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Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia Quintas-Cardama A; Kantarjian HM; Cortes JECancer Control 2009[Apr]; 16 (2): 122-31BACKGROUND: Although the vast majority of patients with chronic myeloid leukemia (CML) respond to the tyrosine kinase inhibitor (TKI) imatinib mesylate, resistance might occur de novo or during treatment. METHODS: The authors reviewed the known mechanisms of primary and secondary resistance to imatinib and other TKIs used in the management of CML. RESULTS: Mutations within the kinase domain of BCR-ABLI account for 30% to 40% of cases of imatinib resistance. Other mechanisms include BCR-ABLI amplification, overexpression of the SRC family of kinases, and pharmacokinetic and pharmacodynamic factors. CONCLUSIONS: Although not all resistance mechanisms have been identified and understood, several agents based on the known mechanisms have already been designed and developed and are beginning clinical trials.|Antineoplastic Agents/therapeutic use[MESH]|Benzamides[MESH]|Clinical Trials as Topic[MESH]|Drug Resistance, Neoplasm/*physiology[MESH]|Fusion Proteins, bcr-abl/genetics[MESH]|Humans[MESH]|Imatinib Mesylate[MESH]|Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy/genetics[MESH]|Mutation[MESH]|Piperazines/pharmacokinetics/*therapeutic use[MESH]|Protein Kinase Inhibitors/pharmacokinetics/*therapeutic use[MESH]|Pyrimidines/pharmacokinetics/*therapeutic use[MESH] |
