【摘 要】
：
The molecular signature of chronic myeloid leukemia (CML) is the BCR-ABL fusion gene originating in a pluripotent hematopoietic stem cell.The BCR-ABL oncopr
【机 构】
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Terry Fox Laboratory British Columbia Cancer Research Centre and Department of Medical Genetics Univ
【出 处】
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BIT Life Sciences' 1st Annual World Cancer Congess-2008(
论文部分内容阅读
The molecular signature of chronic myeloid leukemia (CML) is the BCR-ABL fusion gene originating in a pluripotent hematopoietic stem cell.The BCR-ABL oncoprotein (p210BCR-ABL) has constitutively elevated tyrosine kinase activity that drives CML pathogenesis.Imatinib (IM) and other tyrosine kinase inhibitors have recently been introduced into clinical practice with remarkable effects.Nevertheless, early relapses and the emergence of IM-resistant disease occur and these relapses are frequently associated with BCR-ABL kinase domain mutations.Our recent studies indicate that CML stem cells in chronic phase patients are less responsive to these agents and are a critical target population for IM resistance.
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