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Carcinogenesis Advance Access published online on March 31, 2005
Carcinogenesis, doi:10.1093/carcin/bgi084
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Published by Oxford University Press 2005
Received November 3, 2004
Revised March 2, 2005
Accepted March 25, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

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, Maryland 20892
2 Division of Cancer Epidemiology and Prevention, Cancer Center and M. Sklodowska-Curie Institute of Oncology, 02-781 Warsaw, Poland
3 Core Genotyping Facility, Advanced Technology Center, National Cancer Institute-Frederick, Gaithersburg, Maryland 20892

* To whom correspondence should be addressed.
Wen-Yi Huang, E-mail: huangw{at}mail.nih.gov


  Abstract

Background. 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. Methods. 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). Results. Increased risks of gastric cancer were found for smokers (OR=3.1, CI=1.9-5.1 for pack-years ≥40 vs. never smokers) and subjects with low fruit intake (OR=2.2, CI=1.3-3.6 for 1st vs. 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 and 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. Conslusion. Selected DNA repair polymorphisms did not have independent effects on gastric cancer risk, however, they may modify smoking- and possible diet-related risks for this disease. There results need replication in larger epidemiological studies of gastric cancer.

Keywords: DNA repair; Gastric cancer; Epidemiology; Poland.
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