Throughout its history, chronic myeloid leukemia (CML) has setprecedents for cancer research and therapy, ranging from theidentification of the first specific chromosomal abnormalityassociated with cancer to the development of imatinib as a specific,targeted therapy for the disease.1 In this issue of the Journal,two articles2,3 continue this tradition by describing how anunderstanding of resistance to imatinib has led to a strategyfor circumventing resistance. These articles one concerningnilotinib and the other dasatinib are of fundamentalimportance for at least three reasons. First, they provide immediatehope for patients in whom CML cells . . . [Full Text of this Article]
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From the Howard Hughes Medical Institute, Oregon Health and Science University Cancer Institute, Portland, Oreg.
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