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• W47702910 abstract "Chronic myeloid leukemia cells contain a BCR-ABL oncoprotein with an enhanced tyrosine kinase activity, which is considered to be the principal 'cause' of the leukemia. Though the precise mechanisms underlying the leukemogenesis remains enigmatic, the use of imatinib to inhibit the dysregulated kinase activity has proved remarkably successful in clinical practice. Imatinib was the first small molecule developed to inhibit BCR-ABL tyrosine kinase activity and its success introduced the current era of molecularly targeted therapies for a number of other malignancies. In patients with chronic myeloid leukaemia who develop resistance to imatinib, the Bcr-Abl signaling pathway is often re-established. This has led to the emergence of a number of alternative treatment strategies designed to target the leukemic cell which are resistant to imatinib." @default.
• W47702910 created "2016-06-24" @default.
• W47702910 creator A5020401806 @default.
• W47702910 creator A5090028348 @default.
• W47702910 date "2006-01-01" @default.
• W47702910 modified "2023-10-16" @default.
• W47702910 title "Molecularly targeted treatment of chronic myeloid leukemia: beyond the imatinib era" @default.
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• W47702910 doi "https://doi.org/10.2741/1792" @default.
• W47702910 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16146726" @default.
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