Every human t(11;19) KMT2A::MLLT1 cell line, with accessions fetched and read back - and not one of them is known to be reciprocal-negative
also called t(11;19) cell line enumeration · KMT2A-MLLT1 line panel · MLL-ENL cell lines
There are seven human cell lines with this fusion. All but one come from babies under a year old, six are B-cell leukaemias and one is a therapy-related myeloid leukaemia from an adult. None has been shown to lack the mirror-image gene, which is the one property this project most needs a line to have.
The same thing, for a scientist
Cellosaurus was queried for `KMT2A-MLLT1` and for `"MLL-ENL"` on 2026-09-19 and every human cancer line returned was then re-fetched **by accession** with the primary name read back, because a prior cycle of this project recorded a cell line accession that resolved to an unrelated endometrial carcinoma. Seven human lines carry the fusion as a patient-derived lesion: **KOPN-8 (CVCL_1866)**, **HB11;19 (CVCL_8227)**, **Kasumi-10 (CVCL_8485)**, **KOCL-33 (CVCL_3991)**, **KOCL-51 (CVCL_6865)**, **KOPN-1 (CVCL_3937)** and **TRL-01 (CVCL_W777)** [E1]. Six are childhood B-ALL lines from patients aged 3-11 months (one of unspecified age); TRL-01 is from a 34-year-old woman with therapy-related AML [E2]. The panel's reciprocal status: **one line is reciprocal-positive by inference (HB11;19), six are unassayed, and none is reciprocal-negative** [E3]. Two engineered non-patient entries also returned - the transduced human cord-blood line M9-ENL1 (CVCL_A8IE) and mouse Picalm-knockout lines - and are excluded here because their fusion is a transgene and they are reciprocal-negative trivially rather than informatively [E1].
The panel, with everything that was checked
| line | accession | sex | age | disease | fusion source | YEATS in fusion | reciprocal status |
|---|---|---|---|---|---|---|---|
| KOPN-8 | CVCL_1866 | Female | 3 months | childhood B-ALL | patient | absent 3 | unassayed (reciprocal-capable: intra-MLLT1 break) |
| HB11;19 | CVCL_8227 | unspecified | unspecified | B-ALL, t(v;11q23.3) | patient | present 3 | positive (inferred, 1992) 4 |
| Kasumi-10 | CVCL_8485 | Female | 6 months | childhood B-ALL | patient | unknown | unassayed |
| KOCL-33 | CVCL_3991 | Female | 11 months | childhood B-ALL | patient | unknown | unassayed |
| KOCL-51 | CVCL_6865 | Male | 3 months | childhood B-ALL | patient | unknown | unassayed |
| KOPN-1 | CVCL_3937 | Female | 9 months | childhood B-ALL | patient | unknown | unassayed |
| TRL-01 | CVCL_W777 | Female | 34 years | therapy-related AML | patient | unknown (junction reported at ENL exon 4) | unassayed |
Every accession in this table was fetched individually from https://api.cellosaurus.org/cell-line/<AC>?format=txt and the ID line read back before the row was written 1.
Why 'unassayed' and not 'unknown to me'
Cellosaurus records no reciprocal-transcript information for any of these lines 1, and the searches recorded in absence-no-kmt2a-mllt1-analysis-stratified-by-reciprocal-or-spliced-status return no paper assaying one. The 1994 RT-PCR survey that used several of these lines and detected chimeric mRNAs in 8 of 9 t(11;19) leukaemias was assaying the direct transcript; reciprocal translocation appears in its abstract only as background to how the fusion arises 5. So the absence is a property of the literature, not of this search.
The prior probability says a reciprocal-negative line is already sitting in a freezer
50.7% of t(11;19) patients have an intergenic ACER1-MLLT1 break and make no reciprocal allele 3. Six of these seven lines are from infants with B-ALL, the modal patient group. If breakpoint class is independent of whether a line was successfully established, the probability that none of six unassayed lines is reciprocal-negative is about 0.5^6, roughly 1.6%. The most likely state of the world is that two or three of KOPN-8, Kasumi-10, KOCL-33, KOCL-51, KOPN-1 and TRL-01 are reciprocal-negative and nobody has looked. KOPN-8 is excluded from that count on a technicality that is itself informative: its fusion lacks the YEATS domain, so its break is downstream of MLLT1 exon 2 and therefore intra-genic and reciprocal-capable 3.
