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Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2002-09-2896. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-09-2896v1 102/1/276    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 Branford, S. Articles by Hughes, T. Search for Related Content PubMed PubMed Citation Articles by Branford, S. Articles by Hughes, T. Related Collections Neoplasia Oncogenes and Tumor Suppressors Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 July 2003, Vol. 102, No. 1, pp. 276-283 NEOPLASIA Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis Susan Branford, Zbigniew Rudzki, Sonya Walsh, Ian Parkinson, Andrew Grigg, Jeff Szer, Kerry Taylor, Richard Herrmann, John F. Seymour, Chris Arthur, David Joske, Kevin Lynch, and Tim Hughes From the Institute of Medical and Veterinary Science, Adelaide, South Australia; Royal Melbourne Hospital, Melbourne, Victoria; Mater Hospital, Brisbane, Queensland; Royal Perth Hospital, Perth, Western Australia; Peter MacCallum Cancer Institute, Melbourne, Victoria; Royal North Shore Hospital, Sydney, New South Wales; Sir Charles Gairdner Hospital, Perth, Western Australia; and Novartis Pharmaceuticals Australia, North Ryde, Sydney. Imatinib-treated chronic myeloid leukemia (CML) patients with acquired resistance commonly have detectable BCR-ABL kinase domain mutations. It is unclear whether patients who remain sensitive to imatinib also have a significant incidence of mutations. We evaluated 144 patients treated with imatinib for BCR-ABL kinase domain mutations by direct sequencing of 40 accelerated phase (AP), 64 late chronic phase (≥ 12 months from diagnosis, late-CP), and 40 early-CP patients. Mutations were detected in 27 patients at 17 different residues, 13 (33%) of 40 in AP, 14 (22%) of 64 in late-CP, and 0 of 40 in early-CP. Acquired resistance was evident in 24 (89%) of 27 patients with mutations. Twelve (92%) of 13 patients with mutations in the adenosine triphosphate (ATP) binding loop (P-loop) died (median survival of 4.5 months after the mutation was detected). In contrast, only 3 (21%) of 14 patients with mutations outside the P-loop died (median follow-up of 11 months). As the detection of mutations was strongly associated with imatinib resistance, we analyzed features that predicted for their detection. Patients who commenced imatinib more than 4 years from diagnosis had a significantly higher incidence of mutations (18 [41%] of 44) compared with those treated within 4 years (9 [9%] of 100), P < .0001. Lack of a major cytogenetic response (MCR) was also associated with a higher likelihood of detecting a mutation; 19 (38%) of 50 patients without a MCR had mutations compared with 8 (8.5%) of 94 with an MCR, P < .0001. In conclusion, the detection of kinase domain mutations using a direct sequencing technique was almost always associated with imatinib resistance, and patients with mutations in the P-loop had a particularly poor prognosis. (Blood. 2003; 102:276-283) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Resistance to imatinib: more and more mutations Charles L. Sawyers Blood 2003 102: 4-5. [Full Text] [PDF] This article has been cited by other articles: J. P. Radich How I monitor residual disease in chronic myeloid leukemia Blood, October 15, 2009; 114(16): 3376 - 3381. [Abstract] [Full Text] [PDF] R. D. Press, S. G. Willis, J. Laudadio, M. J. Mauro, and M. W. N. 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