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This Article Full Text Full Text (PDF) 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 Hoover, R. R. Articles by Daley, G. Q. Search for Related Content PubMed PubMed Citation Articles by Hoover, R. R. Articles by Daley, G. Q. Related Collections Neoplasia Brief Reports Related Letter in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 August 2002, Vol. 100, No. 3, pp. 1068-1071 BRIEF REPORT Overcoming STI571 resistance with the farnesyl transferase inhibitor SCH66336 Russell R. Hoover, Francois-Xavier Mahon, Junia V. Melo, and George Q. Daley From the Whitehead Institute for Biomedical Research, Cambridge, MA; Laboratoire Greffe de Moelle, Universite Victor Segalen, Bordeaux, France; Department of Haematology, Imperial College School of Medicine Hammersmith Hospital, London, United Kingdom. The development of chronic myeloid leukemia (CML) is dependent on the deregulated tyrosine kinase of the oncoprotein BCR-ABL. STI571 (imatinib mesylate), an abl tyrosine kinase inhibitor, has proven remarkably effective for the treatment of CML. However, resistance to STI571 because of enhanced expression or mutation of the BCR-ABL gene has been detected in patients. In the current study we show that the farnesyl transferase inhibitor (FTI) SCH66336 (lonafarnib) inhibits the proliferation of STI571-resistant BCR-ABL-positive cell lines and hematopoietic colony formation from peripheral blood samples of STI571-resistant patients with CML. Moreover, SCH66336 enhances STI571-induced apoptosis in STI571-sensitive cells and, in patients with STI571 resistance from gene amplification, cooperates with STI571 to induce apoptosis. Our data provide a rationale for combination clinical trials of STI571 and SCH66336 in CML patients and suggest that combination therapy may be effective in patients with STI571 resistance. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Letter in Blood Online: Apoptotic synergism between STI571 and the farnesyl transferase inhibitor SCH66336 on an imatinib-sensitive cell line Andres L. Brodsky, George Q. Daley, Russell R. Hoover, Donna Carr, and Paul Kirschmeier Blood 2003 101: 2070. [Full Text] [PDF] This article has been cited by other articles: M. Kurokawa, C. Zhao, T. Reya, and S. 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