Abstract
Xeroderma pigmentosum group G (XPG) is a single-strand-specific DNA endonuclease that functions in the nucleotide excision repair pathway. Genetic variations in XPG gene can alter the DNA repair capacity of this enzyme. We evaluated the associations between six single nucleotide polymorphisms (SNPs) in XPG (rs1047768 T>C, rs2296147 T>C, rs2227869 G>C, rs2094258 C>T, rs751402 C>T, and rs873601 G>A) and cancer risk. Forty-seven studies were identified in searches of the PubMed, Scopus, Web of Science, China National Knowledge Infrastructure, and WanFang databases. Crude odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a fixed or random effects model. We found that rs873601 G>A was associated with an increased overall cancer risk (AA vs. GG: OR = 1.14, 95% CI = 1.06–1.24; GA/AA vs. GG: OR = 1.08, 95% CI = 1.02–1.15; A vs. G: OR = 1.06, 95% CI = 1.02–1.10). In a stratified analysis, rs1047768 T>C was associated with an increased risk of lung cancer, rs2227869 G>C was associated with a decreased risk of cancer in population-based studies, and rs751402 C>T and rs873601 G>A were associated with the risk of gastric cancer. Our data indicate that rs873601 G>A is associated with cancer susceptibility.
Highlights
There were an estimated 14.1 million new cancer cases and 8.2 million cancer-related deaths in 2012 worldwide [1, 2]
We evaluated the associations between six single nucleotide polymorphisms (SNPs) in Xeroderma pigmentosum group G (XPG) and cancer risk
We found that rs873601 G>A was associated with an increased overall cancer risk (AA vs. GG: odds ratios (ORs) = 1.14, 95% confidence intervals (CIs) = 1.06–1.24; GA/AA vs. GG: OR = 1.08, 95% CI = 1.02–1.15; A vs. G: OR = 1.06, 95% CI = 1.02–1.10)
Summary
There were an estimated 14.1 million new cancer cases and 8.2 million cancer-related deaths in 2012 worldwide [1, 2]. Chronic disease caused by both endogenous (genetic, immune, and endocrine disorders) and exogenous factors (environmental carcinogens and unhealthy behaviors) [1]. Among these etiological factors, gene-environment interactions have been shown to play key roles in cancer development. DNA damage can occur due to exposure to various chemicals, environmental agents, and ultraviolet radiation. There are five major DNA damage repair pathways in humans: nucleotide excision repair (NER), base excision repair, doublestrand break repair, mismatch repair, and homologous www.impactjournals.com/oncotarget recombination [3]. The versatile NER pathway is responsible for excising DNA lesions including cross-links, bulky adducts, thymidine dimers, alkylating damage, and oxidative DNA damage [3]
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