The KOCL series (CVCL_3993, CVCL_6867, CVCL_3994, CVCL_3995) — four Japanese infant KMT2A::AFF1 lines, all under one year
also called KOCL-45 · KOCL-48 · KOCL-58 · KOCL-69
Four leukaemia cell lines called KOCL were grown from Japanese babies aged five to eight months, all carrying the index fusion. They are an entry about a collection rather than a single line, because the four share one source and one documentation trail.
The same thing, for a scientist
Four lines in the KOCL series carry an explicit Cellosaurus KMT2A-AFF1 gene-fusion annotation and are all derived from infants under one year of age: **KOCL-45** (CVCL_3993, male, 8 months, B-ALL, NSD2 p.Glu1099Lys heterozygous, TP53 p.Arg273Cys), **KOCL-48** (CVCL_6867, female, 5 months, acute **monocytic** leukaemia), **KOCL-58** (CVCL_3994, male, 5 months, B-ALL) and **KOCL-69** (CVCL_3995, female, <1 year, B-ALL, TP53 p.Arg181Cys). All four are recorded as Japanese population and three carry deposited drug-screening data. None is in DepMap, none has a published CRISPR screen, and none carries an STR profile in its Cellosaurus record. KOCL-48 deserves separate notice: it is an infant KMT2A::AFF1 **acute monocytic leukaemia**, not a B-ALL. The index fusion in an infant with a myeloid phenotype is uncommon and makes this line the natural control for any claim that KMT2A::AFF1 biology is intrinsically B-lymphoid.
Why this is one entry and not four1 deeper
The project's standing rule is one entry per thing. The thing here is a series: four lines sharing one originating programme, one annotation source (a 2004 review of MLL-altered haematopoietic lines 1), one TP53 survey 2, and one obtainability answer. Splitting them would produce four records differing only in an accession and an age. Each accession, age, sex, disease term and co-lesion is recorded individually in data.lines, so nothing is lost to a reader who wants one of them.
Per-line facts
| line | accession | sex | age | disease | co-lesions |
|---|---|---|---|---|---|
| KOCL-45 | CVCL_3993 | Male | 8 months | childhood B-ALL, t(v;11q23.3) | NSD2 E1099K het; TP53 R273C |
| KOCL-48 | CVCL_6867 | Female | 5 months | childhood acute monocytic leukaemia | none recorded |
| KOCL-58 | CVCL_3994 | Male | 5 months | childhood B-ALL, t(v;11q23.3) | none recorded |
| KOCL-69 | CVCL_3995 | Female | <1 year | childhood B-ALL, t(v;11q23.3) | TP53 R181C |
All four resolved by accession on 2026-09-19 and the primary name read back in each case 1.
Two of four carry a TP53 mutation, and that is the pattern
KOCL-45 carries TP53 R273C and KOCL-69 carries TP53 R181C 2. Add SEM (R248Q heterozygous), ALL-PO (R248Q homozygous) and the picture is that TP53 mutation is common among KMT2A::AFF1 lines and rare in the disease. Infant KMT2A-rearranged ALL has one of the lowest somatic mutation burdens of any human cancer; a panel in which several members are TP53-mutant is not a sample of that disease at the p53 axis. The survey that measured this in B-precursor ALL lines found the TP53 mutation rate tracks translocation type 2.
| resolved by | Cellosaurus accession lookups 2026-09-19; primary names read back for all four |
|---|---|
| population | Japanese |
| in depmap | false |
| crispr screen published | false |
| str profile recorded | false |
| fusion annotation source | single review, PMID 14671638 — the four are not independent annotations |
| obtainable | No international repository catalogue number found; Japanese originating institutions only |
lines
[
{
"name": "KOCL-45",
"accession": "CVCL_3993",
"sex": "Male",
"age": "8 months",
"infant_derived": true,
"disease": "childhood B-ALL, t(v;11q23.3)",
"co_lesions": [
"NSD2 p.Glu1099Lys het",
"TP53 p.Arg273Cys"
],
"omics": [
"drug screening"
]
},
{
"name": "KOCL-48",
"accession": "CVCL_6867",
"sex": "Female",
"age": "5 months",
"infant_derived": true,
"disease": "childhood acute monocytic leukemia",
"co_lesions": [],
"omics": []
},
{
"name": "KOCL-58",
"accession": "CVCL_3994",
"sex": "Male",
"age": "5 months",
"infant_derived": true,
"disease": "childhood B-ALL, t(v;11q23.3)",
"co_lesions": [],
"omics": [
"drug screening"
]
},
{
"name": "KOCL-69",
"accession": "CVCL_3995",
"sex": "Female",
"age": "<1 year",
"infant_derived": true,
"disease": "childhood B-ALL, t(v;11q23.3)",
"co_lesions": [
"TP53 p.Arg181Cys"
],
"omics": [
"drug screening"
]
}
]- Two of the four are TP53-mutant, which disqualifies them for apoptosis and DNA-damage work in a disease that is almost always TP53 wild-type.
