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Analysismoderate confidence 3 of 5: One strong study, or several smaller consistent ones.Q126-the-partners-named-but-never-written

Do NUP98's seven fusions resemble each other more than they resemble their partners' other fusions? The test cannot be run for six of them, and the seventh resembles neither side

also called the NUP98 shared-address test · cross-partner scan

NUP98 is stuck onto seven different partner genes in seven different leukaemia fusions, which makes it the best case for asking whether a fusion family is really about the shared piece. The answer turned out to be that the question cannot be asked properly here - six of the seven partners appear in no other fusion this project has written - and the one partner that can be compared behaves unlike both groups.

The same thing, for a scientist

**A pre-specified test, run, and returning a negative.** `concept-low-grade-ess-is-a-nua4-to-polycomb-fusion-family` argues that a fusion family can be defined by **the complexes its halves belong to** rather than by a shared gene, and that the analogue of a KMT2A fusion might be **any address-to-effector fusion**. NUP98 is the sharpest available test - one address donated to seven effectors in this corpus - and the prediction is that the seven should resemble each other in mechanism **more** than each resembles its own 3' partner's other fusions. **Result 1. The comparison set is empty for six of seven.** Across all 52 fusion entries in this corpus, only three genes appear as a 3' partner in more than one entry (KMT2A 4, MLLT10 2, NUTM1 2). Of NUP98's seven partners, **only KMT2A has other fusions here** - `fusion-ldb1-kmt2a`, `fusion-vim-kmt2a`, `fusion-yap1-kmt2a-yap1`. DDX10, HOXA9, HOXD13, KDM5A, NSD1 and TOP1 have none [E1]. **Result 2. The one runnable case is an outlier on both sides.** `fusion-nup98-kmt2a` records blasts with **very low** Hoxa5/a7/a9/a10, Meis1, Eya1 and Pbx3 against normal marrow or KMT2A-ENL/KMT2A-AF9 blasts, and resistance to MI-2-2 at 3-12 uM and to JQ1 - because the inversion deletes KMT2A exon 1 and with it the menin-binding motif [E2]. It looks like neither the NUP98 family (HOXA/MEIS1-high, menin-sensitive) nor the KMT2A family (menin-dependent). **Result 3. The axis on which all seven cohere is non-discriminating by construction.** A keyword scan finds condensate/FG-repeat language in **7 of 7** NUP98 fusion entries and **0 of 4** non-NUP98 comparators (the fifth at 2), with no length confound [E1]. But the FG module **is** NUP98, so a plain named-gene family predicts that split exactly as strongly as a complex-defined family does. **The one axis that separates the sets perfectly is the one on which the two competing framings agree** [E1]. **Result 4, and it is the one that actually bears on the claim.** This corpus's own `mechanism-nup98-fusion-menin-mll1-dependency` records that NUP98-fusion menin sensitivity is **partner-graded** - about a six-fold IC50 spread, one of three PDX refractory, NUP98::KMT2A resistant outright - and that the load-bearing downstream node is MEIS1 rather than HOXA, because NUP98-HOXD13 cells lose no Hoxa occupancy at all [E3]. **A dependency that varies across the seven is evidence against the strong form of 'the seven resemble each other most.'** **Verdict: negative, and reported as one.** Q123's framing is not refuted - nothing here touches the ESS biochemistry it rests on - but NUP98 does not supply the support this beat hoped to find, and the sharpest available test came back empty.

Go deeper
Why the empty comparison set is itself the most useful output

The brief expected a scoreable comparison. What the scan found first is that this corpus is organised around 5' donors and almost never sees a 3' partner twice: 52 fusion entries, and exactly three genes recur as a 3' partner 1.

That is a standing limit on the PI's fifth dimension, not a defect of this beat. 'The analogous biology in other fusion families' has been pursued here by comparing named-gene families - the KMT2A family, the NUP98 family, the ETV6 family - and those are all 5'-donor families. A comparison that needs a shared 3' partner has almost no material to work with, and nobody had noticed because nobody had counted.

