Oncofusion

start / graph / noncoding-let-7-microrna-family

Non-codingstrong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.Q133-lin28b-fetal-ontogeny

let-7 microRNA family (12 HGNC loci) - the effector LIN28B blocks. CORRECTED IN-SESSION: the headline 'zero papers in KMT2A leukaemia' was a NAME-LIST ARTEFACT; searching MLL instead of KMT2A returns three, one of them directly on point

also called let-7 · lethal-7 · MIRLET7 family · MIRLET7A1/A2/A3/B/C/D/E/F1/F2/G/I and MIR98 · hsa-let-7

let-7 is a family of tiny RNAs that act like a brake on growth: they switch off genes that keep cells young and dividing, and they build up as a fetus matures. LIN28B works by holding that brake off. This entry first reported that nobody had ever studied let-7 in KMT2A leukaemia - and then found that they had, under the gene's older name, which is the mistake being recorded here as carefully as the biology.

The same thing, for a scientist

let-7 is a deeply conserved microRNA family encoded in humans by **12 HGNC loci** - MIRLET7A1, A2, A3, B, C, D, E, F1, F2, G, I and MIR98 - grouped as HGNC gene group 1697 [E1]. Mature let-7 accumulates as development proceeds; its biogenesis is blocked by the LIN28 proteins. **LIN28A and LIN28B do this by different mechanisms**: LIN28A recruits the TUTase ZCCHC11/TUT4 to pre-let-7 in the cytoplasm to block Dicer, whereas **LIN28B works in the nucleus by sequestering primary let-7 transcripts in the nucleolus, away from the Microprocessor, independently of ZCCHC11** [E2]. In haematopoiesis the axis is a bidirectional developmental clock: Lin28b falls in mouse common myeloid progenitors as maturation proceeds, let-7 rises, inhibiting let-7 in adults recapitulates fetal erythroid-dominant output, and deleting Lin28b or activating let-7 fetally shifts output to adult-like myeloid, with Hmga2 as effector [E3]. **THE CORRECTION THIS ENTRY EXISTS TO CARRY.** It was first written around a bounded absence: zero title/abstract records for let-7 against `KMT2A`, `"MLL-AF4"` or `"t(4;11)"`, verified live with positive controls. Those zeros are real and re-verified [E4]. **But the operand `MLL` was not tried, and it returns three records** - and one of them, Chen et al. 2016, is directly on point: across MLL-fusion-protein mouse AML models the c-Myc/Lin28B/let-7g programme is differentially regulated, **let-7g is highest in the leukaemias with the longest disease latency, and forced let-7g expression induces differentiation of leukaemic blasts** [E5]. So the true statement is much narrower than the one first written: **let-7 has not been measured in KMT2A::AFF1 or in any human infant KMT2A-rearranged leukaemia, but it HAS been measured and manipulated in mouse MLL-fusion AML, where restoring it is differentiating.**

Go deeper
THE CORRECTION, first, because it is the most useful thing here

This entry was drafted with the headline 'zero papers co-mention let-7 with KMT2A leukaemia'. That headline was wrong, and wrong in the standard way - the name list on the target side was too short. Rule 72 in this project's brief says exactly this and it still bit.

querytranslationcount
let-7[tiab] AND KMT2A[tiab]"let-7"[Title/Abstract] AND "KMT2A"[Title/Abstract]0
let-7[tiab] AND "MLL-AF4"[tiab]"let-7"[Title/Abstract] AND "MLL-AF4"[Title/Abstract]0
let-7[tiab] AND "t(4;11)"[tiab]"let-7"[Title/Abstract] AND "t 4 11"[Title/Abstract]0
let-7[tiab] AND "KMT2A-rearranged"[tiab]... AND "KMT2A-rearranged"[Title/Abstract]0
let-7[tiab] AND MLL[tiab]"let-7"[Title/Abstract] AND "MLL"[Title/Abstract]3
let7[tiab] AND MLL[tiab]"let7"[Title/Abstract] AND "MLL"[Title/Abstract]2 (subset)
let-7[tiab] AND "MLL-rearranged"[tiab]... AND "MLL-rearranged"[Title/Abstract]1

Why the failure had this shape. KMT2A became the approved symbol only recently; the microRNA literature on this disease is largely pre-2018 and says MLL. A bounded absence keyed on the current symbol systematically excludes the older literature, and microRNA work on leukaemia is disproportionately old. Any beat in this graph bounding an absence against KMT2A alone is making this error.

