Abstract
Very little is known about how acquired oncogenic mutations arise. In this issue of Cancer Cell, Klemm and colleagues present evidence supporting a role for the antibody diversification enzyme activation-induced deaminase (AID) in the generation of mutations associated with disease progression and drug resistance in chronic myeloid leukemia.
MeSH terms
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Antineoplastic Agents / therapeutic use
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Benzamides
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Blast Crisis / drug therapy*
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Cell Line, Tumor
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Cytidine Deaminase / metabolism*
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Disease Progression
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Drug Resistance, Neoplasm / genetics*
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Humans
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Imatinib Mesylate
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
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Models, Biological
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Mutation*
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Piperazines / therapeutic use*
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Pyrimidines / therapeutic use*
Substances
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Antineoplastic Agents
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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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AICDA (activation-induced cytidine deaminase)
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Cytidine Deaminase