What this does NOT show. It is a statement about this corpus, not about the literature. DDX10, HOXA9, HOXD13, KDM5A, NSD1 and TOP1 may each appear in other fusions that this graph has not written; no PubMed query was run to bound that and none is claimed. Establishing which of the six are genuinely partner-unique and which are merely unwritten is a cheap, well-defined next beat, and it is the prerequisite for ever running this test properly.

The instrument, and the one place it would have inverted the answer

The scan counts regex hits over the whole serialised JSON of each entry on four axes - HOXA programme, menin dependence, condensate/FG, DOT1L/H3K79 - and the full table is in analyses/q126-the-partners-named-but-never-written/nup98-shared-address-cross-partner-scan.json.

It measures what this corpus's beats wrote, not biology, so only the categorical zero/non-zero pattern is used and the magnitudes are discarded. The length control is stated because it is the obvious confound and it does not fire: the non-NUP98 comparators run 17,469-37,231 characters against the NUP98 entries' 15,242-49,672, so their zeros are not short-entry artefacts 1.

And the specific failure this instrument would have produced if trusted. fusion-nup98-kmt2a scores 36 on the menin axis - the second-highest of the seven - and the content of the entry is that the fusion is menin-inhibitor RESISTANT 2. A count of the string 'menin' cannot see the sign of a claim, and on the single most informative entry in the set it would have inverted it. That is why Result 2 was read from the entry's prose and not taken from the table, and it is rule 92's instruction applied before rather than after the verdict.

Facts and figures
scriptanalyses/q126-the-partners-named-but-never-written/nup98-shared-address-cross-partner-scan.json
statusrun
result summaryNEGATIVE on the proposed test. Six of seven NUP98 partners have an empty comparison set in this corpus; the seventh (KMT2A) resembles neither family; the only axis on which all seven cohere is the FG/condensate module, which both competing framings predict equally and which therefore carries no discriminating information; and the corpus's own best-evidenced cross-partner mechanism, menin-MLL1 dependency, is explicitly partner-graded, which cuts against the strong form of the claim.
pre specifiedThe prediction was written in the dispatch brief before the scan was run, together with the instruction not to force it. The scan was run once and its first result - the empty comparison set - was not the result the prediction anticipated and is reported first.
criterion informativeness clauseCycle 86's rule asks what result would make a criterion itself uninformative. For this test it is: IF the axis that separates NUP98 fusions from non-NUP98 fusions is an axis the shared GENE supplies, then a clean separation confirms only that NUP98 fusions contain NUP98, and the criterion is uninformative. THAT IS WHAT HAPPENED - the perfect 7/7-versus-0/4 split is on the FG/condensate axis - so the separation is reported as non-discriminating rather than as a pass.
inputs
[
  "all 52 fusion entries in data/graph/nodes",
  "fusion-nup98-kmt2a",
  "mechanism-nup98-fusion-menin-mll1-dependency",
  "concept-low-grade-ess-is-a-nua4-to-polycomb-fusion-family"
]
what would make it runnable
[
  "Establish, by literature search, which of DDX10, HOXA9, HOXD13, KDM5A, NSD1 and TOP1 genuinely have no other fusion partner and which are merely unwritten here. This was NOT done and is the prerequisite.",
  "Replace keyword counts with a fixed mechanism-feature schema in each fusion entry's data block.",
  "Use the per-partner menin IC50 spread as the quantitative axis; it exists and was not pulled in this beat."
]
corpus snapshot
{
  "node_files": 2374,
  "fusion_entries": 52,
  "date": "2026-09-23"
}
How this could bite us back
  • The most likely misuse of this entry is to read 'NUP98 fusions all have condensates and other fusions do not' as a therapeutic rationale for an FG-repeat- or condensate-directed agent. The 7-of-7 versus 0-of-4 split is a fact about which gene each fusion contains, not a demonstration that condensation is the shared vulnerability, and gene-nup98 records that the same FG region carries wild-type NUP98's own chromatin functions in normal haematopoietic progenitors.
  • The second likely misuse is to read the NUP98::KMT2A outlier as licensing a general claim that menin inhibition fails in NUP98 disease. It does not: the corpus records menin sensitivity across the rest of the family and eviction of the fusion protein itself. NUP98::KMT2A is one fusion, two patients, one mouse and a micromolar tool compound.
  • And the honest structural risk: an analysis whose headline is 'the test cannot be run' can be used to justify not running the follow-up. The follow-up here is cheap and specific - a literature search for other fusions of six named genes - and the value of this entry is entirely contingent on somebody doing it.
Still open
  1. Which of DDX10, HOXA9, HOXD13, KDM5A, NSD1 and TOP1 actually has no other fusion partner in the published literature? This scan establishes only that this corpus has none. The answer decides whether the empty comparison set is a fact about fusion biology - 3' partners genuinely do not recur - or a curation gap, and those are opposite conclusions drawn from the same table.
  2. Is 3'-partner non-recurrence a real property of oncogenic fusions? If a 5' address is promiscuous and a 3' effector is not, that is a structural claim about how fusion oncogenes are built, and it would be independently interesting. Nothing in this beat tests it; the observation that only three genes recur as 3' partners across 52 entries is the prompt, not the answer.
  3. Would the per-partner menin IC50 spread, scored properly, discriminate the two framings? A six-fold spread across the NUP98 family is a quantitative comparator this corpus already holds. If the spread within the NUP98 family is smaller than the spread between families, the shared-address framing gains support; if not, it does not. This beat did not pull the numbers and states no expectation.
  4. Does the empty-comparison-set result generalise to ETV6 and TCF3, the two other multi-fusion 5' donors here? Both have exactly two entries, so the same test would be even weaker for them - but running it would establish whether NUP98 is unusually well covered or unusually badly compared.
Every source behind this entry (3)
  1. E1strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.dataset