A second, smaller instance in the same session: Bolouri et al. write the family member as Let7a-2, with no hyphen after let, so let-7[tiab] cannot match it. Variant spellings of this family in the literature include let-7, let7, let-7a, Let7a-2, lethal-7, MIRLET7* and miR-98, a family member whose name contains no 'let-7' substring at all.

What IS known about let-7 in MLL-rearranged leukaemia, now that the right query was run

Chen et al., Oncotarget 2016 5 - the on-point paper. Mouse AML modelled with several different MLL fusion proteins gave significantly different survival outcomes. RNA-seq identified the c-Myc transcriptional programme as a top distinguishing feature; c-Myc protein correlated with disease latency; Lin28B was differentially expressed in agreement with c-Myc; and examining Lin28B's miRNA targets revealed let-7g significantly increased in the leukaemias with the LONGEST latency, with forced let-7g expression inducing differentiation of leukaemic blasts. The authors conclude that differential regulation of the c-Myc/Lin28/let-7g programme by different MLL-FPs is functionally related to disease latency and to BET-inhibitor resistance.

This is a partner-dependent LIN28B/let-7 result in MLL-rearranged leukaemia, and this graph did not have it. It also lines up in sign with the Magee/Bryder myeloid work: more let-7 means less aggressive disease, and restoring let-7 differentiates blasts. Note the corollary for the index fusion - if the axis is partner-discriminating in MLL-FP AML, then AFF1's position on it is a specific, answerable question and nobody has asked it.

Emmrich et al., Leukemia 2013 6. miR-9 is tumour-suppressive in t(8;21) paediatric AML by cooperating with let-7 to repress the oncogenic LIN28B/HMGA2 axis - and, importantly, those functions were NOT evident in MLL-rearranged blasts. So the one paediatric-AML study that manipulated the LIN28B/let-7/HMGA2 axis in patient material reports it as not operative in MLL-rearranged disease. This graph already holds noncoding-mir-9.

Bolouri et al., PLoS One 2021 7. In infant AML an onco-fetal B-cell gene regulatory network is activated: BRD4 and POU2AF1 with their onco-fetal targets LIN28B and IGF2BP3, all four hypomethylated; and miR Let7a-2 is expressed in a mutually exclusive manner with its target and regulator LIN28B. That mutual exclusivity is a let-7 measurement in infant leukaemia, in human patient material.

What the narrowed absence now says, precisely: there is no let-7 measurement in KMT2A::AFF1, in t(4;11), or in human infant ALL. There are measurements in mouse MLL-FP AML, in paediatric t(8;21) AML, and in human infant AML.

Why the gap that remains still matters

Ling et al. report that LIN28B permits KMT2A::AFF1 transformation by stabilising transcripts - early B-lymphoid genes, epigenetic regulators, cell-cycle and anti-apoptotic genes. That is a direct mRNA activity, not the let-7 mechanism. Eldeeb et al. independently found LIN28B acting on MLL-ENL AML through direct MYBBP1A mRNA binding, explicitly let-7-independent.

So even after the correction, the position stands: both mechanisms ever traced for LIN28B inside a KMT2A fusion are direct mRNA effects, and the let-7 arm in the index fusion remains unmeasured. What changed is that the axis is no longer untouched in MLL-rearranged disease generally - it has been measured in mouse, where it is partner-discriminating, and in human t(8;21) and infant AML. See mechanism-lin28b-has-two-routes-and-the-leukaemia-evidence-is-all-on-the-non-let-7-one.

