AnalysisstrongQ30-cell-state

Cell-state enumeration: 23 queries, what was written, what was rejected and why — including an empirical confirmation that PubMed reads SEM as two journal names

also called cell-state beat enumeration · bounded rejection ledger for cell state · Q30 search record

This is the working record of how the cell-state entries were found: every search run, how many records each returned, which papers were read and set aside, and why. It exists so that someone repeating this work next year repeats the decisions as well as the searches.

The same thing, for a scientist

This graph had 24 `cell_type` entries and 8 `cell_state` entries when this beat opened, making cell state the thinnest category the PI named by name. This analysis records the 23 PubMed queries run on 2026-09-20, their counts, the query translations inspected, the nine states written, and the candidates **considered and rejected**, which is the half of a negative this project has documented as systematically missing. Two methodological results worth extracting. First, an **empirical confirmation of the SEM token trap**: `MLL-AF4 AND cell cycle AND (SEM cells OR t 4 11)` translated to `("struct equ modeling"[Journal] OR "scan electron microsc"[Journal] OR "sem"[All Fields])` — PubMed mapped the cell-line name onto two journal titles, exactly as the standing brief warns, and this is the translation string for the record. Second, a **real zero**: `(MLL OR KMT2A) AND infant leukemia AND minimal residual disease AND single-cell` returns 0 with a sane translation in which all three concept blocks expanded normally, so single-cell profiling of residual disease in infant KMT2A-rearranged ALL genuinely does not exist rather than being hidden by a parser artefact.

Go deeper

Queries run, 2026-09-20

#	Query	Count
1	`(MLL-rearranged OR KMT2A-rearranged OR KMT2A-r) AND leukemia AND (oxidative phosphorylation OR OXPHOS)`	3
2	`(MLL-rearranged OR KMT2A-rearranged) AND leukemia AND metabolism AND mitochondria`	4
3	`(MLL-rearranged OR KMT2A-rearranged) AND leukemia AND BH3 profiling`	4
4	`(MLL OR KMT2A) AND leukemia AND oxidative phosphorylation`	29
5	`(MLL OR KMT2A) AND leukemia AND BH3 profiling`	7
6	`(MLL OR KMT2A) AND infant leukemia AND minimal residual disease AND single-cell`	0
7	`infant acute lymphoblastic leukemia AND single-cell RNA sequencing`	25
8	`(MLL OR KMT2A) AND leukemia AND (single-cell RNA OR scRNA-seq) AND (cell state OR heterogeneity)`	33
9	`KMT2A AND leukemia AND persister`	73
10	`menin inhibitor AND differentiation AND (acute lymphoblastic leukemia OR ALL)`	15
11	`(MLL OR KMT2A) AND leukemia AND interferon signature`	2
12	`(MLL OR KMT2A) AND leukemia AND (hypoxia OR HIF1A)`	23
13	`infant AND (MLL OR KMT2A) AND leukemia AND diagnosis AND relapse AND transcriptome`	22
14	`(MLL OR KMT2A) AND leukemia AND (glutamine OR glutaminase)`	15
15	`(MLL-AF9 OR MLL-AF4 OR KMT2A-rearranged) AND leukemia AND (fatty acid oxidation OR lipid metabolism)`	13
16	`acute myeloid leukemia AND heme biosynthesis AND (dependency OR vulnerability)`	95
17	`(MLL OR KMT2A) AND leukemia AND venetoclax AND BCL-2 dependence`	12
18	`(MOLM-13 OR THP-1 OR MV4-11) AND cell cycle synchronization`	6
19	`MLL-AF4 AND cell cycle AND (SEM cells OR t 4 11)`	17
20	`(MLL OR KMT2A) AND leukemia AND cell cycle checkpoint defect`	6
21	`infant acute lymphoblastic leukemia AND (paired OR matched) AND relapse AND (gene expression OR transcriptomic OR single-cell)`	33
22	`(MLL OR KMT2A) AND leukemia AND (NF-kB OR toll-like receptor OR innate immune)`	62
23	`(MLL-rearranged OR KMT2A-rearranged) AND (senescence OR dormancy)`	9

All counts from NCBI esearch with querytranslation returned and inspected. Note that the hyphenated forms (queries 1–3) return roughly a tenth of what the bare symbol forms return (queries 4–5), which is the recall half of the alias problem the standing brief documents: MLL-rearranged as a token misses everything written as MLL-AF9 or MLL fusion.

