Abstract
Genetic polymorphism of human 8-oxoguanine glycosylase 1 (hOGG1) has been reported to have a relationship with the risk of the development of various cancers. Many studies have described the influence of Ser326Cys polymorphism of the hOGG1 gene on cancer susceptibility. However, the results have remained inconclusive and controversial. Therefore, we performed a meta-analysis to more precisely determine the relationship between the hOGG1 polymorphism and the development of cancer.Electronic databases including PubMed, Embase, Google Scholar, and the Korean Studies Information Service System (KISS) were searched. The odds ratio (OR), 95% confidence interval (CI), and p value were calculated to assess the strength of the association with the risk of cancer using Comprehensive Meta-analysis software (Corporation, NJ, USA). The 127 studies including 38,757 cancer patients and 50,177 control subjects were analyzed for the meta-analysis.Our meta-analysis revealed that G allele of Ser326Cys polymorphism of the hOGG1 gene statistically increased the susceptibility of cancer (all population, OR = 1.092, 95% CI = 1.051-1.134, p < 0.001; in Asian, OR = 1.095, 95% CI = 1.048-1.145, p < 0.001; in Caucasian, OR = 1.097, 95% CI = 1.033-1.179, p = 0.002). Also, other genotype models showed significant association with cancer (p < 0.05, respectively).The present meta-analysis concluded that the G allele was associated with an increased risk of cancer. It suggested that the hOGG1 polymorphism may be a candidate marker of cancer.
Highlights
Cancers are serious problem around the world and complex, multistep, multifactorial, and highly fatal diseases
Our meta-analysis revealed that G allele of Ser326Cys polymorphism of the human 8-oxoguanine glycosylase 1 (hOGG1) gene statistically increased the susceptibility of cancer
A total of 127 genetic studies about the hOGG1 polymorphism and cancer were analyzed for meta-analysis (Supplementary Table 1) [5, 10-143]
Summary
Cancers are serious problem around the world and complex, multistep, multifactorial, and highly fatal diseases. Several recent studies focused on the genetic background and how the single nucleotide polymorphism (SNP) of specific genes, including DNA damage, can enhance cancer susceptibility [2]. DNA damage plays an important role in tumor development. Reactive oxygen species (ROS) increases damage to DNA and causes miscoding by DNA polymerase [3]. The level of ROS in tissue DNA reflects a balance between the rate of damage and repair. Abnormal balance results in DNA mutations that can activate oncogenes or inactivate tumor suppressor genes, which leads to cancer [4]. The base excision repair (BER) pathway is one of the DNA repair process. An important role of BER is to remove DNA damage caused by various carcinogens, such as ionizing radiation or reactive oxidative species [5]. BER has evolved to cope with mutagenic and cytotoxic hydrolytic, oxidative, and alkylation damages. A relationship of BER to cancer progression has been drawn from the observation that mutations or altered expression in BER genes [6]
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