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Javier Pinilla-Ibarz and Alfonso Quintás-Cardama

. 9 Hochhaus A La Rosee P . Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance . Leukemia 2004 ; 18 : 1321 – 1331 . 10 Litzow MR . Imatinib resistance: obstacles and opportunities . Arch

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Jerald P. Radich

not out of the woods yet,” warned Dr. Radich. This approach should only be considered within the context of a clinical trial, he added. “But if I were tolerating these drugs well, I would stay on them.” Mutational Analysis for Imatinib Resistance

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Jorge Cortes, John M. Goldman and Timothy Hughes

-ABL mutation status is critical for determining the best treatment strategy, including the selection of dasatinib versus nilotinib, for patients with CML experiencing imatinib resistance. Detailed analyses have revealed that some BCR-ABL mutations are less

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Jorge Cortes, Clara Chen, Michael Mauro, Neela Kumar, Catherine Davis and Stuart L. Goldberg

associated with dose reductions. Results: Of the 349 pts treated with 1L NIL, 281 (80.5%) started at the standard dose of 300 mg (BID) or the 400 mg (BID) dose for imatinib-resistance/intolerance, and 37 (10.6%) and 31 pts (8.9%) started on 150‒200 mg BID

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Michael Deininger

. 28 Barthe C Cony-Makhoul P Melo JV Mahon JR . Roots of clinical resistance to STI-571 cancer therapy . Science 2001 ; 293 : 2163 . 29 Azam M Latek RR Daley GQ . Mechanisms of autoinhibition and STI-571/imatinib resistance revealed

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Patrick A. Brown and Joseph C. Alvarnas

survival rates, even among elderly patients for whom intensive chemotherapeutic options are inappropriate. TKI resistance has been reported in Ph+ ALL; however, second-generation agents may provide an effective alternative for some patients with imatinib

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Jean McDougall, Scott D. Ramsey and Jerald Radich

myeloid leukemia . N Engl J Med 2003 ; 348 : 994 – 1004 . 15. le Coutre PD Giles FJ Hochhaus A . Nilotinib in patients with Ph+ chronic myeloid leukemia in accelerated phase following imatinib resistance or intolerance: 24-month follow

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Jerald P. Radich

over time and imatinib resistance within 3 years. According to Dr. Radich, “As phase goes up, the probability of acquiring point mutations dramatically increases.” Thus, imatinib-resistant cases are similar to cases of advanced-phase disease, he noted

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George D. Demetri, Robert S. Benjamin, Charles D. Blanke, Jean-Yves Blay, Paolo Casali, Haesun Choi, Christopher L. Corless, Maria Debiec-Rychter, Ronald P. DeMatteo, David S. Ettinger, George A. Fisher, Christopher D. M. Fletcher, Alessandro Gronchi, Peter Hohenberger, Miranda Hughes, Heikki Joensuu, Ian Judson, Axel Le Cesne, Robert G. Maki, Michael Morse, Alberto S. Pappo, Peter W. T. Pisters, Chandrajit P. Raut, Peter Reichardt, Douglas S. Tyler, Annick D. Van den Abbeele, Margaret von Mehren, Jeffrey D. Wayne and John Zalcberg

activity of sunitinib malate against primary KIT and PDGFRA mutations found in GISTs essentially parallels that of imatinib, but this drug also has activity against some forms of KIT with secondary imatinib-resistance mutations. 43 Kinase genotype has

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Susan O'Brien, Ellin Berman, Hossein Borghaei, Daniel J. DeAngelo, Marcel P. Devetten, Steven Devine, Harry P. Erba, Jason Gotlib, Madan Jagasia, Joseph O. Moore, Tariq Mughal, Javier Pinilla-Ibarz, Jerald P. Radich, Neil P. Shah, Paul J. Shami, B. Douglas Smith, David S. Snyder, Martin S. Tallman, Moshe Talpaz and Meir Wetzler

imatinib resistance with a novel ABL kinase inhibitor . Science 2004 ; 305 : 399 – 401 . 22 Talpaz M Shah NP Kantarjian H . Dasatinib in imatinib resistant Philadelphia chromosome-positive leukemias . N Eng J Med 2006 ; 354 : 2531 – 2541