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- W1986058924 abstract "Chronic myeloid leukemia (CML) was the first human malignant disease to be linked to a single, acquired genetic abnormality. Identification of the BCR-ABL kinase fusion protein and its central role in the pathogenesis of CML provided new opportunities to develop rational molecular targeted therapies. This review provides an update on the underlying pathophysiologies of disease progression and imatinib mesylate resistance, leading to the development of new targeted tyrosine kinase inhibitors for managing CML. Imatinib, a selective inhibitor of BCR-ABL, represents a major success in the era of target-directed cancer chemotherapy. However, patients with advanced CML have been less sensitive to therapy and responses have been short. In addition, treatment resistance is an emerging problem at all disease stages. Insight into factors involved in imatinib resistance and disease progression has highlighted a role for such BCR-ABL-dependent factors as amplification and overexpression of the BCR-ABL gene and the emergence of mutant isoforms of BCR-ABL. However, BCR-ABL-independent factors, including leukemogenic pathways involving kinases other than BCR-ABL, also play a part. In light of the limitations of imatinib against these factors, newer tyrosine kinase inhibitors, including dasatinib (a multitargeted kinase inhibitor of BCR-ABL and Src family kinases) and nilotinib (AMN107, a selective BCR-ABL inhibitor), may provide promising treatment options for patients with CML." @default.
- W1986058924 created "2016-06-24" @default.
- W1986058924 creator A5011529063 @default.
- W1986058924 creator A5015101485 @default.
- W1986058924 creator A5030340458 @default.
- W1986058924 creator A5061285204 @default.
- W1986058924 creator A5090435894 @default.
- W1986058924 date "2006-12-19" @default.
- W1986058924 modified "2023-10-15" @default.
- W1986058924 title "New Insights into the Pathophysiology of Chronic Myeloid Leukemia and Imatinib Resistance" @default.
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