Objective Recent studies have demonstrated that gastric adenocarcinoma (GAC), a kind of common malignancy in Guangxi, is possibly related to DNA damage repair ability (DRC), while DNA repair gene XPF is very important ingredient in the nucleotide excision repair (NER) and the polymorphism of this gene (RS#744154) has been reported to relate to the risk of some malignant tumors such as breast cancer, the carcinoma of urinary bladder, lung cancer, and so on. However, it has not been elucidated whether XPF RS#744154 polymorphism modifies the risk of GAC among Guangxi population. Here, we specifically conducted a hospital-based case-control study to investigate the relation between this polymorphism and GAC risk, at the same time, by observing these polymorphism sites in the clinico-pathologic feature of gastric adenocarcinoma and the status of Helicobactor Pyiori( HP ) infection, for further analyze the role of XPF gene polymorphism in pathogenesis of gastric adenocarcinoma.Methods This study, including 99 patients with GAC diagnosed by pathological examination , collecte the genomic DNA from peripheral blood for each patients, and examine the clinico-pathologic feature and HP status,284 controls without any evidence of tumors or family history of tumors, is a hospital-based case-control study. All subjects are Guangxiese. To control possible confounders, cases were frequently matched to controls based on age, gender, and race. XPF RS#744154 polymorphism was testified using TaqMan-PCR method. Hardy-Weinberg analysis was performed via comparing the observed and expected genotype frequencies by using Chi-square test. The distribution of the intergroup was analyzed by using Chi-square test. The odds ratio(OR) and relative 95% confidence interval(CI) were calculated by using anunconditional logistic regression model as appraise risk between the DNA repair gene XPF RS#744154 polymorphism on risk and clinico-pathologic feature of GAC.Results (1)XPF RS#744154 polymorphism among the subjects did not significantly deviate from the expected Hardy-Weinberg equilibrium(p > 0.05).(2)The distribution of three XPF genotypes (namely XPF-GG, -GC, and -CC) among cases was significantly dissimilar to among controls (P < 0.05).(3)These results suggest that XPF RS#744154 polymorphism might associate with the risk of GAC. Compared with GG genotype, CC can increase the risk of GAC (corresponding OR was 2.60 for XPF-CC).(4)Male individuals having genotypes with GC/CC, compared with those without risk genotypes, would face significantly higher risk of GAC(OR = 2.25,95%Cl = 1.27-3.98,P < 0.05).(5)The Han Chinese individuals having genotypes with GC/CC, compared with those without risk genotypes, would face significantly higher risk of the gastric adenocarcinoma (OR = 1.95,95%Cl = 1.02-3.72,P < 0.05). (6)Elders individuals having genotypes with GC/CC, compared with those without risk genotypes, would face significantly higher risk of the gastric adenocarcinoma (OR = 3.00,95%Cl = 1.45-6.20,P < 0.05)。(7)The frequencies of the XPF-GG, GC/CC genotypes were 43.75%, 71.64% in patients with tumor diameter(≤5 cm),and 56.25%,28.36% in patients with tumor diameter(> 5 cm), respectively. The difference was statistical significance(χ2 = 7.198,P = 0.007, OR = 3.69).(8)No relationship was found between XPF gene polymorphisms and tumor sites, pathology grade, Laurén classification,, lymph nodemetastasis, TNM stage.(9) The distribution of HP infection among three XPF genotypes (namely XPF-GG, -GC, and -CC) was not significantly dissimilar in GAC(P > 0.05).Conclusions These results suggest that XPF RS#744154 polymorphism might associate with the risk of gastric adenocarcinoma among Guangxi population, especially among males and elders. The distribution of HP infection and the XPF gene RS#744154 polymorphism was not significantly dissimilar to among juxtacacerous, at the same time , XPF gene polymorphism also was not significantly dissimilar with the clinico-pathologic feature. XPF function decline caused the DNA damage repair disorders may mainly affect start-up phase of gastric cancer, rather than tumor invasion and metastasis-associated genes. Its specific target genes and interaction modes with environment carcinogenic factors, etc, all deserve further study. |