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- W2787823502 endingPage "e88" @default.
- W2787823502 startingPage "e68" @default.
- W2787823502 abstract "Abstract Imatinib, the first-in-class BCR-ABL tyrosine kinase inhibitor (TKI), had been a revolution for the treatment of chronic myeloid leukemia (CML) and had greatly enhanced patient survival. Second- (dasatinib, nilotinib, and bosutinib) and third-generation (ponatinib) TKIs have been developed to be effective against BCR-ABL mutations making imatinib less effective. However, these treatments have been associated with arterial occlusive events. This review gathers clinical data and experiments about the pathophysiology of these arterial occlusive events with BCR-ABL TKIs. Imatinib is associated with very low rates of thrombosis, suggesting a potentially protecting cardiovascular effect of this treatment in patients with BCR-ABL CML. This protective effect might be mediated by decreased platelet secretion and activation, decreased leukocyte recruitment, and anti-inflammatory or antifibrotic effects. Clinical data have guided mechanistic studies toward alteration of platelet functions and atherosclerosis development, which might be secondary to metabolism impairment. Dasatinib, nilotinib, and ponatinib affect endothelial cells and might induce atherogenesis through increased vascular permeability. Nilotinib also impairs platelet functions and induces hyperglycemia and dyslipidemia that might contribute to atherosclerosis development. Description of the pathophysiology of arterial thrombotic events is necessary to implement risk minimization strategies." @default.
- W2787823502 created "2018-02-23" @default.
- W2787823502 creator A5000944048 @default.
- W2787823502 creator A5009413902 @default.
- W2787823502 creator A5018514641 @default.
- W2787823502 creator A5041424887 @default.
- W2787823502 creator A5078686392 @default.
- W2787823502 creator A5079634926 @default.
- W2787823502 date "2018-01-01" @default.
- W2787823502 modified "2023-10-18" @default.
- W2787823502 title "BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?" @default.
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