Abstract
In this issue of Blood, Woyach et al provide compelling evidence that Bruton's tyrosine kinase (BTK) is a critical target of ibrutinib in chronic lymphocytic leukemia (CLL), and Rushworth et al report data suggesting that BTK may also be a viable therapeutic target in acute myeloid leukemia (AML). These studies exemplify the concept that selectively targeting overactive kinases may be therapeutically useful in neoplasia even in the absence of recurrent genetic mutations in those kinases.1,2 © 2014 by The American Society of Hematology.
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CITATION STYLE
Davids, M. S. (2014, February 20). Boldly targeting kinases without mutations. Blood. American Society of Hematology. https://doi.org/10.1182/blood-2013-12-543322
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