title: [Mechanisms of resistance to BCR-ABL kinase inhibitors].
abstract: Since the introduction of imatinib mesylate for the treatment of chronic myeloid leukaemia, impressive clinical responses were observed in the majority of patients in chronic phase. However, not all patients experience an optimal response to imatinib mesylate or even to the more potent, second generation tyrosine kinase inhibitors. Furthermore, responses are not sustained in a number of patients, and it is yet unclear whether the inhibitors can be safely discontinued in patients who achieve long-term remission. The emergence of resistance to second generation tyrosine kinase inhibitors has become a significant problem that led to extensive studies on the causal mechanisms. This review will describe our current state of knowledge on why and how chronic myeloid leukaemia cells can develop resistance to second generation tyrosine kinase inhibitors.
authors.affiliation: Laboratório de Hemato-Oncologia. Unidade de Biologia Molecular. Instituto Português de Oncologia Francisco Gentil. Lisboa. Portugal.. jdiamond@ipolisboa.min-saude.pt.
authors.forename: Joana
authors.initials: J
authors.lastname: Diamond
authors.forename: Maria Gomes
authors.initials: MG
authors.lastname: da Silva
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides / Q000627:therapeutic use; D019008:Drug Resistance, Neoplasm; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors*; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy*; D010879:Piperazines / Q000627:therapeutic use; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl