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Previous Volume 354:2594-2596 June 15, 2006 Number 24 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Throughout its history, chronic myeloid leukemia (CML) has set precedents for cancer research and therapy, ranging from the identification of the first specific chromosomal abnormality associated with cancer to the development of imatinib as a specific, targeted therapy for the disease.¹ In this issue of the Journal, two articles^2,3 continue this tradition by describing how an understanding of resistance to imatinib has led to a strategy for circumventing resistance. These articles — one concerning nilotinib and the other dasatinib — are of fundamental importance for at least three reasons. First, they provide immediate hope 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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