    Across the 52 fusion entries in this corpus, only KMT2A (4), MLLT10 (2) and NUTM1 (2) appear as a 3' partner in more than one entry; of NUP98's seven 3' partners only KMT2A has other fusions here (fusion-ldb1-kmt2a, fusion-vim-kmt2a, fusion-yap1-kmt2a-yap1). Condensate/FG-repeat language appears in 7 of 7 NUP98 fusion entries (4-75 hits) and 0 of 4 non-NUP98 comparators with the fifth at 2, with comparator entry lengths (17,469-37,231 characters) inside the NUP98 range (15,242-49,672).

    Q126 cross-partner scan over all fusion entries in this corpus: 3'-partner recurrence and four-axis keyword presence · Computed by this beat, 2026-09-23 · analyses/q126-the-partners-named-but-never-written/nup98-shared-address-cross-partner-scan.json 2026
    What this evidence cannot show

    SELF-MEASUREMENT OF THIS CORPUS, computed 2026-09-23 over 2,374 node files and 52 fusion entries; it will drift as entries are added and should be re-run rather than quoted later (scripts/check-analysis-staleness.py exists for exactly this). The regex counts were NOT hand-validated item by item; only the categorical zero/non-zero split is used and the magnitudes are explicitly not interpreted. Partner recurrence is read from data.gene5/data.gene3, so a fusion entry that omits those fields would be invisible to the scan - no entry was found to omit them, but that was not separately audited. Above all: this bounds THIS CORPUS and not the literature. Whether DDX10, HOXA9, HOXD13, KDM5A, NSD1 or TOP1 has other fusions in the published literature was NOT searched.

