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Carcinogenesis Advance Access originally published online on August 2, 2006
Carcinogenesis 2007 28(1):118-123; doi:10.1093/carcin/bgl130
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Published by Oxford University Press 2006

Polymorphisms in Th1-type cell-mediated response genes and risk of gastric cancer

L. Hou1,*, E.M. El-Omar2, J. Chen1, P. Grillo3, C.S. Rabkin1, A. Baccarelli3,4, M. Yeager5, S.J. Chanock1,5, W. Zatonski6, L.H. Sobin7, J. Lissowska6, J.F. Fraumeni, Jr1 and W.H. Chow1

1 Division of Cancer Epidemiology and Genetics, National Cancer Institute 6120 Executive Boulevard, EPS 8123, Bethesda, MD 20852-7242, USA
2 Department of Medicine and Therapeutics, Institute of Medical Sciences, University of Aberdeen Foresterhill, Aberdeen, AB25 2ZD, UK
3 Molecular and Genetic Epidemiology Center—Epidemiology Unit, Department of Occupational, Clinical and Preventive Medicine, IRCCS Ospedale Maggiore Policlinico Mangiagalli e Regina Elena, I-20122 Milan, Italy
4 EPOCA Research Center for Clinical, Occupational and Environmental Epidemiology, Department of Occupational Medicine, University of Milan I-20122 Milan, Italy
5 Core Genotyping Facility, Advanced Technology Center, National Cancer Institute Gaithersburg, MD 20892, USA
6 Division of Cancer Epidemiology and Prevention, Cancer Center and M.Sklodowska-Curie Institute of Oncology 02-781 Warsaw, Poland
7 Department of Hepatic and Gastrointestinal Pathology, Armed Forces Institute of Pathology Washington, DC, 20306, USA

*To whom correspondence should be addressed. Tel: +1 301-451-5031 Fax: +1 301 402 4489; Email: lifangh2{at}mail.nih.gov

Helicobacter pylori infection, the dominant risk factor for gastric cancers, has been shown to elicit T helper type 1 (Th1) polarized immunological responses. We conducted a population-based study of 305 gastric cancer cases and 427 age- and gender-matched controls in Warsaw, Poland, to evaluate the association with several variants in genes responsible for Th1-cell-mediated response. Genotyping was performed on genomic DNA by TaqManTM assays to determine TNFA (–308 G>A, –417 G>A, –555 G>A, –1036 C>T, –1042 C>A, –1210 T>C), IL1A (–889 C>T), IFNGR2 (Ex7-128 T>C, Ex2-34 C>G and Ex2-16 A>G) and IL12A (IVS2-798 T>A, IVS2-701 C>A and Ex7+277 G>A) polymorphisms. We used unconditional logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for sex, age, education and smoking status. Out of six single nucleotide polymorphisms (SNPs) tested in TNFA, gastric cancer risk was significantly associated with the TNFA (–308 G>A) polymorphism, with ORs of 1.4 (95% CI: 1.0–2.0) for the G/A and 2.5 (95% CI: 1.3–4.9) for the A/A genotype carriers, when compared with the more frequent genotype (G/G) (P-trend < 0.001). Among the three tested SNPs in the IFNGR2 gene, only the Ex7-128C>T polymorphism was associated with increased risk, with ORs of 1.5 (95% CI: 1.0–2.3) for T/C and 1.7 (95% CI: 1.1–2.7) for C/C carriers when compared with T/T carriers (P-trend = 0.01). Subjects carrying both IFNGR2 Ex7-128 C/C and TNFA –308 A/A genotypes had the highest risk (OR = 5.5, 95% CI: 1.5–19.4), although the interaction was not statistically significant. IL1A (–889 C>T) and the three examined IL12A variants were unrelated to gastric cancer risk. Our findings suggest that two Th1-related polymorphisms (TNFA –308 A>G and IFNGR2 Ex7-128 C>T) may increase the risk of gastric cancer.


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