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Blood, 9 July 2009, Vol. 114, No. 2, pp. 261-263. Prepublished online as a Blood First Edition Paper on May 4, 2009; DOI 10.1182/blood-2008-09-180604. This Article Full Text (PDF) All Versions of this Article: blood-2008-09-180604v1 114/2/261    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 September 25, 2008 Accepted April 24, 2009 Tyrosine kinase inhibitor-induced platelet dysfunction in patients with chronic myeloid leukemia Alfonso Quintas-Cardama, Xin Han, Hagop Kantarjian, and Jorge Cortes* Department of Leukemia, The University of Texas M.D. Anderson Cancer Center, Houston, TX, United States Department of Laboratory Medicine, The University of Texas M.D. Anderson Cancer Center, Houston, TX, United States * Corresponding author; email: jcortes{at}mdanderson.org. Dasatinib is associated with increased risk of bleeding among patients with chronic myeloid leukemia (CML), even in the absence of thrombocytopenia, suggesting the presence of a hemostatic defect. We tested platelet aggregation in 91 patients with CML in chronic phase either off-therapy (n=4) or receiving dasatinib (n=27), bosutinib (n=32), imatinib (n=19), or nilotinib (n=9). All but 3 patients receiving simultaneously imatinib and warfarin had normal coagulation studies. All 4 patients off-therapy had normal platelet aggregation. Impaired platelet aggregation on stimulation with arachidonic acid, epinephrine, or both was observed in 70%, 85%, and 59% of patients on dasatinib, respectively. Eighty-five percent of patients on bosutinib, 100% on nilotinib, and 33% on imatinib had normal platelet aggregation. Dasatinib 400 nM induced rapid and marked prolongation of closure time to collagen/epinephrine in normal whole blood on the PFA-100 system. In conclusion, dasatinib, and to some extent imatinib, produces abnormalities in platelet aggregometry testing. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. E. McKenzie and M. P. Reilly The clot thickens (or not) Blood, August 27, 2009; 114(9): 1722 - 1723. [Abstract] [Full Text] [PDF] M.-P. Gratacap, V. Martin, M.-C. Valera, S. Allart, C. Garcia, P. Sie, C. Recher, and B. Payrastre The new tyrosine-kinase inhibitor and anticancer drug dasatinib reversibly affects platelet activation in vitro and in vivo Blood, August 27, 2009; 114(9): 1884 - 1892. [Abstract] [Full Text] [PDF]

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