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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 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 Citation Map 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. Related Collections Neoplasia Oncogenes and Tumor Suppressors Brief Reports Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CLINICAL TRIALS AND OBSERVATIONS Brief report Dasatinib (BMS-354825) is active in Philadelphia chromosome–positive chronic myelogenous leukemia after imatinib and nilotinib (AMN107) therapy failure Alfonso Quintas-Cardama1, Hagop Kantarjian1, Dan Jones2, Claude Nicaise3, Susan O'Brien1, Francis Giles1, Moshe Talpaz4, and Jorge Cortes1, 1 Department of Leukemia and 2 Department of Hematopathology, The University of Texas M. D. Anderson Cancer Center, Houston; 3 Bristol-Myers Squibb, Wallingford, CT; 4 Department of Internal Medicine, Hematologic Malignancies, University of Michigan, Ann Arbor Developing strategies to counteract imatinib resistance constitutes a challenge in chronic myelogenous leukemia (CML). Therapy with the tyrosine kinase inhibitors nilotinib (AMN107) and dasatinib (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. More than half (13; 57%) of 23 patients responded to dasatinib: 10 (43%) had a complete hematologic response (CHR), including 7 (30%) 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 with both imatinib and nilotinib. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Redaelli, R. Piazza, R. Rostagno, V. Magistroni, P. Perini, M. Marega, C. Gambacorti-Passerini, and F. Boschelli Activity of Bosutinib, Dasatinib, and Nilotinib Against 18 Imatinib-Resistant BCR/ABL Mutants J. Clin. Oncol., January 20, 2009; 27(3): 469 - 471. [Full Text] [PDF] J. Cortes When Imatinib Fails, What Else Is There? ASCO Educational Book, January 1, 2009; 2009(1): 402 - 406. [Abstract] [Full Text] [PDF] J. Wu, F. Meng, L.-Y. Kong, Z. Peng, Y. Ying, W. G. Bornmann, B. G. Darnay, B. Lamothe, H. Sun, M. Talpaz, et al. Association Between Imatinib-Resistant BCR-ABL Mutation-Negative Leukemia and Persistent Activation of LYN Kinase J Natl Cancer Inst, July 2, 2008; 100(13): 926 - 939. [Abstract] [Full Text] [PDF] L. J. Christopher, D. Cui, C. Wu, R. Luo, J. A. Manning, S. J. Bonacorsi, M. Lago, A. Allentoff, F. Y. F. Lee, B. McCann, et al. Metabolism and Disposition of Dasatinib after Oral Administration to Humans Drug Metab. 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