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Journal of the National Cancer Institute Advance Access originally published online on June 24, 2008
JNCI Journal of the National Cancer Institute 2008 100(13):908-909; doi:10.1093/jnci/djn204
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© The Author 2008. Published by Oxford University Press.

EDITORIAL

Persistent LYN Signaling in Imatinib-Resistant, BCR-ABL–Independent Chronic Myelogenous Leukemia

Thomas O'Hare, Christopher A. Eide, Michael W. Deininger

Affiliation of authors: Oregon Health & Science University Cancer Institute, L592, 3181 SW Sam Jackson Park Rd, Portland, OR

Correspondence to: Michael W. Deininger MD, PhD, Oregon Health & Science University Cancer Institute, L592, 3181 SW Sam Jackson Park Rd, Portland, OR 97239 (e-mail: deininge@ohsu.edu).

The first 10% of the full text of this article appears below.

Resistance to imatinib is commonly associated with reactivation of BCR-ABL signaling. Many such patients harbor a mutation in BCR-ABL that confers resistance to imatinib. In other patients, the leukemia cells appear to express increased amounts of BCR-ABL kinase. Identification of a BCR-ABL mutation provides an explanation for onset of imatinib resistance and indicates a clear treatment strategy: second-line therapy with an ABL kinase inhibitor that is active against the particular BCR-ABL variant kinase. In the clinical setting, nilotinib and dasatinib are used for this purpose; additional inhibitors are under development.

However, not all cases of resistance can be attributed to a BCR-ABL mutation or enhanced expression. The phenomenon of BCR-ABL–independent resistance is probably . . . [Full Text of this Article]


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