Genetic polymorphisms in folate metabolism and the risk of stomach cancer

Fang Fang Zhang, Mary Beth Terry, Lifang Hou, Jinbo Chen, Jolanta Lissowska, Meredith Yeager, Witold Zatonski, Stephen Chanock, Alfredo Morabia, Wong Ho Chow

Research output: Contribution to journalArticlepeer-review

Abstract

Folate deficiency has been implicated in the etiology of stomach cancer through abnormal DNA methylation and disrupted DNA synthesis and repair. Enzyme-coding genes involved in folate metabolism are often polymorphic. In a population-based study of 305 cases and 427 controls in Warsaw, Poland, we evaluated the risk of stomach cancer in relation to polymorphisms in folate-metabolizing genes, including MTHFR (Ex5+79C>T and Ex8-62A>C), MTR (Ex26-20A>G), and MTRR (Ex2-64A>G, Ex5+123C>T, Ex15+572C>T, Ex15-405A>T, Ex9-85C>T, Ex15-526G>A, and Ex14+14C>T). Polymorphisms in the MTHFR gene were not associated with stomach cancer risk. No notable effect was found for polymorphisms in MTR or MTRR either, although MTR Ex26-20 A>G and MTRR Ex5+123C>T polymorphisms were associated with a borderline increased risk of stomach cancer (MTR Ex26-20A>G, AG/GG versus AA: odds ratio, 1.35; 95% confidence interval, 0.96-1.90; MTRR Ex5+123C>T, CT/TT versus CC: odds ratio, 1.30; 95% confidence interval, 0.93-1.82). We did not find significant interactions between polymorphisms in MTHFR, MTR, and MTRR genes and dietary folate and alcohol consumption. Our study did not identify strong genetic determinants in the folate metabolism pathway for stomach cancer risk.

Original languageEnglish (US)
Pages (from-to)115-121
Number of pages7
JournalCancer Epidemiology Biomarkers and Prevention
Volume16
Issue number1
DOIs
StatePublished - Jan 2007

ASJC Scopus subject areas

  • Epidemiology
  • Oncology

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