Symposium overview: Genetic polymorphisms in DNA repair and cancer risk

被引:73
作者
Hu, JJ
Mohrenweiser, HW
Bell, DA
Leadon, SA
Miller, MS
机构
[1] Wake Forest Univ, Sch Med, Dept Canc Biol, Winston Salem, NC 27157 USA
[2] Wake Forest Univ, Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27157 USA
[3] Lawrence Livermore Natl Lab, Biol & Biotechnol Res Program, Livermore, CA 94550 USA
[4] NIEHS, Res Triangle Pk, NC 27709 USA
[5] Univ N Carolina, Dept Radiat Oncol, Chapel Hill, NC 27514 USA
关键词
DNA repair; SNPs; cancer risk;
D O I
10.1006/taap.2002.9518
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
A symposium, Genetic Polymorphisms in DNA Repair and Cancer Risk, was presented at the 40th Annual Meeting of the Society of Toxicology, held in San Francisco, California, in March 2001. A brief report of the symposium was published (Kaiser, Science 292, 837-838, 2001). Molecular epidemiological studies have shown that polymorphic variants of genes involved in the metabolism and repair of carcinogens can act as cancer susceptibility genes. These variants of drug metabolic and DNA-repair enzymes either increase the activation of chemical carcinogens or decrease the cells' ability to detoxify/repair mutagenic damages. Although on an individual basis these variant alleles may only slightly change catalytic activity and increase cancer risk, their polymorphic frequency in the human population may contribute to a high proportion of cancer cases. Studies conducted over the past few years have identified variant alleles for a number of DNA-repair genes, some of which have been shown to change DNA-repair capacity. Identifying these genotypic alterations in DNA-repair enzymes and their association with cancer may help to elucidate the mechanisms of cancer etiology and to predict both disease risk and response to cancer therapy, since most antineoplastic treatments mediate their effects through DNA damage. (C) 2002 Elsevier Science (USA).
引用
收藏
页码:64 / 73
页数:10
相关论文
共 87 条
[1]   BRCA1 expression restores radiation resistance in BRCA1-defective cancer cells through enhancement of transcription-coupled DNA repair [J].
Abbott, DW ;
Thompson, ME ;
Robinson-Benion, C ;
Tomlinson, G ;
Jensen, RA ;
Holt, JT .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (26) :18808-18812
[2]   The 399Gln polymorphism in the DNA repair gene XRCC1 modulates the genotoxic response induced in human lymphocytes by the tobacco-specific nitrosamine NNK [J].
Abdel-Rahman, SZ ;
El-Zein, RA .
CANCER LETTERS, 2000, 159 (01) :63-71
[3]   Variant XRCC3 implicated in cancer is functional in homology-directed repair of double-strand breaks [J].
Araujo, FD ;
Pierce, AJ ;
Stark, JM ;
Jasin, M .
ONCOGENE, 2002, 21 (26) :4176-4180
[4]   Markers of DNA repair and susceptibility to cancer in humans: An epidemiologic review [J].
Berwick, M ;
Vineis, P .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2000, 92 (11) :874-897
[5]   XRCC3 is required for efficient repair of chromosome breaks by homologous recombination [J].
Brenneman, MA ;
Weiss, AE ;
Nickoloff, JA ;
Chen, DJ .
MUTATION RESEARCH-DNA REPAIR, 2000, 459 (02) :89-97
[6]   Genetic polymorphisms in DNA repair genes and risk of lung cancer [J].
Butkiewicz, D ;
Rusin, M ;
Enewold, L ;
Shields, PG ;
Chorazy, M ;
Harris, CC .
CARCINOGENESIS, 2001, 22 (04) :593-597
[7]   Sequence diversity in 36 candidate genes for cardiovascular disorders [J].
Cambien, F ;
Poirier, O ;
Nicaud, V ;
Herrmann, SM ;
Mallet, C ;
Ricard, S ;
Behague, I ;
Hallet, V ;
Blanc, H ;
Loukaci, V ;
Thillet, J ;
Evans, A ;
Ruidavets, JB ;
Arveiler, D ;
Luc, G ;
Tiret, L .
AMERICAN JOURNAL OF HUMAN GENETICS, 1999, 65 (01) :183-191
[8]  
Chen PC, 2000, CANCER EPIDEM BIOMAR, V9, P843
[9]   Common pathways for ultraviolet skin carcinogenesis in the repair and replication defective groups of xeroderma pigmentosum [J].
Cleaver, JE .
JOURNAL OF DERMATOLOGICAL SCIENCE, 2000, 23 (01) :1-11
[10]   Nucleotide excision repair "a legacy of creativity" [J].
Cleaver, JE ;
Karplus, K ;
Kashani-Sabet, M ;
Limoli, CL .
MUTATION RESEARCH-DNA REPAIR, 2001, 485 (01) :23-36