The X-ray repair cross-complementing group 7 (XRCC7) plays a key role in DNA repair that protects against genetic instability and carcinogenesis. To determine whether XRCC7 rs#7003908 polymorphism (XRCC7P) is associated with Helicobacter pylori (H. pylori) infection-related gastric antrum adenocarcinoma (GAA) risk, we conducted a hospital-based case-control study, including 642 patients with pathologically confirmed GAA and 927 individually matched controls without any evidence of tumours or precancerous lesions, among Guangxi population. Increased risks of GAA were observed for individuals with cagA positive (odds ratio (OR) 6.38; 95% confidence interval (CI) 5.03–8.09). We also found that these individuals with the genotypes of XRCC7 rs#7003908 G alleles (XRCC7-TG or -GG) featured increasing risk of GAA (ORs 2.80 and 5.13, resp.), compared with the homozygote of XRCC7 rs#7003908 T alleles (XRCC7-TT). GAA risk, moreover, did appear to differ more significantly among individuals featuring cagA-positive status, whose adjusted ORs (95% CIs) were 15.74 (10.89–22.77) for XRCC7-TG and 38.49 (22.82–64.93) for XRCC7-GG, respectively. Additionally, this polymorphism multiplicatively interacted with XRCC3 codon 241 polymorphism with respect to HCC risk ( ). These results suggest that XRCC7P may be associated with the risk of Guangxiese GAA related to cagA. 1. Introduction Gastric cancer is the fourth most common cancer worldwide and the second most common cause of death from cancer [1, 2]. The predominant type of this tumor in Guangxi Zhuang Autonomous Region is gastric antrum adenocarcinoma (GAA) [3]. Clinic-epidemiological evidence suggests that Helicobacter pylori (H. pylori) infection is a major risk factor [4, 5]. Increasing evidence has shown that cagA protein, an important H. pylori-produced virulent factor for gastric mucosa injury, could induce many kinds of DNA damage including DNA base damage, DNA double-strand break (DSBs), and oxidative damage [5–10]. Among these DNA damages, DSBs are the most detrimental form [11, 12], because they may lead to both chromosomal breakage and rearrangement and ultimately lead to tumorigenesis of cancers such as GAA. DNA repair gene “X-ray repair cross-complementing group 7” (XRCC7) is necessary for DNA ligation in the nonhomologous end-joining (NHEJ) pathway, which is responsible for repairing most double-strand breaks [13, 14]. Recently, several studies have shown that XRCC7 rs#7003908 polymorphism (XRCC7P) may be associated with DNA repair capacity and tumor risk [15–17]. However, the association between this
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