Abstract
BackgroundAssociation between the single nucleotide polymorphism rs3218536 (known as Arg188His) located in the X-ray repair cross complementing group 2 (XRCC2) gene and cancer susceptibility has been widely investigated. However, results thus far have remained controversial. A meta-analysis was performed to identify the impact of this polymorphism on cancer susceptibility.MethodsPubMed and Embase databases were searched systematically until September 7, 2013 to obtain all the records evaluating the association between the XRCC2 Arg188His polymorphism and the risk of all types of cancers. We used the odds ratio (OR) as measure of effect, and pooled the data in a Mantel-Haenszel weighed random-effects meta-analysis to provide a summary estimate of the impact of this polymorphism on breast cancer, ovarian cancer and other cancers. All the analyses were carried out in STATA 12.0.ResultsWith 30868 cases and 38656 controls, a total of 45 case-control studies from 26 publications were eventually included in our meta-analysis. No significant association was observed between the XRCC2 Arg188His polymorphism and breast cancer susceptibility (dominant model: OR = 0.94, 95%CI = 0.86–1.04, P = 0.232). However, a significant impact of this polymorphism was detected on decreased ovarian cancer risk (dominant model: OR = 0.83, 95%CI = 0.73–0.95, P = 0.007). In addition, we found this polymorphism was associated with increased upper aerodigestive tract (UADT) cancer susceptibility (dominant model: OR = 1.51, 95%CI = 1.04–2.20, P = 0.032).ConclusionThe Arg188His polymorphism might play different roles in carcinogenesis of various cancer types. Current evidence did not suggest that this polymorphism was directly associated with breast cancer susceptibility. However, this polymorphism might contribute to decreased gynecological cancer risk and increased UADT cancer risk. More preclinical and epidemiological studies were still imperative for further evaluation.
Highlights
As the core component of cell nucleus, DNA suffers from various damaging agents such as chemicals, radiations and some endogenous elements
It has been demonstrated that accumulation of unrepaired double strand breaks (DSBs) can cause cell death and initiate malignancies [2], which highlights the disorder of DNA repair as the key role in tumorigenesis
A wide range of crucial molecules have been identified to participate in the homologous recombination repair (HRR) process [4].Recently, researches have revealed that RAD51 paralogs (RAD51B, RAD51C, RAD51D, Xray repair cross complementing group 2 (XRCC2), XRCC3) could serve as central proteins during the HRR process [5]
Summary
As the core component of cell nucleus, DNA suffers from various damaging agents such as chemicals, radiations and some endogenous elements. Under these damages, single strand breaks (SSBs) occur. Unrepaired SSBs lead to double strand breaks (DSBs) during the S phase of cell cycle [1]. There are several mechanisms repairing DSBs, among which homologous recombination repair (HRR) is the key pathway functioning in the S phase of somatic mammalian cell cycle [2]. Association between the single nucleotide polymorphism rs3218536 (known as Arg188His) located in the Xray repair cross complementing group 2 (XRCC2) gene and cancer susceptibility has been widely investigated. A meta-analysis was performed to identify the impact of this polymorphism on cancer susceptibility
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