    Evidence that argues against this (1)
    • Two readings of the empty comparison set are equally consistent with the data and the entry cannot distinguish them. It may be that 3' effectors genuinely do not recur across fusions - an interesting structural claim - or that this corpus simply has not written the other fusions of those six genes, in which case the finding is about curation and says nothing about biology. There is also a naming hazard: the same effector appearing under a different symbol in another entry would be invisible to a gene5/gene3 string match, and no alias resolution was performed.
  2. E2strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.dataset

    NUP98::KMT2A arises from inv(11)(p15q23) and deletes KMT2A exon 1, removing the menin-binding motif at Q03164 residues 6-25 and the LEDGF IBM1/IBM2 sites; in an inducible transgenic mouse the leukaemic blasts express very low Hoxa5/a7/a9/a10, Meis1, Eya1 and Pbx3 relative to normal marrow or to KMT2A-ENL/KMT2A-AF9 blasts, matching low HOXA in the two reported patients, and the cells are resistant to MI-2-2 at 3-12 uM and to JQ1 at 0.05-0.5 uM, concentrations at which KMT2A-AF9 cells arrest.

    fusion-nup98-kmt2a, this corpus (entry read in full this session; its own primary citations are E1/E2/E5 of that entry and were not independently re-fetched here) · Oncofusion Knowledge Graph, comparative beat · data/graph/nodes/comparative/fusion-nup98-kmt2a.json 2026
    What this evidence cannot show

    THIS IS A CITATION OF ANOTHER ENTRY IN THIS GRAPH, NOT OF A PAPER, and it is marked as such deliberately. The underlying primary sources are cited inside fusion-nup98-kmt2a and this beat did NOT re-fetch them, so the strength of Result 2 is inherited from that entry rather than established here. Two patients and one mouse model: the clinical n is 2. The resistance measurement uses MI-2-2, a micromolar tool compound, and that entry's own open questions already name the genetic MEN1-deletion arm as the experiment that would make the resistance claim decisive - so Result 2 rests on a weak reagent, which this project has been burned by before.

    Evidence that argues against this (1)
    • This is a citation of another entry in this graph rather than of a paper, so its strength is inherited and not established here, and the underlying clinical n is two patients. The resistance measurement uses MI-2-2 at 3-12 uM, a micromolar tool compound - and this project has already published a negative headline that turned out to be a fact about a weak tool compound rather than about the biology. A genetic MEN1-deletion arm, which fusion-nup98-kmt2a's own open questions call for, could reverse Result 2 entirely.
  3. E3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.dataset

    NUP98-fusion menin-MLL1 dependency is partner-graded rather than uniform: roughly a six-fold IC50 spread across partners, one of three PDX refractory, and NUP98::KMT2A resistant outright; and the load-bearing downstream node is MEIS1 rather than HOXA, because MEIS1 re-expression abrogates sensitivity while NUP98-HOXD13 cells lose no Hoxa occupancy at all.

    mechanism-nup98-fusion-menin-mll1-dependency, this corpus (read in full this session) · Oncofusion Knowledge Graph, comparative beat · data/graph/nodes/comparative/mechanism-nup98-fusion-menin-mll1-dependency.json 2026
    What this evidence cannot show

    Again a citation of another entry rather than of a paper; that entry's own E1/E5/E6 carry the primary sources and were not re-fetched here. This is the axis that WOULD discriminate the two framings, and the reason it is quoted rather than recomputed is that recomputing it needs per-partner IC50s that this beat did not pull. Anyone strengthening this analysis should start there, because a six-fold spread with named partners is a real quantitative comparator and everything else in this scan is categorical.

    Evidence that argues against this (1)
    • A partner-graded dependency does not cleanly refute the shared-address framing, and Result 4 overstates its force. A shared mechanism modulated by partner-specific co-lesions - FLT3-ITD accompanies NUP98::NSD1 in most patients, and this corpus holds an entry on that confound - would also produce an IC50 spread across partners. Grading is therefore compatible with one shared mechanism plus context, and distinguishing that from seven partner-specific mechanisms needs the co-lesions controlled, which no published comparison in this beat's reading does.
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