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Blood, 1 April 2005, Vol. 105, No. 7, pp. 2640-2653. Prepublished online as a Blood First Edition Paper on December 23, 2004; DOI 10.1182/blood-2004-08-3097. This Article Full Text (PDF) All Versions of this Article: 2004-08-3097v1 105/7/2640    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 Deininger, M. Articles by Druker, B. J Search for Related Content PubMed PubMed Citation Articles by Deininger, M. Articles by Druker, B. J Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 11, 2004 Accepted November 29, 2004 The development of imatinib as a therapeutic agent for chronic myeloid leukemia Michael Deininger*, Elisabeth Buchdunger, and Brian J Druker Oregon Health & Science University Cancer Institute, Portland, OR, USA Novartis Institutes for Biomedical Research, Novartis Pharma AG, Basel, Switzerland Oregon Health & Science University Cancer Institute, Portland, OR, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA * Corresponding author; email: deininge{at}ohsu.edu. Imatinib has revolutionized drug therapy of chronic myeloid leukemia (CML). Preclinical studies were promising but the results of clinical trials by far exceeded expectations. Responses in chronic phase are unprecedented, with rates of complete cytogenetic response (CCR) of more than 40% in patients after failure of interferon- (IFN) and more than 80% in newly diagnosed patients, a level of efficacy that led to regulatory approval in record time. While most of these responses are stable, resistance to treatment after an initial response is common in more advanced phases of the disease. Mutations in the kinase domain (KD) of BCR-ABL that impair imatinib binding have been identified as the leading cause of resistance. Patients with CCR who achieve a profound reduction of BCR-ABL mRNA have a very low risk of disease progression. However, residual disease usually remains detectable with reverse transcription-polymerase chain reaction (RT-PCR), indicating that disease eradication may pose a significant challenge. The mechanisms underlying the persistence of minimal residual disease are unknown. In this manuscript, we review the preclinical and clinical development of imatinib for the therapy of CML, resistance and strategies that may help to eliminate resistant or residual leukemia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. A. Byers, B. Sen, B. Saigal, L. Diao, J. Wang, M. Nanjundan, T. Cascone, G. B. Mills, J. V. Heymach, and F. M. Johnson Reciprocal Regulation of c-Src and STAT3 in Non-Small Cell Lung Cancer Clin. Cancer Res., November 15, 2009; 15(22): 6852 - 6861. [Abstract] [Full Text] [PDF] P. Ceppi, M. Papotti, V. Monica, M. L. Iacono, S. Saviozzi, M. Pautasso, S. Novello, S. Mussino, E. Bracco, M. Volante, et al. Effects of Src kinase inhibition induced by dasatinib in non-small cell lung cancer cell lines treated with cisplatin Mol. Cancer Ther., November 1, 2009; 8(11): 3066 - 3074. [Abstract] [Full Text] [PDF] X. Li, Y. He, C. H. Ruiz, M. Koenig, and M. D. 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