TOM-1

Cat.No.: CSC-C0583

Species: Homo sapiens (Human)

Source: Bone Marrow

Morphology: small round cells growing in suspension singly or in clumps, some cells are loosely adherent

Culture Properties: suspension

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Cat.No.
CSC-C0583
Description
Established in 1983 from the bone marrow of a 54-year-old woman with refractory Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL); described to carry the ALL-variant (m-bcr) of the BCR-ABL1 fusion gene (e1-a2)
Species
Homo sapiens (Human)
Source
Bone Marrow
Recommended Medium
Culture Properties
suspension
Morphology
small round cells growing in suspension singly or in clumps, some cells are loosely adherent
Karyotype
Human hyperdiploid karyotype with 7% polyploidy - 47(47-48)<2n>X, -X, +8, +16, del(7)(p14), der(9)del(9)(q13q34)t(9;22)(q34;q11), der(22)t(9;22)(q34;q11) - carries t(9;22) effecting BCR-ABL1 rearrangement - resembles published karyotype
Disease
Adult B Acute Lymphoblastic Leukemia
Quality Control
Mycoplasma: negative in microbiological culture, PCR assays
Immunology: CD2 -, CD3 -, CD4 -, CD7 -, CD10 +, CD13 +, CD19 +, CD20 +, CD34 +, CD37 +, CD38 +, cyCD79a +, CD80 -, CD138 -, HLA-DR +, sm/cyIgG -, sm/cyIgM -, sm/cykappa -, sm/cylambda -
Viruses:
Storage and Shipping
Frozen with 70% medium, 20% FBS, 10% DMSO at about 6 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen
Synonyms
TOM1
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

The TOM-1 cell line is a human B-cell precursor leukemia line established in 1983 from the bone marrow of a 54-year-old female patient with refractory Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). It is characterized by a hyperdiploid karyotype with a t(9;22) translocation, resulting in the expression of the p190 BCR-ABL1 fusion protein (e1a2 junction). Morphologically, TOM-1 cells are small, round lymphocytes that grow in suspension, either singly or in loose clusters, though some may show loose adherence. They are positive for HLA-DR, CD10, CD19, CD20, CD34, and terminal deoxynucleotidyl transferase (TdT), but negative for surface and cytoplasmic immunoglobulins, confirming their early pre-B cell stage. Culturally, they are maintained in a nutrient-rich basal medium supplemented with serum under standard conditions (37°C, 5% CO₂). The line has a doubling time of approximately 50-70 hours and is sub-cultured upon reaching appropriate density.

TOM-1 is a valuable model for studying Ph+ ALL pathogenesis, BCR-ABL1 signaling, tyrosine kinase inhibitor sensitivity, and mechanisms of leukemic stem cell differentiation and drug resistance.

Biological Effects of LIMKi in BCR::ABL+ Cell Lines

Despite advances with TKIs, Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia (Ph+ B-ALL) remains a high-risk malignancy, necessitating less toxic strategies, particularly for elderly patients. Berrou et al. evaluated targeting LIMK1/2-key downstream effectors of BCR::ABL that regulate apoptosis via cofilin phosphorylation.

As BCR::ABL activates the ROCK-LIMK axis, they investigated the efficacy of the LIMK inhibitor CEL_Amide in Ph+ B-ALL cell lines (TOM-1, BV-173). CEL_Amide significantly inhibited cell viability with IC50s of 580 nM (TOM-1) and 1090 nM (BV-173) (Fig. 1A). Treatment induced dose-dependent apoptosis, reaching 45% (TOM-1) and 50% (BV-173) at 48 h (Fig. 1B), and caused G1/S cell cycle arrest (Fig. 1C). These findings suggest that LIMK inhibition disrupts critical survival pathways in Ph+ B-ALL.

In vitro effect of LIMKi on viability, apoptosis, and cell cycle in BCR::ABL1+ ALL cell lines

Fig. 1. In vitro effect of LIMKi on viability, apoptosis, and cell cycle in BCR::ABL1+ ALL cell lines (Berrou J, Dupont M, et al., 2022).

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