What mapping these breakpoints would give the field
The first reciprocal-negative KMT2A-rearranged cell line of any partner. There is none for t(4;11) either - RS4;11 and SEMK2-M1 both express MLL-AF4 and AF4-MLL - so every preclinical package in this disease is unstratified in a known direction. A reciprocal-negative t(11;19) line paired against HB11;19 would be partner-matched, and against a YEATS-status-matched line would be architecture-matched too. The work is long-distance inverse PCR or targeted sequencing across the MLLT1 locus in six lines: a week, no new patients, no consent.
Bounded rejection: what was returned and set aside
- M9-ENL1 (CVCL_A8IE) - human umbilical cord blood transduced with a KMT2A-MLLT1 transgene, described as mimicking primary human pro-B ALL. Excluded as a model of transduction, not of the translocation: it carries no der(19) at all, so calling it reciprocal-negative is true and uninformative.
- PICALM6A/6B/6D (CVCL_B3QV/B3QW/B3QX) - mouse Picalm-knockout embryonic liver cells transduced with KMT2A-MLLT1. Excluded: mouse, transgenic, and the experimental variable is Picalm.
- IMS-M1 (CVCL_A623) - returned by the
KMT2A-MLLT1query but its fusion is KMT2A-MLLT3. Excluded, and recorded here as the alias-precision failure this query class produces. - KARPAS-45, ML-2, MOLM-13, THP-1, MV4;11, SEM, RS4;11 - not returned; other partners. Not investigated further.
| status | run |
|---|---|
| result summary | Seven human patient-derived t(11;19) KMT2A::MLLT1 cell lines exist. One is reciprocal-positive by inference, six are unassayed, none is known to be reciprocal-negative. On breakpoint-class priors, two or three of the unassayed six are expected to be reciprocal-negative. |
| reciprocal negative lines | 0 |
| prior probability none of six is reciprocal negative | 0.016 |
inputs
[ "Cellosaurus API searches for KMT2A-MLLT1 and \"MLL-ENL\"", "individual accession fetches for each returned human patient-derived line" ]
lines
[
{
"name": "KOPN-8",
"accession": "CVCL_1866",
"sex": "Female",
"age": "3 months",
"disease": "childhood B-ALL",
"yeats_in_fusion": false,
"reciprocal_status": "unassayed (reciprocal-capable)",
"depmap": "ACH-001106"
},
{
"name": "HB11;19",
"accession": "CVCL_8227",
"sex": "unspecified",
"age": "unspecified",
"disease": "B-ALL t(v;11q23.3)",
"yeats_in_fusion": true,
"reciprocal_status": "positive (inferred)",
"depmap": "ACH-001736"
},
{
"name": "Kasumi-10",
"accession": "CVCL_8485",
"sex": "Female",
"age": "6 months",
"disease": "childhood B-ALL",
"yeats_in_fusion": null,
"reciprocal_status": "unassayed",
"co_lesions": [
"FLT3-ITD"
],
"note": "XXY karyotype from a female patient; JCRB1410"
},
{
"name": "KOCL-33",
"accession": "CVCL_3991",
"sex": "Female",
"age": "11 months",
"disease": "childhood B-ALL",
"yeats_in_fusion": null,
"reciprocal_status": "unassayed"
},
{
"name": "KOCL-51",
"accession": "CVCL_6865",
"sex": "Male",
"age": "3 months",
"disease": "childhood B-ALL",
"yeats_in_fusion": null,
"reciprocal_status": "unassayed"
},
{
"name": "KOPN-1",
"accession": "CVCL_3937",
"sex": "Female",
"age": "9 months",
"disease": "childhood B-ALL",
"yeats_in_fusion": null,
"reciprocal_status": "unassayed",
"co_lesions": [
"TP53 p.Arg248Gln"
]
},
{
"name": "TRL-01",
"accession": "CVCL_W777",
"sex": "Female",
"age": "34 years",
"disease": "therapy-related AML",
"yeats_in_fusion": null,
"reciprocal_status": "unassayed",
"note": "stroma-dependent, established by NOG-mouse xenotransplantation; ENL exon 4 junction reported"
}
]excluded
[
{
"name": "M9-ENL1",
"accession": "CVCL_A8IE",
"reason": "transduced human cord blood, transgene not translocation"
},
{
"name": "PICALM6A/6B/6D",
"accession": "CVCL_B3QV / CVCL_B3QW / CVCL_B3QX",
"reason": "mouse, transgenic, Picalm-knockout background"
},
{
"name": "IMS-M1",
"accession": "CVCL_A623",
"reason": "returned by the query but is KMT2A-MLLT3, not MLLT1"
}
]- Every preclinical result for this fusion comes from lines that are reciprocal-positive or reciprocal-unassayed. If the reciprocal product modifies drug response, no existing cell-based experiment in this partner could have detected it, and the same is true for t(4;11).
