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Previous Volume 355:2481-2482 December 7, 2006 Number 23 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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Genetic abnormalities that occur during neoplastic transformation can cause the dysregulation of protein kinases — a critical event in tumorigenesis. The inhibition of protein kinases is one of the most impressive new approaches to targeted cancer therapy. Imatinib mesylate (Gleevec, Novartis; formerly known as STI571) was one of the first selective protein kinase inhibitors developed for the treatment of chronic myelogenous leukemia (CML). The principal target of imatinib is BCR-ABL, a fusion protein made up of part of the breakpoint cluster region (BCR) protein and part of the tyrosine kinase Abelson murine leukemia (ABL). Imatinib directly binds to the tyrosine . . . [Full Text of this Article]

Source Information

From the Department of Obstetrics and Gynecology, School of Medicine, J.W. Goethe University, Frankfurt, Germany (K.S.); the Singapore Oncogenome Laboratory, Centre of Molecular Medicine, Institute of Molecular and Cell Biology, Proteos, Singapore (A.U.); and the Department of Molecular Biology, Max Planck Institute of Biochemistry, Martinsried, Germany (A.U.).

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