Facts and figures
element classmicroRNA family (12 loci, trans-acting)
hgnc gene group ID1697
hgnc gene group nameMicroRNA MIRLET7 family
n members12
identifier provenanceHGNC REST gene_group_id/1697 and fetch/symbol/MIRLET7A1 fetched live 2026-09-23. Accessions for the other eleven loci were NOT individually fetched and are recorded as symbols only.
regulatorLIN28B (nuclear/nucleolar sequestration of pri-let-7, ZCCHC11-independent) and LIN28A (cytoplasmic ZCCHC11/TUT4-dependent uridylation of pre-let-7)
measured in kmt2a rearranged leukaemiaCORRECTED. Zero under the symbol KMT2A, zero for MLL-AF4 and t(4;11), but THREE records under the operand MLL, of which PMID 27007052 measures and manipulates let-7g across MLL-fusion AML models in mouse. The absence that survives is narrower: no let-7 measurement in KMT2A::AFF1, in t(4;11), or in human infant ALL.
shown for fusionMouse MLL-fusion-protein AML: YES - let-7g varies with partner and with disease latency, and forced let-7g differentiates blasts (PMID 27007052; which partners were compared is unread). Human paediatric t(8;21) AML: YES (PMID 24270738), and in the SAME study the axis was NOT operative in MLL-rearranged blasts. Human infant AML: YES as an expression anticorrelation (PMID 34793513). KMT2A::AFF1 / t(4;11) / human infant ALL: NOBODY HAS LOOKED.
subcellular site of regulationpri-let-7 is held in the NUCLEOLUS by LIN28B, away from the Microprocessor; pre-let-7 is uridylated by LIN28A/ZCCHC11 in the CYTOPLASM. Two compartments, two paralogues, one output.
members
[
  "MIRLET7A1",
  "MIRLET7A2",
  "MIRLET7A3",
  "MIRLET7B",
  "MIRLET7C",
  "MIRLET7D",
  "MIRLET7E",
  "MIRLET7F1",
  "MIRLET7F2",
  "MIRLET7G",
  "MIRLET7I",
  "MIR98"
]
representative locus
{
  "symbol": "MIRLET7A1",
  "hgnc_id": "HGNC:31476",
  "location": "9q22.32",
  "ensembl_gene_id": "ENSG00000199165",
  "mirbase": "MI0000060"
}
known effectors in haematopoiesis
[
  "HMGA2 (mouse myeloerythroid developmental timing; and the LIN28B/HMGA2 axis in paediatric t(8;21) AML)",
  "IGF2BP1 (reported as a LIN28B/let-7 target in AML)",
  "IGF2BP3 (co-hypomethylated with LIN28B in the infant-AML onco-fetal network)"
]
querytranslations recorded
[
  "\"let-7\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract] -> 0",
  "\"let-7\"[Title/Abstract] AND \"MLL-AF4\"[Title/Abstract] -> 0",
  "\"let-7\"[Title/Abstract] AND \"t 4 11\"[Title/Abstract] -> 0",
  "\"let-7\"[Title/Abstract] AND \"KMT2A-rearranged\"[Title/Abstract] -> 0",
  "\"let-7\"[Title/Abstract] AND \"MLL\"[Title/Abstract] -> 3  <- THE OPERAND THAT BROKE THE FIRST DRAFT'S HEADLINE",
  "\"let7\"[Title/Abstract] AND \"MLL\"[Title/Abstract] -> 2",
  "\"let-7\"[Title/Abstract] AND \"MLL-rearranged\"[Title/Abstract] -> 1",
  "\"let-7a\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract] -> 0",
  "\"let7a-2\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract] -> 0",
  "\"lethal-7\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract] -> 0",
  "\"MIRLET7\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract] -> 0",
  "\"miR-98\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract] -> 0",
  "\"LIN28B\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract] -> 1 (positive control)",
  "\"LIN28B\"[Title/Abstract] AND \"lymphoblastic\"[Title/Abstract] -> 3 (positive control)"
]
name variants of this family
[
  "let-7",
  "let7",
  "let-7a",
  "let-7g",
  "Let7a-2",
  "lethal-7",
  "MIRLET7A1..I",
  "MIR98 / miR-98 (a family member with no 'let-7' in its name)"
]
How this could bite us back
  • let-7 restoration as a therapy is a growth brake applied to every tissue that expresses the targets, in an infant. The family has hundreds of targets and the axis is a developmental clock, so 'restore let-7' is closer to 'advance the patient's developmental age' than to inhibiting an enzyme.
  • If LIN28B acts on KMT2A::AFF1 through direct transcript stabilisation rather than let-7, then a let-7 mimetic is targeting the wrong arm of the axis and would fail for a reason nobody had measured.
  • Twelve loci is twelve chances for compensation. Silencing or losing one is unlikely to move mature let-7 much, which also means a CRISPR knockout screen at the single-locus level would report the family as non-essential and be wrong.
Still open
  1. Which MLL fusion partners did Chen et al. 2016 compare, and was AF4/AFF1 among them? The paper reports the c-Myc/Lin28/let-7g programme as PARTNER-DISCRIMINATING in MLL-FP AML, so where AFF1 sits on that axis may already be answerable by opening one full text.
  2. Is mature let-7 detectable in human fetal liver CD34+ cells before and after LIN28B knockout in the CRISPR-KMT2A::AFF1 system? This is a small-RNA qPCR panel on material that already exists in the Ling et al. laboratory, and it is the single measurement that would convert the assumed mechanism into a measured one.
  3. Does let-7 restoration phenocopy LIN28B loss - i.e. does it block transformation - or does LIN28B permit transformation through a let-7-independent stabilisation route, as it suppresses AML through a let-7-independent MYBBP1A route? See exp-let-7-restoration-versus-lin28b-loss-fetal-liver-kmt2a-aff1.
  4. Are let-7 levels different between infant KMT2A::AFF1 ALL and childhood KMT2A::AFF1 ALL? The graph already holds that fetal-specific expression is retained in the infant form and not the childhood form, which makes this a directly testable prediction on banked diagnostic material.
  5. Which of the 12 loci carries the signal? Family-level measurement is the norm and it hides the possibility that one locus, silenced or amplified, does the work - the same granularity failure this project has hit with gene families elsewhere.
  6. Why is the let-7/LIN28B/HMGA2 axis reported as NOT operative in MLL-rearranged paediatric AML blasts (Emmrich 2014) while being partner-discriminating in mouse MLL-FP AML (Chen 2016)? Species, or the human MLL group being underpowered, or a real difference - and the answer decides whether the mouse result transfers.
Every source behind this entry (7)
  1. E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    The human let-7 microRNA family comprises 12 HGNC-approved loci - MIRLET7A1, MIRLET7A2, MIRLET7A3, MIRLET7B, MIRLET7C, MIRLET7D, MIRLET7E, MIRLET7F1, MIRLET7F2, MIRLET7G, MIRLET7I and MIR98 - assembled as HGNC gene group 1697 'MicroRNA MIRLET7 family'; MIRLET7A1 is HGNC:31476 at 9q22.32, ENSG00000199165, miRBase MI0000060.

