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Blood, 15 February 2008, Vol. 111, No. 4, pp. 2378-2381. Prepublished online as a Blood First Edition Paper on November 2, 2007; DOI 10.1182/blood-2007-06-096396. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-06-096396v1 111/4/2378    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 Khorashad, J. S. Articles by Kaeda, J. S. Search for Related Content PubMed PubMed Citation Articles by Khorashad, J. S. Articles by Kaeda, J. S. Related Collections Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief Report In vivo kinetics of kinase domain mutations in CML patients treated with dasatinib after failing imatinib Jamshid S. Khorashad1, Dragana Milojkovic1, Puja Mehta1, Mona Anand1, Sara Ghorashian1, Alistair G. Reid1, Valeria De Melo1, Anna Babb1, Hugues de Lavallade1, Eduardo Olavarria1, David Marin1, John M. Goldman1, Jane F. Apperley1, and Jaspal S. Kaeda1 1 Department of Haematology, Hammersmith Hospitals Trust and Imperial College London, London, United Kingdom We sought kinase domain (KD) mutations at the start of treatment with dasatinib in 46 chronic myeloid leukemia (CML) patients resistant to or intolerant of imatinib. We identified BCR-ABL mutant subclones in 12 (26%) cases and used pyrosequencing to estimate subsequent changes in their relative size after starting dasatinib. Four patients lost their mutations, which remained undetectable, 3 patients retained the original mutation or lost it only transiently, 3 lost their original mutations but acquired a new mutation (F317L), and 2 developed another mutation (T315I) in addition to the original mutation within the same subclone. This study shows that expansion of a mutant Ph-positive clone that responds initially to a second generation tyrosine kinase inhibitor may be due either to late acquisition of a second mutation in the originally mutated clone, such as the T315I, or to acquisition of a completely new mutant clone, such as F317L. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. Jabbour, J. E. Cortes, and H. M. Kantarjian Suboptimal Response to or Failure of Imatinib Treatment for Chronic Myeloid Leukemia: What Is the Optimal Strategy? Mayo Clin. Proc., February 1, 2009; 84(2): 161 - 169. [Abstract] [Full Text] [PDF] E. Jabbour, H. M. Kantarjian, D. Jones, N. Reddy, S. O'Brien, G. Garcia-Manero, J. Burger, and J. Cortes Characteristics and outcome of chronic myeloid leukemia patients with F317L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors Blood, December 15, 2008; 112(13): 4839 - 4842. [Abstract] [Full Text] [PDF]

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