- Six of the seven lines are infant B-ALL, and the fusion's adverse clinical reputation comes from paediatric AML. The panel is therefore mismatched to the population in which the drug question is sharpest.
- Which of Kasumi-10, KOCL-33, KOCL-51, KOPN-1 and TRL-01 has an intergenic ACER1-MLLT1 break? Long-distance inverse PCR or targeted sequencing across the locus in five lines would very probably yield the field's first reciprocal-negative KMT2A-rearranged cell line.
- Do any of these lines still express a reciprocal transcript after decades of passage? Reciprocal allele loss during clonal progression is documented, and an RT-PCR panel across all seven is a single afternoon.
- Is TRL-01's ENL exon-4 junction YEATS-partial? Exon 4 is the last YEATS-coding exon, so an exon-4 junction sits exactly on the boundary between the partial-inclusion (6.0%) and exclusion (9.9%) classes, and this line would be the only model of that architecture.
- E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database
A Cellosaurus search for KMT2A-MLLT1 returns 11 entries, of which the human patient-derived cancer lines are HB11;19 (CVCL_8227), Kasumi-10 (CVCL_8485), KOCL-51 (CVCL_6865), KOPN-1 (CVCL_3937), KOCL-33 (CVCL_3991) and KOPN-8 (CVCL_1866), plus the transduced human cord-blood line M9-ENL1 (CVCL_A8IE) and three mouse Picalm-knockout transductants; a search for 'MLL-ENL' additionally returns TRL-01 (CVCL_W777), a female 34-year-old therapy-related AML line. Individual accession fetches confirm KOCL-33 as female 11 months, KOCL-51 as male 3 months and KOPN-1 as female 9 months, all with NCIt terms 'Childhood B acute lymphoblastic leukemia' and 'B acute lymphoblastic leukemia with t(v;11q23.3) MLL rearranged'; none of the seven records carries any reciprocal-transcript annotation.
Cellosaurus: search for KMT2A-MLLT1 and individual accession records CVCL_1866, CVCL_8227, CVCL_8485, CVCL_3991, CVCL_6865, CVCL_3937, CVCL_W777 · Bairoch A, et al.; Cellosaurus · Cellosaurus (SIB) 2026What this evidence cannot show
Queried and each accession re-fetched on 2026-09-19 with the primary ID read back. Cellosaurus completeness is the limiting factor: a line whose fusion has never been annotated there would not be returned, and the 'MLL-ENL' query surfaced TRL-01 that the 'KMT2A-MLLT1' query did not, which shows the annotations are not uniform. The IMS-M1 hit in the KMT2A-MLLT1 result set is a KMT2A-MLLT3 line and was excluded by reading its record.
Evidence that argues against this (1)
- Cellosaurus fusion annotations for several of these lines cite panel or survey papers rather than breakpoint-mapping studies, so 'carries KMT2A-MLLT1' is established at gene level and not at junction level for most of the panel. Drexler HG et al. 2004
- E2moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
TRL-01 was established from therapy-related acute myeloid leukaemia with t(11;19) by xenotransplantation into NOD/SCID IL-2Rgamma-null mice; it is CD13, CD33, CD11a, CD18, CD29, CD49d, CD49e, CD54, CD62L and CD117 positive and CD3, CD4, CD8, CD19, CD34, CD41a, CD41b, CD135 and myeloperoxidase negative; and the translocation in both the original sample and the line generated MLL-ENL chimeric transcripts joining exon 6 and exon 4, described by the authors as a novel isoform.
