Abstract
BackgroundThe X-ray repair cross-complementing group 3 (XRCC3) in homologous recombination repair (HRR) pathway plays a very important role in DNA double-strand break repair (DSBR). Variations in the XRCC3 gene might lead to altered protein structure or function which may change DSBR efficiency and result in cancer. The XRCC3 C18067T polymorphism has been reported to be associated with skin cancer susceptibility, yet the results of these previous results have been inconsistent or controversial. To derive a more precise estimation of the association, we conducted a meta-analysis.MethodsThe quality of the studies was assessed according to a predefined scale. The association between the XRCC3 C18067T polymorphism and skin cancer risk was assessed by odds ratios (ORs) together with their 95% confidence intervals (CIs).ResultsOverall, no significant association was observed between XRCC3 C18067T polymorphism and skin cancer risk in any genetic model. Stratified analyses according to tumor type, significant association was found in the relationship between XRCC3 C18067T polymorphism and nonmelanoma skin cancer risk (homozygote comparison TT versus CC: OR = 0.74, 95%CI = 0.61–0.90, P = 0.003; recessive model TT versus TC/CC: OR = 0.81, 95%CI = 0.68–0.95, P = 0.01). Furthermore, significant association was also observed in XRCC3 C18067T polymorphism with both basal cell carcinoma risk (homozygote comparison TT versus CC: OR = 0.70, 95%CI = 0.53–0.92, P = 0.011; recessive model TT versus. TC/CC: OR = 0.74, 95%CI = 0.60–0.92, P = 0.007) and squamous cell carcinoma risk (heterozygote comparison TT versus .CC: OR = 0.81, 95%CI = 0.67–0.99, P = 0.04; dominant model TT/TC versus .CC: OR = 0.81, 95%CI = 0.68–0.98, P = 0.029).ConclusionThe present meta-analysis demonstrates that XRCC3 C18067T polymorphism was not associated with risk of cutaneous melanoma but contributed a decreased risk to both basal cell carcinoma and squamous cell carcinoma.
Highlights
Skin cancer is one of the most frequent malignant diseases in humans, especially in the Western world [1]
Further subgroup analysis by subtype of nonmelanoma, we found that the X-ray repair cross-complementing group 3 (XRCC3) C18067T polymorphism contributed decreased risk to basal cell carcinoma
DNA repair pathways are of great importance in the removal of damages, repair of base alterations caused by UV radiation, recombination of homologous or nonhomologous end joining, and other injuries caused by many carcinogenic agents [35,36]
Summary
Skin cancer is one of the most frequent malignant diseases in humans, especially in the Western world [1]. Many studies have demonstrated that the incidence of skin cancer varies greatly between different countries and different ethnicities, suggesting genetic factors play important roles in the development of skin cancer [5,6,7]. It is well accepted that UV radiation could cause various kinds of DNA damage and the cellular response to DNA damage promotes activation of many DNA repair pathways involving dozens of genes with unique repair functions. The DNA repair systems play an important role in maintaining the integrity of the genome and protecting against mutations that can lead to cancer, including skin cancer. The X-ray repair cross-complementing group 3 (XRCC3) in homologous recombination repair (HRR) pathway plays a very important role in DNA double-strand break repair (DSBR). Variations in the XRCC3 gene might lead to altered protein structure or function which may change DSBR efficiency and result in cancer. To derive a more precise estimation of the association, we conducted a meta-analysis
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