Division of Clinical Sciences, National Cancer Institute, Building 10, Room 12N226, Bethesda, MD, 20892, U.S.A. E-mail,
Cytotechnology. 1998 Sep;27(1-3):187-201. doi: 10.1023/A:1008016922425.
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.
DNA 修复是抗肿瘤药物耐药性的重要效应因子。近年来，人们已经明显认识到 DNA 修复是一个极其复杂的过程。在 DNA 修复过程中，可能导致一种或多种耐药表型的过程包括：O-6-烷基转移酶活性、碱基切除修复、错配修复、核苷酸切除修复和基因特异性修复。显然，在任何一个时间点，在单个细胞或肿瘤中，其中几种过程都可能表现出活性增强。这篇综述简要地探讨了这些特定途径之间的区别问题；然后探讨了核苷酸切除修复作为细胞和临床对铂类抗癌治疗耐药性的一种可能效应因子。
