Oncofusion

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Explainerestablished confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.Q21-index-fusion-models

MV4-11 (CVCL_0064) — KMT2A::AFF1, yes, but a ten-year-old's acute monocytic leukaemia with FLT3-ITD

also called MV-4-11 · MV4;11 · MV411 · MV(4;11) · CVCL_0064 · ACH-000045

MV4-11 does carry the index fusion, which surprises people. But it is a myeloid leukaemia from a ten-year-old boy and it also carries a FLT3 mutation, so results from it are not straightforwardly about infant B-cell leukaemia.

The same thing, for a scientist

MV4-11 (CVCL_0064, DepMap ACH-000045, ATCC CRL-9591, DSMZ ACC-102) **does** carry KMT2A::AFF1 — the brief's instruction to check is answered yes — with a karyotype of 48,XY,t(4;11)(q21;q23),+8,+19. But the line is from a **10-year-old male** with childhood acute monocytic leukaemia (NCIt C9163, FAB M5), not B-ALL, and it carries a **FLT3 internal tandem duplication**. It is CSF2- and IL3-dependent in its original description. It is the KMT2A::AFF1 line that appears in this project's own eleven-line DepMap panel as a *myeloid* line, and its MEN1 gene effect (-1.198) is the strongest of the three index-fusion lines with screen data.

Go deeper
The three ways MV4-11 differs from the index disease at once

Lineage. Monocytic AML, not pro-B ALL. This graph already holds the standing correction that the differentiation narrative in KMT2A-rearranged leukaemia is an AML story and should not be inherited by infant ALL entries; MV4-11 is the vehicle by which it is inherited.

Age. Ten years 1. Older than SEM, far older than any infant line.

FLT3-ITD. A constitutively active receptor tyrosine kinase 1. FLT3 is highly expressed in KMT2A-rearranged infant ALL but FLT3-ITD is uncommon in it; ITD is an AML lesion. MV4-11 is the standard FLT3-inhibitor sensitivity line in oncology, which means a large fraction of its literature is about FLT3 and not about the fusion at all.

The fusion is genuinely there. Everything around it is different.

Why it still earns its place

MV4-11 is the only KMT2A::AFF1 line with a myeloid phenotype that is in DepMap, catalogued at ATCC and DSMZ, and deeply characterised. That makes it the natural control for the question this graph keeps meeting: is a given KMT2A::AFF1 dependency a property of the fusion or of B-lymphoid identity? Comparing MV4-11 against SEM and RS4;11 holds the fusion fixed and varies lineage — the design the project's DepMap work has repeatedly needed and has had to approximate with cross-fusion comparisons instead 2.

Facts and figures
accessionCVCL_0064
depmap IDACH-000045
resolved byCellosaurus accession lookup 2026-09-19; primary name read back as MV4-11
age at derivation10 years
infant derivedfalse
sexMale
populationCaucasian
sitePeripheral blood
disease termChildhood acute monocytic leukemia (NCIt C9163)
lineagemyeloid / monocytic
fusionKMT2A::AFF1 — confirmed present
msiMSS
in depmaptrue
depmap crispr gene effecttrue
men1 gene effect-1.198
repositoryATCC CRL-9591; DSMZ ACC-102
obtainableYes — ATCC and DSMZ catalogue line
co lesions
[
  "FLT3 internal tandem duplication",
  "+8",
  "+19"
]
derived sublines
[
  "CVCL_F4CE (TP53 KO)",
  "CVCL_F1S5 (CEBPA KO)",
  "CVCL_C3HG (MV-4-11B)"
]
How this could bite us back
  • FLT3-ITD makes MV4-11 exquisitely sensitive to FLT3 inhibitors, so combination results in this line will overstate FLT3-directed benefit in infant KMT2A::AFF1 ALL, where ITD is uncommon.
  • MV4-11 is a monocytic AML line. Differentiation endpoints measured in it — the framing menin inhibitors are usually described with — do not transfer to infant ALL, where revumenib kills rather than differentiates.
  • Three named sublines share the MV4-11 name, including TP53- and CEBPA-knockout derivatives. A paper that says 'MV4-11' without an accession may not be reporting this cell line.
Still open
  1. How much of the KMT2A::AFF1 literature is actually MV4-11 literature about FLT3? A citation-level split of MV4-11 papers by whether the manipulated gene is FLT3 would size the problem.
  2. Held against SEM and RS4;11, which dependencies are shared across lineage and which are not? That is the cleanest fusion-versus-lineage test available in existing data and this graph has not run it on the index fusion alone.
Every source behind this entry (2)
  1. E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    Cellosaurus accession CVCL_0064 records MV4-11 as a Caucasian male human cancer cell line aged 10 years at sampling, derived in situ from peripheral blood, with NCIt disease terms 'Childhood acute monocytic leukemia' and ORDO 'Acute monoblastic/monocytic leukemia', a KMT2A-AFF1 gene-fusion annotation, a FLT3 internal tandem duplication, karyotype 48,XY,t(4;11)(q21;q23),+8,+19, CSF2 and IL3 dependence, microsatellite-stable status, DepMap identifier ACH-000045, ATCC catalogue CRL-9591 and DSMZ catalogue ACC-102.

    Cellosaurus cell line MV4-11 (CVCL_0064) · Bairoch A, et al. (SIB Swiss Institute of Bioinformatics) · Cellosaurus 2025
    What this evidence cannot show

    Fetched by accession 2026-09-19 with the primary name read back. The karyotype is ATCC's. Cellosaurus records three derived sublines (a TP53 knockout, a CEBPA knockout and MV-4-11B), so 'MV4-11' in a paper may not be this accession — a name-based match to this line is unsafe and the accession must be checked.

    Evidence that argues against this (1)
    • A monocytic phenotype in a t(4;11) line is exactly the ambiguity this beat found in the Perth panel, where B-lymphoid infant leukaemias produced CD19-negative monocytoid lines. MV4-11's original description is of a biphenotypic B-myelomonocytic leukaemia rather than a pure AML, so treating it as a clean lineage control assumes a sharper distinction than the founding material supports. Lange B et al. 1987
  2. E2strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.database

    In DepMap CRISPR screens queried through the Open Targets Platform on 2026-09-19, the MEN1 gene effect is -1.198 in MV4-11 (ACH-000045, recorded disease Acute Myeloid Leukemia), -0.959 in SEM (ACH-000782, B-ALL), -1.667 in SEM-K2 (ACH-001735, B-ALL), -0.463 in RS4;11 (ACH-000874, B-ALL) and -1.983 in HB11;19 (ACH-001736, B-ALL).

    DepMap CRISPR (Chronos) gene-effect screens for MEN1 (ENSG00000133895), queried via the Open Targets Platform GraphQL API · Broad Institute Cancer Dependency Map; Open Targets Platform · Open Targets Platform / DepMap 2026
    What this evidence cannot show

    Five values from one API call on one release; no confidence intervals were retrieved and the values are not lineage-adjusted or floor-corrected. With n=3 index-fusion lines, one of them a duplicate patient of another, nothing about a lineage effect can be concluded from this spread — it is recorded as a range, not as a comparison.

    Evidence that argues against this (1)
    • The spread runs the wrong way for a simple fusion story: the strongest menin dependency in this set belongs to HB11;19, a KMT2A::MLLT1 line, and the weakest to RS4;11, a KMT2A::AFF1 line. Within these five lines, menin dependency tracks neither the partner nor the lineage, which is what a line-level confound looks like. Broad Institute Cancer Dependency Map; Open Targets Platform 2026
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