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• W1488809246 abstract "The nitrogen mustard anticancer drugs are widely used for treating many forms of cancer. However, a number of toxic side effects, including secondary tumors, limit their clinical utility. There is strong evidence that the effectiveness for killing cancer cells (cytotoxicity) of these drugs is directly related to the ability of their metabolites to form interstrand DNA crosslinks. These crosslinks are formed by the sequential alkylation of two bases on complementary DNA strands. Other products, including monoalkylated adducts and intrastrand crosslinks are much less cytotoxic, and can mutate the DNA in normal cells leading to the formation of secondary tumors. The nitrogen mustards have a complex DNA-alkylation chemistry. They form monoalkylation adducts at a number of different sites on DNA and the predominant lesions vary between mustards and are strongly modulated by conjugation with DNA-targeting groups including intercalators, minor groove binders, and triplex-forming DNA oligomers. Only a small fraction of the DNA-alkylation events proceed to the formation of the therapeutically useful, highly cytotoxic crosslinks. For this reason there is considerable ongoing research to improve the efficiency of crosslink formation, and reduce the mutagenic effects of the other mustard-induced lesions. The phosphoramide mustard prodrugs including cyclophosphamide and ifosfamide, produce acrolein as a metabolic byproduct. Like the mustards themselves, acrolein has a complex DNA-alkylation chemistry, leading to a diversity of DNA adducts." @default.
• W1488809246 created "2016-06-24" @default.
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• W1488809246 date "2002-01-01" @default.
• W1488809246 modified "2023-09-23" @default.
• W1488809246 title "DNA-alkylating events associated with nitrogen mustard based anticancer drugs and the metabolic byproduct Acrolein" @default.
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• W1488809246 doi "https://doi.org/10.1016/s1067-568x(02)80004-4" @default.
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