New insights into the pathophysiology of chronic myeloid leukemia and imatinib resistance
作者： Hagop M. Kantarjian , Moshe Talpaz , Francis Giles , Susan O'Brien , Jorge Cortes
DOI: 10.7326/0003-4819-145-12-200612190-00008
关键词: Dasatinib 、 Medicine 、 Kinase 、 Nilotinib 、 Imatinib mesylate 、 Cancer research 、 Myeloid leukemia 、 Tyrosine kinase 、 Leukemia 、 Imatinib
摘要: Chronic myeloid leukemia (CML) was the first human malignant disease to be linked a single, acquired genetic abnormality. Identification of BCR-ABL kinase fusion protein and its central role in pathogenesis CML provided new opportunities develop rational molecular targeted therapies. This review provides an update on underlying pathophysiologies progression imatinib mesylate resistance, leading development tyrosine inhibitors for managing CML. Imatinib, selective inhibitor BCR-ABL, represents major success era target-directed cancer chemotherapy. However, patients with advanced have been less sensitive therapy responses short. In addition, treatment resistance is emerging problem at all stages. Insight into factors involved has highlighted such BCR-ABL-dependent as amplification overexpression gene emergence mutant isoforms BCR-ABL. BCR-ABL-independent factors, including leukemogenic pathways involving kinases other than also play part. light limitations against these newer inhibitors, dasatinib (a multitargeted Src family kinases) nilotinib (AMN107, inhibitor), may provide promising options
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