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Carcinogenesis Advance Access originally published online on March 31, 2005
Carcinogenesis 2005 26(8):1354-1359; doi:10.1093/carcin/bgi084
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Carcinogenesis vol.26 no.8 © Oxford University Press 2005; all rights reserved.

Selected DNA repair polymorphisms and gastric cancer in Poland

Wen-Yi Huang 1, *, Wong-Ho Chow 1, Nat Rothman 1, Jolanta Lissowska 2, Victor Llaca 3, Meredith Yeager 3, Witold Zatonski 2 and Richard B. Hayes 1

1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA, 2 Division of Cancer Epidemiology and Prevention, Cancer Center and M.Sklodowska-Curie Institute of Oncology, 02-781 Warsaw, Poland and 3 Core Genotyping Facility, Advanced Technology Center, National Cancer Institute-Frederick, Gaithersburg, MD 20892, USA

* To whom correspondence should be addressed: Division of Cancer Epidemiology and Genetics, National Cancer Institute, EPS 8113, MSC 7240, Bethesda, MD 20892, USA. Tel: +301 435 4710; Fax: +301 402 1819; Email: huangw{at}mail.nih.gov

Impaired DNA repair capacity may adversely affect cancer risk, particularly in subjects exposed to DNA damaging carcinogens, as found in tobacco smoke, or among subjects deficient for protective factors, as found in fruits and vegetables. We studied tobacco use, fruit and vegetable intake, and common non-synonymous single nucleotide polymorphisms in four DNA repair genes in relation to gastric cancer risk, in a population-based, case–control study of 281 incident gastric cancer cases and 390 controls, in Warsaw, Poland. Multivariate logistic regression analysis was performed to calculate odds ratios (OR) and 95% confidence intervals (CI). Increased risks of gastric cancer were found for smokers (OR = 3.1, CI = 1.9–5.1 for pack-years ≥40 versus never smokers) and subjects with low fruit intake (OR = 2.2, CI = 1.3–3.6 for 1st versus 4th quartile); risk associated with vegetable intake was not statistically significant. Allele frequencies among the controls were consistent with those previously reported for the 5 polymorphisms studied: XRCC1-Arg399Gln, XPD-Lys751Gln, MGMT-Ile143Val, Leu84Phe, and XRCC3-Thr241Met. None of the studied polymorphisms were independently associated with gastric cancer risk. Smoking-associated risks, however, were greatest for carriers of the XRCC1-399 ArgArg genotype (Pinteraction = 0.004). Risks associated with low intake of fruits or vegetables tended to be modified by selected polymorphisms in XRCC1, XPD and MGMT (Pinteraction = 0.1–0.2). Risk modification was not found for the other repair polymorphisms. Selected DNA repair polymorphisms did not have independent effects on gastric cancer risk; however, they may modify smoking- and probably diet-related risks for this disease. These results need replication in larger epidemiological studies of gastric cancer.


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