Abstract
Rarely has progress in treatment of leukemia been as dramatic and convincing as with the BCR-ABL tyrosine kinase inhibitor imatinib.(1) Imatinib induces remissions of CML as fast as hydroxyurea, achieves rates of cytogenetic remissions that by far exceed those induced by interferon alpha and has a toxicity profile as favourable as that of hydroxyurea and much superior to that of interferon alpha.(2) In addition, the causal approach of this new drug, which may well serve as a model for new treatment modalities in other neoplasias is reassuring.
MeSH terms
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Antineoplastic Agents / therapeutic use
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Benzamides
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Clinical Trials as Topic
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Enzyme Inhibitors / therapeutic use
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Fusion Proteins, bcr-abl
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Humans
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Hydroxyurea / therapeutic use
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Imatinib Mesylate
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Interferon-alpha / therapeutic use
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
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Piperazines / therapeutic use
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Protein-Tyrosine Kinases / antagonists & inhibitors
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Protein-Tyrosine Kinases / metabolism
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Pyrimidines / therapeutic use
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Stem Cell Transplantation
Substances
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Antineoplastic Agents
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Benzamides
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Enzyme Inhibitors
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Interferon-alpha
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Piperazines
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Pyrimidines
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Imatinib Mesylate
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Protein-Tyrosine Kinases
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Fusion Proteins, bcr-abl
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Hydroxyurea