    What this evidence cannot show

    Fetched live 2026-09-23; numFound was 12. Note that MIR98 is a let-7 family member by sequence and by HGNC grouping despite a name that does not say 'let-7' - a naming trap of exactly the kind this graph's symbol-collision registry exists for, and a reason a `let-7*` text search under-counts the family. Ensembl/miRBase identifiers were confirmed for MIRLET7A1 only; the other eleven were taken from the group listing and their individual accessions were not fetched.

    Evidence that argues against this (1)
    • Only MIRLET7A1's accessions were individually fetched; the other eleven loci are recorded as symbols taken from a group listing. If HGNC's grouping is wrong or has changed for any member, this entry's membership list is wrong in a way nothing here would catch - and MIR98's inclusion is exactly the kind of grouping judgement that can move. source 2026
  2. E2established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.paper

    LIN28A and LIN28B block let-7 biogenesis by distinct mechanisms: LIN28A recruits the TUTase ZCCHC11/TUT4 to let-7 precursors in the cytoplasm to block Dicer processing, whereas LIN28B represses let-7 through a ZCCHC11-independent mechanism, functioning in the nucleus by sequestering primary let-7 transcripts and inhibiting their processing by the Microprocessor.

    Lin28A and Lin28B inhibit let-7 microRNA biogenesis by distinct mechanisms. · Piskounova E, Polytarchou C, Thornton JE, LaPierre RJ, Pothoulakis C, Hagan JP, Iliopoulos D, Gregory RI · Cell 2011
    PMID 22118463DOI
    What this evidence cannot show

    Abstract read; full text not opened. The work is in human colon and breast cancer cells and xenografts, not haematopoietic cells and not any leukaemia. This is also the paper UniProt cites with ECO:0000269 for the nucleolar localisation of Q6ZN17, and - unusually for this graph's experience with rule 91 - it IS the founding observation for that fact rather than a pointer at an unrelated study.

