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Blood, 15 August 2006, Vol. 108, No. 4, pp. 1421-1423. Prepublished online as a Blood First Edition Paper on April 6, 2006; DOI 10.1182/blood-2006-02-001933. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-02-001933v1 108/4/1421    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 Jabbour, E. Articles by de Lima, M. Search for Related Content PubMed PubMed Citation Articles by Jabbour, E. Articles by de Lima, M. Related Collections Neoplasia Transplantation Oncogenes and Tumor Suppressors Brief Reports Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents TRANSPLANTATION Brief report Allogeneic stem cell transplantation for patients with chronic myeloid leukemia and acute lymphocytic leukemia after Bcr-Abl kinase mutation–related imatinib failure Elias Jabbour, Jorge Cortes, Hagop M. Kantarjian, Sergio Giralt, Dan Jones, Roy Jones, Francis Giles, Borje S. Andersson, Richard Champlin, and Marcos de Lima From the Departments of Blood and Marrow Transplantation, Leukemia, and Hematopathology, University of Texas M. D. Anderson Cancer Center, Houston. Resistance to imatinib mesylate is an emerging problem in the treatment of chronic myeloid leukemia (CML), often associated with point mutations in the Bcr-Abl kinase domain. Outcome of patients with such mutations after allogeneic stem cell transplantation (Allo-SCT) is unknown. Ten imatinib-resistant patients with Bcr-Abl kinase mutations received a transplant: 9 had CML (3 in chronic phase, 4 in accelerated phase, and 2 in blast phase) and 1 had Philadelphia-positive acute lymphocytic leukemia (ALL). Patients harbored 9 different protein kinase mutations (T315I mutation, n = 2). Preparative regimens were ablative (n = 7) and nonablative (n = 3). All patients engrafted; there were no treatment-related deaths. Disease response was complete molecular (CMR; n = 7), major molecular (n = 2), and no response (n = 1). Three patients (mutations Q252H, E255K, and T315I) died of relapse after Allo-SCT. Seven patients are alive (6 in CMR) for a median of 19 months. Allo-SCT remains an important salvage option for patients who develop resistance to imatinib through Bcr-Abl mutations. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. M. Goldman How I treat chronic myeloid leukemia in the imatinib era Blood, October 15, 2007; 110(8): 2828 - 2837. [Abstract] [Full Text] [PDF] H. de Lavallade, J. S. Khorashad, H. P. Davis, D. Milojkovic, J. S. Kaeda, J. M. Goldman, J. F. Apperley, and D. Marin Interferon-{alpha} or homoharringtonine as salvage treatment for chronic myeloid leukemia patients who acquire the T315I BCR-ABL mutation Blood, October 1, 2007; 110(7): 2779 - 2780. [Full Text] [PDF] F. E. Nicolini, S. Hayette, S. Corm, E. Bachy, D. Bories, M. Tulliez, F. Guilhot, L. Legros, F. Maloisel, J.-J. Kiladjian, et al. Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation Haematologica, September 1, 2007; 92(9): 1238 - 1241. [Abstract] [Full Text] [PDF] F. J. Giles, J. Cortes, D. Jones, D. Bergstrom, H. Kantarjian, and S. J. Freedman MK-0457, a novel kinase inhibitor, is active in patients with chronic myeloid leukemia or acute lymphocytic leukemia with the T315I BCR-ABL mutation Blood, January 15, 2007; 109(2): 500 - 502. [Abstract] [Full Text] [PDF] S. Branford Chronic Myeloid Leukemia: Molecular Monitoring in Clinical Practice Hematology, January 1, 2007; 2007(1): 376 - 383. [Abstract] [Full Text] [PDF]

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