Two query-translation findings worth keeping

1. SEM is read as two journals. Query 19's translation, in full for the relevant block:

(("struct equ modeling"[Journal] OR "scan electron microsc"[Journal] OR "sem"[All Fields])
   AND ("cell s"[All Fields] OR "cells"[MeSH Terms] OR "cells"[All Fields]))
 OR ("t"[All Fields] AND "4"[All Fields] AND "11"[All Fields])

So SEM cells retrieves Structural Equation Modeling and Scanning Electron Microscopy before it retrieves the cell line, and t 4 11 decomposes into three independent all-fields tokens. The standing brief asserts this trap; this is the measured translation string behind it. Searching by cell-line name is not a usable retrieval strategy for SEM, and the same is true for RS4;11, which the brief records translating to rs4 11.

2. Query 6's zero is real. Translation showed the MLL/KMT2A block expanding through the supplementary-concept mapping, the infant block through MeSH, the leukemia block through MeSH, and the MRD and single-cell blocks through their normal synonym sets. No [UID] term appeared and no block collapsed. So the absence of single-cell profiling of residual disease in infant KMT2A-rearranged ALL is a real absence, and it is recorded as a bounded absence in cell-state-diagnosis-versus-relapse-quiescent-subclone.

Written

Nine state entries, one hypothesis, two experiments and this analysis:

cell-state-unsynchronisable-cell-cycle — the five lines refractory to three synchronisation agents; fusion level constant through the cycle
cell-state-oxphos-dependence — OXPHOS in AML, its inversion in B-ALL LICs, the published heme dependency
cell-state-hypoxic-glycolytic — three convergent lines of evidence and two genetic counter-results
cell-state-lipid-pufa-dependence — ACSL4/PUFA against ELOVL1/saturated elongation
cell-state-apoptotic-priming-bcl2 — BH3 profiling, the BCL-XL-independence exception, the MCL-1 shift
cell-state-relapse-initiating-persister — the characterised persister state at diagnosis
cell-state-diagnosis-versus-relapse-quiescent-subclone — paired samples, quiescent subclone, bounded absence
cell-state-early-lymphocyte-precursor — ELP dominance and the cell-of-origin constraint
cell-state-under-menin-inhibition — three exits: differentiate, die, switch
cell-state-interferon-herv-mhc2 — the induced interferon state; no baseline exists
cell-state-innate-immune-lamp5 — the NF-kB/interferon routing state
cell-state-cns-niche-adapted — the sanctuary state and its repopulation deficit

Rejected, with reasons — bounded rejection

Recorded because a reader would reasonably expect each to be cited and it is not.

Considered as candidate states and not written:

Senescence as a state distinct from quiescence. Query 23 returns 9 records and none characterises a senescent state in KMT2A-rearranged leukaemia. The senescence-associated stem-like state that exists in the paediatric literature is Ph-like ALL and is already recorded, with its reversibility contradiction, inside cell-state-quiescence. Would change my mind: a KMT2A-rearranged sample with SA-beta-gal or a validated senescence signature plus a demonstration of irreversibility.
Glutamine dependence. Query 14 returns 15 records, none KMT2A-stratified; the relevant mechanisms (ASCT2, PMID 31535081; glutaminase in selected AML subtypes, PMID 27806325) are AML-class findings. Would change my mind: a KMT2A-versus-comparator glutamine flux or dependency measurement.
Glucocorticoid-resistant state as its own entry. It is already the substance of cell-state-pro-b-arrest (the NG2/FLT3/AP-1/NR3C1 axis) and of cell-state-relapse-initiating-persister (basal GC-response activation). A third entry would be a duplicate.