Establishment of a myeloid leukemia cell line, TRL-01, with MLL-ENL fusion gene. · Ninomiya M, Abe A, Yokozawa T, Ozeki K, et al. · Cancer Genet Cytogenet 2006What this evidence cannot show
ABSTRACT ONLY; Europe PMC returns pmcid null and isOpenAccess N. The phrase 'joining exon 6 and exon 4, respectively' is ambiguous in the abstract between an MLL exon 6 to ENL exon 4 junction and two different junctions in sample and line; the body was not read and this entry does not resolve it. The line is stroma-dependent and did not support long-term culture, so it is not a drop-in model.
Evidence that argues against this (1)
- Therapy-related KMT2A::MLLT1 was described in 2007 as very rare with a single t-AML case in the literature, so this line represents a subgroup that the 2023 recombinome still counts at only 9 t-AML cases out of 460. Meyer C et al. 2023
- E3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
Read in full text (PMC11246743): KOPN8 cells harbour MLL-ENL fusion proteins lacking the YEATS domain while HB1119 cells are driven by MLL-ENL fusion proteins containing it; and of 302 t(11;19) patients, 50.7% (n = 153) harbour genomic breaks 5' upstream of MLLT1 but 3' downstream of ACER1, 33.4% (n = 101) break within MLLT1 intron 1 and 15.9% (n = 48) break downstream of exon 2.
The ENL YEATS epigenetic reader domain critically links MLL-ENL to leukemic stem cell frequency in t(11;19) Leukemia. · Hu H, Saha N, Yang Y, Ahmad E, et al. · Leukemia 2023What this evidence cannot show
Read via the PMC HTML page after fullTextXML returned HTTP 500 and efetch db=pmc returned HTTP 429. The paper says nothing about reciprocal alleles in any line; the inference that a YEATS-less fusion implies an intra-MLLT1 and therefore reciprocal-capable break is this graph's reasoning from the breakpoint geometry.
Evidence that argues against this (1)
- The prior-probability argument assumes breakpoint class is independent of whether a line could be established, which has never been tested; if intergenic breaks were associated with any biological property affecting immortalisation, the six unassayed lines could be systematically non-representative. Iida S et al. 1992
- E4strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
In a t(11;19)-carrying cell line, fusion transcripts are expressed from both derivative chromosomes, the more abundant derivative 11 transcript coding for a chimeric protein containing the AT hook motifs fused to ENL.
Involvement of a homolog of Drosophila trithorax by 11q23 chromosomal translocations in acute leukemias. · Tkachuk DC, Kohler S, Cleary ML · Cell 1992What this evidence cannot show
Abstract only; no PMCID in Europe PMC, so routes 2-4 of the unreadable test are unavailable. The abstract does not name the line, and the attribution to HB11;19 rests on Cellosaurus citing this paper for that line's fusion.
Evidence that argues against this (1)
- Reciprocal alleles can be lost during clonal progression, so a 1992 observation is not a statement about the line as distributed in 2026. Meyer C et al. 2023
- E5moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
An RT-PCR survey of 25 leukaemias with 11q23 abnormalities amplified chimeric mRNAs in 6 of 7 leukaemias with t(4;11), 6 of 8 with t(9;11) and 8 of 9 with t(11;19), and found the chimeric mRNAs heterogeneous with differential usage of MLL exons irrespective of partner chromosome.
A reverse transcriptase-polymerase chain reaction detects heterogeneous chimeric mRNAs in leukemias with 11q23 abnormalities. · Yamamoto K, Seto M, Iida S, et al. · Blood 1994What this evidence cannot show
Abstract only; PubMed returns no DOI for this record and Europe PMC no PMCID. The assay detects DIRECT chimeric transcripts; 'reciprocal translocation' appears in the abstract only as background to how the fusion arises, and no reciprocal transcript assay is described. This paper is a Cellosaurus reference for KOCL-33, KOCL-51 and KOPN-1, which is why it is checked here.
Evidence that argues against this (1)
- One of nine t(11;19) cases gave no amplifiable chimeric mRNA, which a partner-specific primer panel would also produce for an unusual junction - so even the direct-transcript detection rate is a property of the primer set rather than of the biology. Fu JF et al. 2007
the complete human model panel for this fusion
panel member
panel member; the only reciprocal-positive line
the patient comparison has no in vitro counterpart, and on breakpoint priors two or three lines should already be reciprocal-negative
extends the preclinical control-arm problem to the t(11;19) panel
the same audit for the paralogous partner