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Nucleotide excision repair and anti-cancer chemotherapy

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Abstract

DNA repair is an important effector of anti-cancer drug resistance. In recent years, it has become apparent that DNA repair is an extremely complex process. Processes within DNA repair that may contribute to one or more drug resistance phenotypes include; O-6-alkyltransferase activity, base excision repair, mismatch repair, nucleotide excision repair, and gene specific repair. Clearly, several of these processes may show increased activity within any single cell, or tumor, at any one time. This review attempts to touch briefly upon the question of the distinctions between each of these specific pathways; and then seeks to expand on nucleotide excision repair as a possible effector of cellular and clinical resistance to platinum-based anticancer therapy.

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  1. Division of Clinical Sciences, National Cancer Institute, Building 10, Room 12N226, Bethesda, MD, 20892, U.S.A. E-mail

    Eddie Reed

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Reed, E. Nucleotide excision repair and anti-cancer chemotherapy. Cytotechnology 27, 187–201 (1998). https://doi.org/10.1023/A:1008016922425

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