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- W2034346237 abstract "The majority of chronic myeloid leukemia (CML) (actually all, according to WHO) and ~30% of acute lymphoblastic leukemia (ALL) cases in adults originate from transformation of a hematopoietic stem cell by the oncogenic kinase Bcr-Abl1.1 Despite the indisputable success of small-molecule inhibitors of Bcr-Abl1 in prolonging the survival of patients with Bcr-Abl1-positive leukemia, leukemic stem cells (LSCs) remain detectable in the bone marrow.2, 3, 4 There are two well-documented mechanisms of Bcr-Abl1-dependent resistance to tyrosine kinase inhibitor (TKI) treatment, both leading to cell autonomous activation of Bcr-Abl1 kinase: mutations in the catalytic domain and amplification of the oncogene.5, 6, 7 In addition, detailed mechanistic studies of imatinib mesylate (IM) resistance and persistence of Bcr-Abl1-containing hematopoietic stem cells (HSCs) have shown that primitive CML cells are capable of survival in the absence of Bcr-Abl1 kinase activity.2, 4, 8 These studies suggested the existence of a kinase activity-independent mechanism of acquired drug resistance. It is thought that primitive LSCs that are insensitive to the presence of TKI are responsible for relapse after TKI discontinuation. In this scenario, non-catalytic, adapter functions of Bcr-Abl1 are believed to contribute to the oncogenic characteristics of CML stem cells, indicating the necessity of identifying Bcr-Abl1 kinase-independent mechanisms of survival of LSCs in the presence of TKI." @default.
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- W2034346237 date "2014-12-01" @default.
- W2034346237 modified "2023-09-25" @default.
- W2034346237 title "New Abelson interactor-1 (Abi-1)-driven mechanism of acquired drug resistance" @default.
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- W2034346237 doi "https://doi.org/10.1038/leusup.2014.4" @default.
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