BACKGROUND: The relationship between Helicobacter pylori infection and gastric antrum adenocarcinoma (GAA) has previously been demonstrated and supported with strong epidemiological evidence. However, the role of genetic polymorphism of X-ray cross-complementing group 3 (XRCC3) Thr241Met (rs#861539), which may be involved in the repair of DNA double-strand breaks caused by carcinogens such as CagA, a protein produced by H. pylori, has been less well elaborated. METHODS: We conducted a hospital-based case-control study, including 721 patients with pathologically confirmed GAA and 989 individually matched controls without any evidence of tumors or precancerous lesions to evaluate the associations between this polymorphism and GAA risk in the Guangxi population. XRCC3 codon 241 genotypes and CagA status were determined using TaqMan-PCR and PCR, respectively. RESULTS: Increased risks of GAA were found for cagA-positive individuals [odds ratio (OR), 7.31; 95% confidence interval (CI), 5.87-9.09]. We also found that individuals with the XRCC3 genotypes with codon 241 Met (namely XRCC3-TM or XRCC3-MM) had an increased risk of GAA compared with those with the homozygote of XRCC3 codon 241 Thr alleles (namely XRCC3-TT, adjusted ORs 1.76 and 3.73; 95% CIs 1.37-2.24 and 2.66-5.23, respectively). The risk of GAA, moreover, appeared to differ more significantly among individuals featuring cagA-positive status, whose adjusted ORs (95% CIs) were 11.31 (8.34-15.33) and 27.48 (15.17-49.78), respectively. CONCLUSION: These results suggest that XRCC3 Thr241Met polymorphism may be associated with the risk of GAA related to CagA. Crown
BACKGROUND: The relationship between Helicobacter pyloriinfection and gastric antrum adenocarcinoma (GAA) has previously been demonstrated and supported with strong epidemiological evidence. However, the role of genetic polymorphism of X-ray cross-complementing group 3 (XRCC3) Thr241Met (rs#861539), which may be involved in the repair of DNA double-strand breaks caused by carcinogens such as CagA, a protein produced by H. pylori, has been less well elaborated. METHODS: We conducted a hospital-based case-control study, including 721 patients with pathologically confirmed GAA and 989 individually matched controls without any evidence of tumors or precancerous lesions to evaluate the associations between this polymorphism and GAA risk in the Guangxi population. XRCC3 codon 241 genotypes and CagA status were determined using TaqMan-PCR and PCR, respectively. RESULTS: Increased risks of GAA were found for cagA-positive individuals [odds ratio (OR), 7.31; 95% confidence interval (CI), 5.87-9.09]. We also found that individuals with the XRCC3 genotypes with codon 241 Met (namely XRCC3-TM or XRCC3-MM) had an increased risk of GAA compared with those with the homozygote of XRCC3 codon 241 Thr alleles (namely XRCC3-TT, adjusted ORs 1.76 and 3.73; 95% CIs 1.37-2.24 and 2.66-5.23, respectively). The risk of GAA, moreover, appeared to differ more significantly among individuals featuring cagA-positive status, whose adjusted ORs (95% CIs) were 11.31 (8.34-15.33) and 27.48 (15.17-49.78), respectively. CONCLUSION: These results suggest that XRCC3 Thr241Met polymorphism may be associated with the risk of GAA related to CagA. Crown