On-topic titles read and set aside:

PMID 30670779, A novel small molecule that kills a subset of MLL-rearranged leukemia cells by inducing mitochondrial dysfunction — a compound-discovery paper about one tool molecule, not a characterisation of the metabolic state, and 'a subset' is not resolved. Would change my mind: if the subset turned out to be definable by a state property rather than by sensitivity to the compound.
PMID 32999332, High-fat diet intensifies MLL-AF9-induced acute myeloid leukemia through activation of FLT3 signaling — genuinely on-beat for a lipid state and a dietary rather than cellular intervention in mouse; deferred rather than rejected, and it is the best single candidate for a future metabolic-environment entry.
PMID 38822412, Sequential drug treatment targeting cell cycle and cell fate regulatory programs blocks non-genetic cancer evolution in acute lymphoblastic leukemia — directly about non-genetic state transitions under therapy, but not KMT2A-stratified in its abstract. Deferred.
PMID 40579588 (multipotent lineage potential in B-ALL and cellular origins) and PMID 40294241 (single-cell transcriptional atlas of human haematopoiesis and aberrant AML differentiation) — both are reference-atlas-scale resources whose value here is as the reference against which state is measured, not as state findings. They belong to a lineage or atlas beat.
PMID 36052997 (stromal acetate secretion) and PMID 32966766 (marrow MSC support of AML bioenergetics) — niche metabolism, already the marrow-niche beat's territory; 32966766 is already cited in mechanism-niche-chemoprotection-kmt2a.
PMID 33555272 (RUNX2 and metabolism) is T-ALL; PMID 35108652 (SIRT2 in MLL-ENL) concerns proliferation and chemotherapy response rather than a state; PMID 39841459 (GATA2 and chemoresistance) is AML-wide.
PMID 38234854, KMT2A oncoproteins induce epigenetic resistance to targeted therapies — a 2024 bioRxiv preprint from the same group and overlapping in subject with the peer-reviewed PMID 39472576 used in cell-state-under-menin-inhibition. The published paper was preferred. Would change my mind: if the preprint contains the lineage-switch chromatin data at a depth the published version does not.

Known but unreadable: PMID 41711432 (menin inhibitors differ in in vitro sensitivity in KMT2A-rearranged infant ALL), checked by all four routes and recorded in cell-state-under-menin-inhibition E5.

What a reader should conclude about coverage

The alias coverage here is MLL and KMT2A and their hyphenated fusion spellings only. Not searched: the retired symbols ALL-1, HRX, HTRX, nor the spelled-out phrase mixed lineage leukemia as a standalone term. The standing brief's septin lesson — that retired symbols can carry nine-tenths of a literature — means every count above is a floor, and the 2-record interferon count in particular should be re-run over the retired symbol set before anyone builds on it as an absence.

What was not searched at all, and is the honest gap in this beat: ferroptosis as a state, autophagy, the unfolded-protein or integrated stress response, and proteostasis. The last is notable because this graph already holds mechanism-immunoproteasome material via PMID 38049829 and a proteasome-inhibition paper (PMID 36781850) appeared in query 13 without being pursued.

Facts and figures

status	run
run date	2026-09-20
queries run	23
recall note	hyphenated forms (MLL-rearranged, KMT2A-rearranged) return roughly a tenth of the bare-symbol forms: 3 versus 29 for the OXPHOS query and 4 versus 7 for the BH3 query

inputs

[
  "NCBI eutils esearch, db=pubmed, querytranslation inspected for every query",
  "NCBI eutils esummary and efetch (rettype=abstract, retmode=xml, itertext-safe parsing) for citation blocks",
  "Europe PMC core records and PMC HTML pages for full-text retrieval"
]

zero counts with translation verified

[
  {
    "query": "(MLL OR KMT2A) AND infant leukemia AND minimal residual disease AND single-cell",
    "count": 0,
    "verdict": "real absence"
  }
]

query translation traps confirmed

[
  {
    "token": "SEM",
    "query": "MLL-AF4 AND cell cycle AND (SEM cells OR t 4 11)",
    "translation_fragment": "(\"struct equ modeling\"[Journal] OR \"scan electron microsc\"[Journal] OR \"sem\"[All Fields])",
    "consequence": "cell-line-name retrieval for SEM is unusable; searching by mechanism plus partner symbol is the working alternative"
  },
  {
    "token": "t 4 11",
    "translation_fragment": "(\"t\"[All Fields] AND \"4\"[All Fields] AND \"11\"[All Fields])",
    "consequence": "bare karyotype tokens decompose into independent all-fields terms; parenthesised karyotypes return a clean, false zero"
  }
]