    Evidence that argues against this (1)
    • The nucleolar-sequestration model is a mechanism for let-7 repression, and LIN28B's leukaemia-relevant activities reported since are direct mRNA-stabilising ones (MYBBP1A in MLL-ENL AML; B-lymphoid, epigenetic, cell-cycle and anti-apoptotic transcripts in KMT2A::AFF1). Neither of those requires let-7 and neither requires the nucleolar pool. Cell Rep 2023
  3. E3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    Lin28b expression decreases in mouse common myeloid progenitors as haematopoiesis matures, coinciding with accumulation of mature let-7; inhibiting let-7 in the adult haematopoietic system recapitulates fetal erythroid-dominant haematopoiesis, while deleting Lin28b or ectopically activating let-7 in the fetal state induces a shift toward adult-like myeloid-dominant output, with Hmga2 identified as an effector of the switch.

    Developmental regulation of myeloerythroid progenitor function by the Lin28b-let-7-Hmga2 axis. · Rowe RG, Wang LD, Coma S, Han A, Mathieu R, Pearson DS, Ross S, Sousa P, Nguyen PT, Rodriguez A, Wagers AJ, Daley GQ · J Exp Med 2016
    PMID 27401346DOI
    What this evidence cannot show

    Abstract read; full text not opened. MOUSE, NORMAL haematopoiesis, MYELOERYTHROID output. No fusion oncogene, no leukaemia, no B-lineage measurement in the abstract, and no human cells. It establishes the axis as a developmental clock, which is a different claim from the axis being the route by which LIN28B permits KMT2A::AFF1 transformation.

    Evidence that argues against this (1)
    • The axis being causal for developmental timing in normal myeloerythroid progenitors does not establish it as the route in fetal B-lymphopoiesis, and the two published leukaemia mechanisms for LIN28B in KMT2A-rearranged disease are both direct mRNA stabilisation, not let-7 de-repression. Blood 2026
  4. E4strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.database

    Live PubMed esearch on 2026-09-23 returns 0 records for each of `let-7[tiab] AND KMT2A[tiab]`, `let-7[tiab] AND "MLL-AF4"[tiab]`, `let-7[tiab] AND "t(4;11)"[tiab]` and `let-7[tiab] AND "KMT2A-rearranged"[tiab]`, each with a non-empty querytranslation; but the same session returns 3 for `let-7[tiab] AND MLL[tiab]` and 1 for `let-7[tiab] AND "MLL-rearranged"[tiab]`.

    What this evidence cannot show

    **THIS ITEM WAS CORRECTED WITHIN THE SESSION THAT WROTE IT AND THE CORRECTION IS THE POINT.** The four zeros are real and re-verified. The entry's first draft presented them as 'let-7 has never been studied in KMT2A leukaemia'. That was FALSE: adding the operand `MLL` returns three records, one of which (PMID 27007052) measures and manipulates let-7g across MLL-fusion AML models. The zeros were a fact about the SYMBOL, not about the field. Rule 80 also still applies - these bound titles and abstracts only, and the paper most likely to hold a let-7 figure in the index fusion (Ling et al. 2026) is paywalled and absent from PMC, so its figures could not be searched. Name variants tried on the microRNA side: `let-7`, `let7`, `let-7a`, `let7a`, `let7a-2`, `lethal-7`, `MIRLET7`, `miR-98` - all zero against KMT2A. Name variants on the target side: `KMT2A` (0), `KMT2A-rearranged` (0), `MLL-AF4` (0), `t(4;11)` (0), `MLL` (3), `MLL-rearranged` (1).

    Evidence that argues against this (1)
    • The operand-widening check that rule 72 mandates was run AFTER the entry was drafted rather than before, and it overturned the headline. The lesson generalises beyond this entry: a bounded absence in this graph keyed on the modern symbol `KMT2A` will systematically miss the pre-2018 literature, which for microRNA work is most of it. Oncotarget 2016
  5. E5strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    Across mouse AML models transformed with different MLL fusion proteins, the c-Myc transcriptional programme was a top distinguishing feature and c-Myc protein correlated with disease latency; the Myc target Lin28B was differentially expressed in agreement with c-Myc; examination of Lin28B's miRNA targets showed let-7g significantly increased in the leukaemic cells associated with the LONGEST disease latency, and forced let-7g expression induced differentiation of leukaemic blasts; high c-Myc cells were more resistant to Brd4 inhibition.

