Abstract
Gastric cancer remains a major health problem in China. We hypothesized that XRCC1 Arg194Trp and ADPRT Val762Ala may be associated with risk. We designed a multicenter 1:1 matched case- control study of 307 pairs of gastric cancers and controls between October 2010 and August 2011. XRCC1 Arg194Trp and ADPRT Val762Ala were sequenced, and demographic data as well as lifestyle factors were collected using a self-designed questionnaire. Individuals carrying XRCC1 Trp/Trp or Arg/Trp variant genotype had a significantly increased risk of gastric cancer (OR, 1.718; 95% CI, 1.190-2.479), while the OR for ADPRT Val762Ala variant genotype (Ala/Ala or Val/Ala) was 1.175 (95% CI, 0.796-1.737). No gene-gene or gene-environment interactions were found. In addition, family history of cancer and drinkers proportion were higher among cases than among controls (P<0.05). XRCC1 194 Arg/Trp or Trp/Trp genotype, family history of cancer, and drinking are suspected risk factors of gastric cancer from our study. Our findings may offer insight into further similar large gene-environment and gene-gene studies in this region.
Highlights
Cancer has been one of the leading causes of death among Chinese adults (He et al, 2005)
The results showed that individuals with both X-ray repair cross-complementing group 1 (XRCC1) Arg194Trp and adenosine diphosphate ribosyl transferase (ADPRT) Val762Ala variant genotypes (XRCC1 Trp/Trp or Arg/ Trp + ADRRT Ala/Ala or Val/Ala) had a significantly increased risk of gastric cancer (OR, 2.063; 95%confidence interval (CI), 1.2023.540), compared to subjects who were wild type for both polymorphisms
Genetic variation in DNA repair genes has been postulated as an important component for the etiology of gastric cancer (Gonzalez et al, 2002; Goode et al, 2002; Capella et al, 2008; Palli et al, 2010)
Summary
Cancer has been one of the leading causes of death among Chinese adults (He et al, 2005). ADPRT binds to DNA strand breaks where it is autoactivated and recruits the XRCC1-Ligase IIIα complex to stimulate BER, and as a result, XRCC1 interacts with ADPRT to recruit other partner proteins such as DNA polymerase β (Ploβ) to execute BER (Masson et al, 1998; Keith, 2003). In this regard, functional variants of XRCC1 and ADPRT may alter BER functions and play an essential role in the evolution of gastric lesions (Li et al, 2009)
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call