alias coverage

{
  "searched": [
    "MLL",
    "KMT2A",
    "MLL-AF4",
    "MLL-AF9",
    "MLL-rearranged",
    "KMT2A-rearranged",
    "KMT2A-r"
  ],
  "not_searched": [
    "ALL-1",
    "HRX",
    "HTRX",
    "mixed lineage leukemia as a standalone phrase"
  ],
  "consequence": "all counts are floors; the 2-record interferon count should be re-run over the retired symbol set before being used as an absence"
}

entries written

[
  "cell-state-unsynchronisable-cell-cycle",
  "cell-state-oxphos-dependence",
  "cell-state-hypoxic-glycolytic",
  "cell-state-lipid-pufa-dependence",
  "cell-state-apoptotic-priming-bcl2",
  "cell-state-relapse-initiating-persister",
  "cell-state-diagnosis-versus-relapse-quiescent-subclone",
  "cell-state-early-lymphocyte-precursor",
  "cell-state-under-menin-inhibition",
  "cell-state-interferon-herv-mhc2",
  "cell-state-innate-immune-lamp5",
  "cell-state-cns-niche-adapted",
  "hyp-cell-state-splits-by-lineage-not-by-fusion",
  "exp-elutriation-phase-and-size-resolved-kmt2a",
  "exp-dynamic-bh3-profiling-under-menin-inhibition"
]

rejected candidates

[
  {
    "candidate": "senescence as a state distinct from quiescence",
    "count": 9,
    "disposition": "rejected",
    "reason": "no record characterises a senescent state in KMT2A-rearranged leukaemia; the Ph-like senescence-associated stem-like state is already recorded inside cell-state-quiescence with its reversibility contradiction",
    "would_change_my_mind": "a KMT2A-rearranged sample with SA-beta-gal or a validated senescence signature plus a demonstration of irreversibility"
  },
  {
    "candidate": "glutamine / glutaminase dependence",
    "count": 15,
    "disposition": "rejected",
    "reason": "no record is KMT2A-stratified; ASCT2 (PMID 31535081) and glutaminase in selected AML subtypes (PMID 27806325) are AML-class findings",
    "would_change_my_mind": "a KMT2A-versus-comparator glutamine flux or dependency measurement"
  },
  {
    "candidate": "glucocorticoid-resistant state as its own entry",
    "disposition": "rejected as duplicative",
    "reason": "already the substance of cell-state-pro-b-arrest (NG2/FLT3/AP-1/NR3C1) and of cell-state-relapse-initiating-persister (basal GC-response activation)"
  },
  {
    "candidate": "PMID 30670779, small molecule killing a subset of MLL-r cells via mitochondrial dysfunction",
    "disposition": "read and set aside",
    "reason": "compound-discovery paper about one tool molecule; 'a subset' is unresolved and no state is characterised",
    "would_change_my_mind": "if the sensitive subset is definable by a state property rather than by sensitivity to the compound"
  },
  {
    "candidate": "PMID 32999332, high-fat diet intensifies MLL-AF9 AML via FLT3",
    "disposition": "deferred",
    "reason": "on-beat for a lipid/metabolic-environment state but a dietary intervention in mouse; best single candidate for a future metabolic-environment entry"
  },
  {
    "candidate": "PMID 38822412, sequential drug treatment blocking non-genetic evolution in ALL",
    "disposition": "deferred",
    "reason": "directly about non-genetic state transitions under therapy but not KMT2A-stratified in the abstract"
  },
  {
    "candidate": "PMID 40579588 and PMID 40294241, reference-scale single-cell atlases",
    "disposition": "deferred to a lineage or atlas beat",
    "reason": "these are the references against which state is measured rather than state findings in this disease"
  },
  {
    "candidate": "PMID 36052997 stromal acetate secretion; PMID 32966766 marrow MSC bioenergetic support",
    "disposition": "rejected as out of beat",
    "reason": "niche metabolism; 32966766 is already cited in mechanism-niche-chemoprotection-kmt2a"
  },
  {
    "candidate": "PMID 33555272 (RUNX2, T-ALL); PMID 35108652 (SIRT2, MLL-ENL); PMID 39841459 (GATA2, AML)",
    "disposition": "rejected",
    "reason": "wrong disease, or proliferation and chemoresistance rather than a state"
  },
  {
    "candidate": "PMID 38234854, KMT2A oncoproteins induce epigenetic resistance to targeted therapies (bioRxiv 2024)",
    "disposition": "rejected in favour of the peer-reviewed overlap",
    "reason": "same group, overlapping subject with PMID 39472576 which is used instead",
    "would_change_my_mind": "if the preprint contains lineage-switch chromatin data at a depth the published version does not"
  }
]

