Abstract
Despite high rates of hematologic and cytogenetic responses to imatinib therapy, the emergence of resistance to imatinib has been recognized as a major problem in the treatment of Ph-positive leukemia. The high frequency of BCR-ABL mutations and amplifications represents the high degree of heterogeneity in patients with advanced phase of CML, in whom multiple leukemic clones may exist. Therefore, a single inhibitor is unlikely to able to block all mutants.
MeSH terms
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Benzamides
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Drug Resistance, Neoplasm*
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Fusion Proteins, bcr-abl / antagonists & inhibitors
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Fusion Proteins, bcr-abl / genetics
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Genetic Heterogeneity
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Humans
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Imatinib Mesylate
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Leukemia / drug therapy*
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
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Mutation
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Piperazines / pharmacology
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Piperazines / therapeutic use*
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Pyrimidines / pharmacology
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Pyrimidines / therapeutic use*
Substances
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Benzamides
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Piperazines
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Pyrimidines
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Imatinib Mesylate
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Fusion Proteins, bcr-abl