Cytarabine-resistant (160nM) acute myeloid leukemia (AML) MOLM-13 cell line
Invented by Disha Malani at University Of Helsinki
Catalogue Number | 159680 |
Antigen/Gene or Protein Targets | Acute myeloid leukemia |
Parental Line | MOLM-13 |
Tissue | Blood |
Disease Keywords | Cancer, acute myeloid leukemia, cytarabine-resistance, AML, chemotherapy resistance |
Model | Cancer Model |
Relevance | Acute myeloid leukaemia (AML) is a cancer of the myeloid line of blood cells, characterised by the rapid growth of abnormal cells that build up in the bone marrow and blood and interfere with normal blood cell production. Cytarabine is a common chemotherapy treatment for AML. Resistance to it in AML cells was shown to be linked to aberrant expression of equilibrative nucleoside transporters (ENT1) and metabolic enzymes deoxycytidine kinase (DCK) and cytosolic 5′-nucleotidase-II (NT5C2). The MOLM-13 cell line was derived from the peripheral blood of a patient at relapse of acute monocytic leukaemia. |
Production Details | This cell line and the others in this set were generated through long-term treatment of MOLM-13 cells with cytarabine. Doses were doubled when the AML cells started to proliferate at an equal rate as theuntreated parental cells. |
Conditional | No |
Research Area | Cancer |
Growth/Phenotype Keywords | cytarabine-resistant |
Notes |
This cell line comes in a set of 4 cytarabine-resistant cell lines, with resistance to increasing doses of cytarabine. This cell line is resistant to 1240nM of cytarabine. The parental MOLM-13 cell line can be used as a negative control for cytarabine resistance. Cytarabine resistance was found by the inventors of these cell lines to lead to glucocorticoid sensitivity as long as the cells had a wild- type fms like tyrosine kinase 3 (FLT-3) gene. This set of 4 MOLM-13 cells which have been made cytarabine resistant have a mutant form of FLT-3 (an an internal tandem duplication) and thus do not display glucocorticoid sensitivity. The related SHI-1 cell line which has similarly been made cytarabine resistant, contains the wild-type gene and thus is now sensitive to glucocorticoids. See Malani et al, Leukemia volume 31, pages1187–1195(2017) for details. |
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Disha Malani |
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Olli Kallioniemi |