ArticleMolecular medicine reports2017
Semi‑random mutagenesis profile of BCR‑ABL during imatinib resistance acquirement in K562 cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- BCR-ABL triggers a glucose-dependent survival program during leukemogenesis through the suppression of TXNIP.Cell death & disease · 2023Article
- The effects of cannabidiol via TRPV2 channel in chronic myeloid leukemia cells and its combination with imatinib.Cancer science · 2022Article
- Somatic Mutations in Oncogenes Are in Chronic Myeloid Leukemia AcquiredFrontiers in oncology · 2021Article
- A combined computational and experimental strategy identifies mutations conferring resistance to drugs targeting the BCR-ABL fusion protein.Communications biology · 2020Article
- Article
- Homoharringtonine enhances the effect of imatinib on chronic myelogenous leukemia cells by downregulating ZFX.Molecular medicine reports · 2019Article
- HDAC1,2 Knock-Out and HDACi Induced Cell Apoptosis in Imatinib-Resistant K562 Cells.International journal of molecular sciences · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
Although imatinib is effective in chronic myeloid leukemia treatment, imatinib resistance due to the T315I mutation and/or other mutations is a challenge to be overcome. However, how DNA mutation occurs, particularly the T315I mutation, remains unclear. In the current study, the mutagenesis of BCR‑ABL was analyzed via focusing on the process of drug resistance, rather than the final results. Clone sequencing of the BCR‑ABL gene and other control genes was applied in two imatinib‑resistant cell models. The results have indicated that imatinib actively and selectively causes sporadic mutations in the BCR‑ABL gene, however not in the control genes. The majority of the mutations of BCR‑ABL were not the clinically observed T315I mutation, suggesting that the T315I mutation may be due to clonal expansion of cells with survival advantages. Taken together, the results of the current study elucidated the mutagenesis process during drug resistance and thus aids in the management of chemotherapy.
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