is INDIRECT: SET-NUP214 interacts with MLL via the SET acidic region of the fusion, and the two cooperatively enhance HOXA10 promoter activity, with neither region alone sufficient. Menin binds wild-type MLL1, not the fusion - so no anti-menin blot on a SET-NUP214 immunoprecipitate would have been designed in 2008 even by authors who had considered the idea, and the absence of that blot is close to uninformative about the hypothesis it is cited against. Cigdem S et al. 2021