Abstract
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 (ORinteraction = 1.49). These results suggest that XRCC7P may be associated with the risk of Guangxiese GAA related to cagA.
Highlights
Gastric cancer is the fourth most common cancer worldwide and the second most common cause of death from cancer [1, 2]
To the best of our knowledge, there has been no report on the association between XRCC7 rs#7003908 polymorphism (XRCC7P) and the risk of gastric antrum adenocarcinoma (GAA), especially from high H. pylori infection areas
In this hospital-based case-control study, we analyzed the association between aforementioned polymorphism and the risk of GAA among Guangxi population from a high H. pylori infection area
Summary
Gastric cancer is the fourth most common cancer worldwide and the second most common cause of death from cancer [1, 2]. 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 [5,6,7,8,9,10]. Among these DNA damages, DSBs are the most detrimental form [11, 12], because they may lead to both chromosomal breakage and rearrangement and lead to tumorigenesis of cancers such as GAA. We evaluated whether XRCC7P modifies H. pylori infection-related GAA risk
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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
