SCMC-L1 (CVCL_7125) — a four-month-old's KMT2A::AFF1 line carrying NSD2 E1099K
also called SCMC-L-1 · SCMCL-L1 · Saitama Children's Medical Center-Leukemia 1 · CVCL_7125
SCMC-L1 comes from a four-month-old Japanese girl with the index fusion. It also carries a second mutation, in a gene called NSD2, that is known to make leukaemia cells resistant to steroids.
The same thing, for a scientist
SCMC-L1 (CVCL_7125) is a B-precursor ALL line established at Saitama Children's Medical Center from a **4-month-old Japanese female**, with an explicit Cellosaurus KMT2A-AFF1 gene-fusion annotation and a heterozygous **NSD2 p.Glu1099Lys** mutation. It is microsatellite-stable and has deposited drug-screening data. NSD2 E1099K is a recurrent gain-of-function ALL lesion; SCMC-L1 shares it with RS4;11 (CVCL_0093) and with the infant line KOCL-45 (CVCL_3993), so three of the KMT2A::AFF1 lines in this inventory carry the same secondary lesion. The line features in published work on glucocorticoid-receptor mutations and glucocorticoid resistance in B-cell precursor ALL, and in a copy-number survey of ALL lines by genetic subtype.
NSD2 E1099K is a shared confound, not a private one
Cellosaurus annotates NSD2 p.Glu1099Lys in SCMC-L1, in RS4;11 and in KOCL-45 12. That is three of roughly a dozen KMT2A::AFF1 lines carrying an identical activating mutation in a histone methyltransferase. NSD2 deposits H3K36me2, so a line panel in which a quarter of the members carry an NSD2 gain-of-function is not a clean background for any chromatin claim about the fusion — and the histone-mark work in this graph is built on lines, not on patient material.
The same lesion is associated with glucocorticoid resistance 3, which makes it a confound for steroid-sensitivity claims specifically. Infant KMT2A-rearranged ALL is clinically steroid-poor-responding; if the lines used to study that are enriched for an NSD2 lesion the patients mostly do not carry, the mechanism inferred will be the line's, not the disease's.
| accession | CVCL_7125 |
|---|---|
| resolved by | Cellosaurus accession lookup 2026-09-19; primary name read back as SCMC-L1 |
| secondary accession | CVCL_G317 |
| age at derivation | 4 months |
| infant derived | true |
| sex | Female |
| population | Japanese |
| lineage | B-precursor |
| fusion | KMT2A::AFF1 (Cellosaurus gene-fusion annotation) |
| msi | MSS |
| in depmap | false |
| crispr screen published | false |
| obtainable | Originating institution (Saitama Children's Medical Center) / Japanese collaborators; no international repository catalogue number found |
synonyms
[ "SCMC-L-1", "SCMCL-L1" ]
co lesions
[ "NSD2 p.Glu1099Lys heterozygous" ]
omics available
[ "drug screening" ]
- An NSD2 gain-of-function mutation raises H3K36me2 genome-wide. Any chromatin-state claim about KMT2A::AFF1 made in this line, in RS4;11 or in KOCL-45 has an NSD2 confound that is not usually declared.
- If the panel's steroid resistance is NSD2-driven rather than fusion-driven, combinations designed to restore steroid sensitivity in infants are being optimised against the wrong lesion.
- What fraction of primary infant KMT2A::AFF1 leukaemias carry NSD2 E1099K? If it is low, the line panel is enriched for it and every H3K36me2-adjacent claim built on lines needs re-examination.
- Is SCMC-L1 glucocorticoid-resistant, and if so is that attributable to NSD2 rather than to a glucocorticoid-receptor lesion? The papers exist; the specific answer for this line was not retrievable from abstracts.
- E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database
Cellosaurus accession CVCL_7125 records SCMC-L1 as a female human cancer cell line aged 4 months at sampling, of Japanese population, microsatellite stable, with disease terms 'Childhood B acute lymphoblastic leukemia' and 'B acute lymphoblastic leukemia with t(v;11q23.3) MLL rearranged', an explicit KMT2A-AFF1 gene-fusion annotation, and a heterozygous NSD2 p.Glu1099Lys (c.3295G>A) mutation.
Cellosaurus cell line SCMC-L1 (CVCL_7125) · Bairoch A, et al. (SIB Swiss Institute of Bioinformatics) · Cellosaurus 2025What this evidence cannot show
Fetched by accession 2026-09-19. The fusion annotation traces to a 2004 review (PMID 14671638) rather than to a primary junction-sequencing report. The founding description is a 1991 Japanese-language institutional report (CelloPub CLPUB00110) that was not retrieved, so the patient's presentation and the line's immunophenotype at derivation are not established here.
Evidence that argues against this (1)
- Cellosaurus also records an older, now-secondary accession (CVCL_G317) merged into this record, meaning the line was at some point entered twice under variant spellings. Duplicate entries in cell-line registries are the mechanism by which one line gets counted as two, and this inventory's whole purpose is a count. Bairoch A et al. 2025
- E2established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database
The same NSD2 p.Glu1099Lys heterozygous mutation annotated in SCMC-L1 is also annotated in RS4;11 (CVCL_0093) and in the infant line KOCL-45 (CVCL_3993), so multiple independent KMT2A::AFF1 lines in current use share this secondary lesion.
Cellosaurus records for RS4;11 (CVCL_0093) and KOCL-45 (CVCL_3993) — NSD2 p.Glu1099Lys annotations · Bairoch A, et al. (SIB Swiss Institute of Bioinformatics) · Cellosaurus 2025What this evidence cannot show
Fetched by accession on 2026-09-19 for both lines. Cellosaurus attributes the RS4;11 call to both a publication (PMID 35124168) and DepMap (ACH-000874), and the KOCL-45 call to the publication only. Shared annotation across three lines does not establish whether the mutation was present in the patients or acquired in culture.
Evidence that argues against this (1)
- If NSD2 E1099K arose independently in three separate patients' leukaemias it is a co-occurring lesion worth studying; if it arose in culture it is an artefact of immortalisation. Nothing in the annotation distinguishes these, and the primary samples for the older lines no longer exist to check. Tomoyasu C et al. 2018
- E3moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper
SCMC-L1 is one of the B-cell precursor ALL cell lines used in a study establishing that glucocorticoid receptor gene mutations confer glucocorticoid resistance in B-cell precursor acute lymphoblastic leukaemia.
Glucocorticoid receptor gene mutations confer glucocorticoid resistance in B-cell precursor acute lymphoblastic leukemia · Tamai M, Kasai S, Akahane K, et al. · Journal of Steroid Biochemistry and Molecular Biology 2022What this evidence cannot show
Bibliographic record fetched from PubMed on 2026-09-19; abstract not read in full and the paper was not read. SCMC-L1's inclusion in this study is taken from the Cellosaurus reference list, which cites this paper as the source of the NSD2 annotation — so what role this line played in the study is not established, and in particular it is NOT established that SCMC-L1 carries a glucocorticoid-receptor mutation.
Evidence that argues against this (1)
- Being in a panel is not being a positive. The citation supports that this line was surveyed for NSD2, and the graph should not infer from it that SCMC-L1 is glucocorticoid-resistant; that would be exactly the error class of a correct PMID attached to a claim the paper does not make. Watanabe A et al. 2019
- related to →KMT2A::AFF1 (MLL-AF4), t(4;11)(q21;q23)
Cellosaurus KMT2A-AFF1 annotation; 4-month-old donor
infant-derived KMT2A::AFF1 B-precursor line