    PMID 27007052DOI
    What this evidence cannot show

    Abstract read; full text not opened, so which MLL fusion partners were compared, how many, and the effect sizes are not known here - and the partner identities are the single most useful fact in the paper for this project. MOUSE, MYELOID, retroviral MLL-FP models. Whether AFF1/AF4 was among the partners is UNKNOWN and should be checked before this is cited as partner-discriminating in a way that includes the index fusion. Oncotarget is a journal whose editorial standards over this period have been questioned; the result is treated as a strong pointer rather than as established.

    Evidence that argues against this (1)
    • In human paediatric AML material, the let-7/LIN28B/HMGA2 axis was reported NOT to be operative in MLL-rearranged blasts, in contrast to t(8;21) blasts where it is - which argues the mouse MLL-FP result may not transfer to human MLL-rearranged disease. Leukemia 2014
  6. E6strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    In a miRNA expression profiling of 90 cytogenetically characterised de novo paediatric AML cases, forced miR-9 expression reduced leukaemic growth and induced monocytic differentiation of t(8;21) AML lines in vitro and in vivo, acting through cooperation with let-7 to repress the oncogenic LIN28B/HMGA2 axis; these tumour-suppressive functions were specific to t(8;21) and were NOT evident in AML blasts from patients with MLL rearrangements.

    miR-9 is a tumor suppressor in pediatric AML with t(8;21). · Emmrich S, Katsman-Kuipers JE, Henke K, Khatib ME, Jammal R, Engeland F, Dasci F, Zwaan CM, den Boer ML, Verboon L, Stary J, Baruchel A, de Haas V, Danen-van Oorschot AA, Fornerod M, Pieters R, Reinhardt D, Klusmann JH, van den Heuvel-Eibrink MM · Leukemia 2014
    PMID 24270738DOI
    What this evidence cannot show

    Abstract read; full text not opened. The MLL-rearranged arm is a NEGATIVE result reported in passing within a paper about t(8;21), so its statistical power against the MLL-rearranged group is unknown and the MLL group's partner composition is unstated - it is almost certainly mostly myeloid partners, not AFF1, since these are AML cases. A negative in a subgroup of a paper about a different subgroup is weak evidence of absence.

    Evidence that argues against this (1)
    • This is a NEGATIVE result about MLL-rearranged blasts reported inside a paper about t(8;21), so the MLL-rearranged group's size, partner composition and statistical power are all unstated. A subgroup null in a paper about a different subgroup is among the weakest forms of evidence of absence, and it is being used here against a positive mouse result. Oncotarget 2016
  7. E7strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    Integrative mRNA, miRNA and DNA-methylation analysis of diagnosis-stage infant AML found an onco-fetal B-cell developmental gene regulatory network activated, comprising 18 genes including the epigenetic regulators BRD4 and POU2AF1 and their onco-fetal targets LIN28B and IGF2BP3, all four hypomethylated in infant AML; and micro-RNA Let7a-2 is expressed in a mutually exclusive manner with its target and regulator LIN28B.

    A B-cell developmental gene regulatory network is activated in infant AML. · Bolouri H, Ries R, Pardo L, Hylkema T, Zhou W, Smith JL, Leonti A, Loken M, Farrar JE, Triche TJ, Meshinchi S · PLoS One 2021
    PMID 34793513DOI
    What this evidence cannot show

    Abstract read; full text not opened. INFANT AML, not infant ALL, and the analysis is correlative expression and methylation across ~1500 paediatric AML samples - there is no perturbation. The mutual exclusivity of Let7a-2 and LIN28B is an expression-anticorrelation, which is what the axis predicts but is not a demonstration of it. NOTE THE SPELLING: the paper writes `Let7a-2`, which the query string `let-7[tiab]` cannot match - this is the second name-list failure recorded in this entry.

    Evidence that argues against this (1)
    • This is a correlative expression and methylation analysis with no perturbation, in infant AML rather than infant ALL. An anticorrelation between Let7a-2 and LIN28B is what the axis predicts, but it is equally consistent with both being downstream readouts of one methylation state - which is what the same paper's own network model proposes. Leukemia 2024
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