Abstract
Various mechanisms have been implicated in nitrogen mustard drug resistance. The role of these mechanisms in the development of chlorambucil drug resistance in chronic lymphocytic leukemia (CLL) is discussed. We review these mechanisms with emphasis on the emerging role of DNA repair, and specifically, recombinational repair. Inhibition of these repair processes may lead to new therapies, not only in CLL, but in other malignancies as well.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antineoplastic Agents, Alkylating / pharmacology*
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Apoptosis
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Biological Transport
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Chlorambucil / pharmacology*
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Cross-Linking Reagents / pharmacology
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DNA Repair*
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Drug Resistance, Neoplasm*
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Genes, p53 / genetics
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Glutathione / genetics
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Glutathione Transferase / genetics
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Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy*
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Leukemia, Lymphocytic, Chronic, B-Cell / metabolism*
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Mechlorethamine / pharmacology*
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Models, Genetic
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Mutation
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Recombination, Genetic
Substances
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Antineoplastic Agents, Alkylating
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Cross-Linking Reagents
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Chlorambucil
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Mechlorethamine
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Glutathione Transferase
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Glutathione