- All four fusion assignments come from a single 2004 compilation. If that review erred for one line, nothing downstream would catch it — there is no STR profile, no karyotype and no sequenced junction in any of the four records.
- A panel that cannot be obtained cannot be a replication set. Quoting 'four infant lines exist' as reassurance is only honest if someone has checked that they can be shipped.
- Are viable KOCL stocks still distributed, and would STR profiling match? Four documented infant KMT2A::AFF1 lines that cannot be obtained are, for practical purposes, a gap rather than a resource.
- Was KOCL-48's patient really myeloid at presentation? If yes it is the only infant KMT2A::AFF1 AML line in existence and belongs in every lineage-destination experiment in this graph.
- Do the four share a KMT2A breakpoint intron? A single RT-PCR panel would place all four on the recombinome distribution and would confirm or remove their AFF1 assignments at the same time.
- E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database
Cellosaurus accessions CVCL_3993, CVCL_6867, CVCL_3994 and CVCL_3995 record KOCL-45 (male, 8 months), KOCL-48 (female, 5 months), KOCL-58 (male, 5 months) and KOCL-69 (female, under 1 year) as Japanese human cancer cell lines each carrying an explicit KMT2A-AFF1 gene-fusion annotation; KOCL-45, -58 and -69 are annotated as childhood B acute lymphoblastic leukaemia with t(v;11q23.3) MLL rearrangement and KOCL-48 as childhood acute monocytic leukaemia.
Cellosaurus cell lines KOCL-45 (CVCL_3993), KOCL-48 (CVCL_6867), KOCL-58 (CVCL_3994) and KOCL-69 (CVCL_3995) · Bairoch A, et al. (SIB Swiss Institute of Bioinformatics) · Cellosaurus 2025What this evidence cannot show
Each of the four fetched by accession on 2026-09-19 with the primary name read back. In all four the fusion annotation is attributed to one source, a 2004 review of MLL-altered haematopoietic cell lines (PMID 14671638), so the four annotations are not independent of each other. KOCL-69's age is recorded only as '<1Y', not as a number of months. None of the four records an STR profile or a karyotype.
Evidence that argues against this (1)
- Four fusion assignments from one review are one observation, not four. The review itself is a compilation of published line descriptions rather than a re-typing exercise, so if a line was mis-assigned in the original report the review propagates it — and that same review is the sole fusion source for BLIN-3, EU-8, Kid92 and BEL-1 as well. Drexler HG et al. 2004
- E2moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
KOCL-45 carries TP53 p.Arg273Cys and KOCL-69 carries TP53 p.Arg181Cys, both attributed to a survey linking TP53 mutation incidence in B-precursor ALL cell lines to the type of chromosomal translocation the line carries.
A specific linkage between the incidence of TP53 mutations and type of chromosomal translocations in B-precursor acute lymphoblastic leukemia cell lines · Inukai T, Zhang X, Kameyama T, et al. · American Journal of Hematology 2010What this evidence cannot show
Bibliographic record fetched from PubMed on 2026-09-19; the paper was not read and the abstract was not read in full. The per-line TP53 alleles come from the Cellosaurus records, which cite this paper. Whether these mutations were present in the patients or acquired during immortalisation is not addressed.
Evidence that argues against this (1)
- Immortalisation selects for p53 loss regardless of translocation, which predicts the same observation with no fusion-specific mechanism. Lines from low-mutation-burden leukaemias such as infant KMT2A-rearranged ALL would be the ones most dependent on acquiring it, so the association could run entirely through culture. Tomoyasu C et al. 2018
- E3moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database
KOCL-48 is annotated as a childhood acute monocytic leukaemia carrying KMT2A-AFF1, derived from a 5-month-old female, so at least one infant KMT2A::AFF1 line has a myeloid rather than a B-lymphoid phenotype.
Cellosaurus cell line KOCL-48 (CVCL_6867) · Bairoch A, et al. (SIB Swiss Institute of Bioinformatics) · Cellosaurus 2025What this evidence cannot show
Fetched by accession 2026-09-19. The record is the thinnest of the four: no omics, no karyotype, no co-lesions, and the disease term (NCIt C9163, childhood acute monocytic leukemia) is a database assignment whose primary source was not retrieved. A monocytic phenotype in a cultured line can also be a derivation artefact, as the Perth panel demonstrates for PER-485 and PER-703.
Evidence that argues against this (1)
- This graph's own Perth-panel reading shows that lines derived from B-lymphoid infant leukaemias can emerge as CD19-negative and monocytoid, with the matched patient sample still CD19-positive. So a monocytic disease term on a cultured line is weak evidence that the patient's leukaemia was myeloid, and KOCL-48 should not be quoted as an infant KMT2A::AFF1 AML case without the founding report. Cheung LC et al. 2021
- related to →KMT2A::AFF1 (MLL-AF4), t(4;11)(q21;q23)
four Japanese infant lines annotated KMT2A-AFF1
all four donors under one year of age
two of four lines are TP53-mutant in a disease that is almost always TP53 wild-type