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BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet by Simona Soverini, Andreas Hochhaus, Franck E. Nicolini, Franz Gruber, Thoralf Lange, Giuseppe Saglio, Fabrizio Pane, Martin C. Müller, Thomas Ernst, Gianantonio Rosti, Kimmo Porkka, Michele Baccarani, Nicholas C. P. Cross, and Giovanni Martinelli Blood Volume 118(5):1208-1215 August 4, 2011 ©2011 by American Society of Hematology Map of all the amino acid substitutions in the Bcr-Abl KD identified in clinical samples from patients reported to be resistant to imatinib in published papers. Simona Soverini et al. Blood 2011;118:1208-1215 ©2011 by American Society of Hematology Flow chart summarizing when mutation analysis is recommended in CML patients treated with imatinib first-line. Simona Soverini et al. Blood 2011;118:1208-1215 ©2011 by American Society of Hematology Cellular IC50 (nM) of imatinib (IM), nilotinib (NI), and dasatinib (DA) and fold increase with respect to the IC50 for wild-type (WT) Bcr-Abl of the M244V, L248V, G250E, Q252H, Y253H, Y253F, E255K, E255V, E279K, and V299L mutant forms. Simona Soverini et al. Blood 2011;118:1208-1215 ©2011 by American Society of Hematology Cellular IC50 (nM) of imatinib (IM), nilotinib (NI), and dasatinib (DA) and fold increase with respect to the IC50 for wild-type (WT) Bcr-Abl of the F311L, T315I, F317L, M351T, F359V, V379I, L384M, L387M, H396R, H396P, and F486S mutant forms. Simona Soverini et al. Blood 2011;118:1208-1215 ©2011 by American Society of Hematology