Abstract
Genetic variations in DNA repair genes are thought to modulate DNA repair capacity and are suggested to be related to lung cancer risk. We conducted a meta-analysis of epidemiologic studies on the association between genetic polymorphisms in both base excision repair and nucleotide excision repair pathways, and lung cancer. We found xeroderma pigmentosum complementation group A (XPA) G23A (odds ratio (OR) = 0.76, 95% confidence interval (CI) = 0.61–0.94), 8-oxoguanine DNA glycosylase 1 (OGG1) Ser326Cys (OR = 1.22, 95% CI = 1.02–1.45), and excision repair cross-complementing group 2 (ERCC2) Lys751Gln (OR = 1.27, 95% CI = 1.10–1.46) polymorphisms were associated with lung cancer risk. Considering the data available, it can be conjectured that if there is any risk association between a single SNP and lung cancer, the risk fluctuation will probably be minimal. Advances in the identification of new polymorphisms and in high-throughput genotyping techniques will facilitate the analysis of multiple genes in multiple DNA repair pathways. Therefore, it is likely that the defining feature of future epidemiologic studies will be the simultaneous analysis of large samples of cases and controls.
Highlights
Sporadic cancer is a multifactorial disease that results from complex interactions between many genetic and environmental factors [1]
We found xeroderma pigmentosum complementation group A (XPA) G23A (odds ratio (OR) = 0.76, 95% confidence interval (CI) = 0.61–0.94), 8-oxoguanine DNA glycosylase 1 (OGG1) Ser326Cys (OR = 1.22, 95% CI = 1.02–1.45), and excision repair cross-complementing group 2 (ERCC2) Lys751Gln (OR = 1.27, 95% CI = 1.10–1.46) polymorphisms were associated with lung cancer risk
The aim of this article is to review and evaluate associations between genes in the Base excision repair (BER) and nucleotide excision repair (NER) pathways, focusing on genetic polymorphisms in OGG1, XRCC1, XPA, and ERCC2 genes, which have been reported a sufficient number of studies to conduct a meta-analysis
Summary
Sporadic cancer is a multifactorial disease that results from complex interactions between many genetic and environmental factors [1]. This means that there will not be a single gene or single environmental factor that has large effects on cancer susceptibility. Cigarette smoke contains several thousand chemicals that are known to chemically modify DNA [2] and lead to the formation of mutations [3]. Most of these compounds are procarcinogens that must be activated by Phase I enzymes, such as cytochrome P450s. A critical cellular response that counteracts the carcinogenic effects of DNA damage is DNA repair
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