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Blood, 15 January 2007, Vol. 109, No. 2, pp. 497-499. Prepublished online as a Blood First Edition Paper on September 21, 2006; DOI 10.1182/blood-2006-07-035493. This Article Full Text (PDF) All Versions of this Article: blood-2006-07-035493v1 109/2/497    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Quintas-Cardama, A. Articles by Cortes, J. Search for Related Content PubMed PubMed Citation Articles by Quintas-Cardama, A. Articles by Cortes, J. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 20, 2006 Accepted September 4, 2006 Dasatinib (BMS-354825) is active in Philadelphia chromosome-positive chronic myelogenous leukemia after imatinib and nilotinib (AMN107) therapy failure Alfonso Quintas-Cardama, Hagop Kantarjian, Dan Jones, Claude Nicaise, Susan O'Brien, Francis Giles, Moshe Talpaz, and Jorge Cortes* Dept of Leukemia, University of Texas, MD Anderson Cancer Center, Houston, TX Dept of Hematopathology, University of Texas, MD Anderson Cancer Center, Houston, TX Briston-Myers Squibb, Wallingford, CT University of Texas MD Anderson Cancer Center, Houston, TX University of Michigan, Ann Arbor, MI * Corresponding author; email: jcortes{at}mdanderson.org. Developing strategies to counteract imatinib-resistance constitutes a challenge in chronic myelogenous leukemia (CML). Therapy with the tyrosine kinase inhibitors nilotinib (Tasigna; AMN107) and dasatinib (Sprycel; BMS-354825) has produced high rates of hematologic and cytogenetic response. Src kinase activation has been linked to Bcr-Abl-mediated leukemogenesis and CML progression. In addition to binding Abl kinase with less stringent conformational requirements than imatinib, dasatinib is a potent Src kinase inhibitor. In the current study, we report on 23 patients with CML (19 of them in accelerated or blastic phases) treated with dasatinib after treatment failure with both imatinib and nilotinib. Thirteen (57%) of 23 patients responded to dasatinib: 10 (43%) had a complete hematologic response (CHR), including 7 (32%) who had a cytogenetic response (2 complete, 4 partial, and 1 minor). These results suggest that dasatinib may be active in some patients after failure to both imatinib and nilotinib. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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