not searched at all

[
  "ferroptosis as a state",
  "autophagy",
  "unfolded protein response / integrated stress response",
  "proteostasis and proteasome dependence (PMID 36781850 surfaced in query 13 and was not pursued; PMID 38049829 immunoproteasome material already exists in this graph)"
]

unreadable after four routes

[
  {
    "pmid": "41711432",
    "title": "Menin inhibitors display differential in vitro sensitivity in KMT2A-rearranged infant acute lymphoblastic leukemia",
    "routes": "EPMC core pmcid null; no PMCID so fullTextXML and efetch db=pmc unavailable; elink pubmed->pmc empty; NCBI ID converter 'Identifier not found in PMC'; PubMed record carries no abstract; DOI resolves to publisher HTTP 403"
  }
]

full text retrieved by route 4

[
  {
    "pmid": "17908926",
    "pmcid": "PMC1993870",
    "route": "fullTextXML HTTP 500, then PMC HTML page",
    "stripped_characters": 91692,
    "title": "Bimodal degradation of MLL by SCFSkp2 and APCCdc20 assures cell cycle execution: a critical regulatory circuit lost in leukemogenic MLL fusions.",
    "authors": "Liu H, Cheng EH, Hsieh JJ",
    "venue": "Genes Dev",
    "year": 2007,
    "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."
  }
]

atlas refs

[
  {
    "label": "Reversible, niche-imposed dormancy constrains every ex vivo state measurement in this beat",
    "pmid": "27916615",
    "title": "Characterization of Rare, Dormant, and Therapy-Resistant Cells in Acute Lymphoblastic Leukemia.",
    "authors": "Ebinger S, Özdemir EZ, Ziegenhain C, et al.",
    "venue": "Cancer Cell",
    "year": 2016,
    "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."
  }
]

How this could bite us back

Every count in this entry is a floor over an incomplete alias set, so any decision that rests on one of these numbers being small should first be re-run over the retired symbols.
Recording rejections makes a beat auditable and also makes it look more complete than it is: four state classes were never searched at all, and that omission is more consequential than any individual rejection listed here.
The states enumerated are the states the literature names. A state that has been measured but not named would be invisible to this method, and nothing in this analysis would reveal that.

Still open

What does the interferon query return over the retired symbols ALL-1, HRX and HTRX? The 2-record count is the weakest absence claim in this beat and the cheapest to strengthen.
Is there a proteostasis or integrated-stress-response state in this disease? It was not searched, a proteasome-inhibition paper surfaced incidentally, and this graph already holds immunoproteasome material — so the gap is known rather than merely possible.
Can an enumeration keyed to state VOCABULARY find states described only by their constituent genes? This project has twice been caught by complex-level framing making a paper unreachable from subunit symbols, and the analogous failure here would be silent.

Every source behind this entry (2)

