Journal
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
Volume 37, Issue 6, Pages 1316-1325Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ije/dyn145
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Funding
- European Commission FP5 [QLG1-CT-2001-01049]
- Ligue contre le Cancer (France)
- Societe 3M (France)
- Mutuelle Generale de l'Education Nationale
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- German Cancer Aid
- German Cancer Research Center
- German Federal Ministry of Education and Research
- Danish Cancer Society
- Instituto de Salud Carlos III of the Spanish Ministry of Health (CIBER Epidemiologia y Salud Publica
- RETIC [RD06/0020]
- AGAUR [2002-PIR-00333]
- Generalitat de Catalunya
- Cancer Research UK
- Medical Research Council, UK
- Stroke Association, UK
- British Heart Foundation
- Department of Health, UK
- Food Standards Agency, UK
- Wellcome Trust, UK
- Greek Ministry of Health
- Greek Ministry of Education
- Italian Association for Research on Cancer (AIRC)
- Dutch Ministry of Public Health, Welfare and Sports
- Dutch Ministry of Health
- Dutch Prevention Funds
- LK Research Funds
- Dutch ZON (Zorg Onderzoek Nederland)
- World Cancer Research Fund (WCRF)
- Swedish Cancer Society
- Swedish Scientific Council
- Regional Government of Skane, Sweden
- Norwegian Cancer Society
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Background The contribution of genetic variation in DNA repair genes to gastric cancer (GC) risk remains essentially unknown. The aim of this study was to explore the relative contribution of DNA repair gene polymorphisms to GC risk and severe chronic atrophic gastritis (SCAG). Method A nested case control study within the EPIC cohort was performed including 246 gastric adenocarcinomas and 1175 matched controls. Controls with SCAG (n 91), as defined by low pepsinogen A (PGA) levels, and controls with no SCAG (n 1061) were also compared. Twelve polymorphisms at DNA repair genes (MSH2, MLH1, XRCC1, OGG1 and ERCC2) and TP53 gene were analysed. Antibodies against Helicobacter pylori were measured. Results No association was observed for any of these polymorphisms with stomach cancer risk. However, ERCC2 K751Q polymorphism was associated with an increased risk for non-cardial neoplasm [odds ratio (OR) 1.78; 95 confidence interval (CI) 1.023.12], being ERCC2 K751Q and D312N polymorphisms associated with the diffuse type. ERCC2 D312N (OR 2.0; 95 CI 1.093.65) and K751Q alleles (OR 1.82; 95 CI 1.013.30) and XRCC1 R399Q (OR 1.69; 95 CI 1.022.79) allele were associated with an increased risk for SCAG. Conclusion Our study supports a role of ERCC2 in non-cardial GC but not in cardial cancer. A concordant result was observed for subjects with low PGA levels. XRCC1 allele was associated also with SCAG. This is the first prospective study suggesting that individual variation in DNA repair may be relevant for gastric carcinogenesis, a finding that will require further confirmation validation in larger independent studies.
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