E1strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.database
NCBI E-utilities esearch against db=pubmed, run 2026-09-20, returns the record counts tabulated in this entry and supplies for each query a querytranslation string showing how PubMed rewrote the submitted terms; the translation for a query containing the token SEM maps it onto the journal titles Structural Equation Modeling and Scanning Electron Microscopy before any all-fields match, and the translation for the infant KMT2A MRD single-cell query shows all concept blocks expanding normally with no [UID] term, confirming its zero count as a genuine absence.
NCBI Entrez Programming Utilities (E-utilities) esearch endpoint, db=pubmed, with querytranslation returned · US National Library of Medicine 2026
What this evidence cannot show
PubMed counts are not stable: they change as records are indexed, as MeSH mappings are revised and as the supplementary-concept entries for KMT2A and MEN1 are updated, so every number here is dated 2026-09-20 and will drift. The counts are also a floor with respect to alias coverage, which here is MLL and KMT2A only and excludes the retired symbols ALL-1, HRX and HTRX and the spelled-out phrase 'mixed lineage leukemia'. Title-checking was applied where a count was used to support an absence; it was not applied exhaustively to the larger counts (queries 9, 16, 22), which were used for discovery rather than for enumeration.
Evidence that argues against this (1)
- A search-based enumeration cannot see literature that is on-topic without being retrievable by topic terms, and this project has documented the failure twice: a paper establishing that five NUP98 fusions bind the NSL complex appears in no query built from any subunit symbol, and a Mediator shRNA screen naming MED23 is unreachable from MED23 because its abstract frames the work at complex level. The direct analogue here is that a paper characterising a cell state may describe it only by its constituent genes, so an enumeration keyed to state vocabulary - 'quiescence', 'persister', 'metabolic' - will miss it. The nine states written here are the states the literature NAMES, not necessarily the states that have been measured. Read: this note restates a documented methodological finding of this project; the citation is one of the two papers on which it rests. Bhagwat AS et al. 2016
E2strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
The eight cell_state entries existing in this graph before this beat were cell-state-cell-cycle-g1-cdk6, cell-state-differentiation-block, cell-state-fetal-program-retention, cell-state-gmp-like, cell-state-primed-bivalent-chromatin, cell-state-pro-b-arrest, cell-state-quiescence and cell-state-stem-like-self-renewal, against 24 cell_type entries, making cell_state the thinnest of the standing saturation priorities apart from pathway; one of those eight, the quiescence entry, already records that the dormant compartment in ALL patient-derived xenografts is reversible and niche-imposed, which constrains every ex vivo state measurement made in this beat.
Characterization of Rare, Dormant, and Therapy-Resistant Cells in Acute Lymphoblastic Leukemia · Ebinger S, Ozdemir EZ, Ziegenhain C, Tiedt S, Castro Alves C, Grunert M, et al., Jeremias I · Cancer Cell 2016
PMID 27916615 DOI
What this evidence cannot show
The inventory of eight is a fact about this repository on 2026-09-20 and not a claim about the literature. The attached citation is the primary paper underlying the reversibility constraint referenced in the claim, re-fetched from PubMed for this entry rather than copied from cell-state-quiescence which also cites it; it is a paediatric and adult ALL PDX study not selected for KMT2A rearrangement, so the reversibility finding is imported into this disease by analogy. Read: abstract only.
Evidence that argues against this (1)
- If dormancy is fully niche-imposed and reverses on removal from the mouse, then every ex vivo measurement this beat relies on - BH3 profiling, metabolic flux, drug sensitivity, and the single-cell transcriptomes taken from aspirated marrow - was made on cells that had already begun leaving the state that matters. That does not invalidate the entries, but it means the beat's states are states of cells outside their niche, and the direction of the bias is toward greater sensitivity and greater proliferation than the patient's disease has. Read: abstract only (same paper). Ebinger S et al. 2016

Connected to

supports →Cell state in KMT2A-rearranged leukaemia is organised by lineage, not by the fusion — five independent axes split the same way, and every one of them splits AML from ALL rather than partner from partner
the enumeration is where the lineage split was noticed: it recurred across five independently searched axes
related to →The non-synchronisable state: five KMT2A-rearranged lines refuse mimosine, double thymidine and nocodazole, and the fusion protein does not fluctuate through the cycle
records the four-route read of PMID 17908926 (fullTextXML HTTP 500, PMC HTML 91,692 stripped characters) that this entry rests on
related to →Quiescence (G0) — the state 15 entries invoke to explain measurable residual disease, defined here for the first time
the reversible, niche-imposed dormancy recorded there constrains every ex vivo state measurement in this beat
related to →The interferon state is not baseline in this disease — it is something a menin inhibitor creates, through endogenous retrovirus induction and MHC class II
the 2-record interferon count is the weakest absence claim in the beat; alias coverage excludes ALL-1, HRX and HTRX
← related toExpressed, required, maintains — three different claims about where a gene matters, and the graph must label which one it has
the existing enumeration of cell states this beat connects genes to
← related toThe corpus citation index reads `PMID nnnnnnnn` in prose and never the `pmid` citation field — it sees 1,908 of 3,991 papers, undercounts 872 of the rest, and its headline single-cell absence was an artefact
both enumerate what the corpus holds on the cell-type/cell-state axis; this one measures the instrument that does the enumerating