Abstract
Catechol-O-methyltransferase (COMT) is involved in estrogen metabolism and is vital to estrogen-induced carcinogenesis, including that of ovarian cancer. Although many recent epidemiologic studies have investigated associations between the COMT rs4680 polymorphism and ovarian cancer risk, the results remain inconclusive. We therefore performed a meta-analysis to derive a more precise estimate of associations. Systematic searches of the PubMed, Embase, Web of Science, Cochrane Library, Wanfang, China National Knowledge Infrastructure, and Chinese Biomedicine databases were undertaken to retrieve eligible studies. Odds ratios (ORs) with their corresponding 95% confidence intervals (CIs) were pooled to assess the strength of the association. In total, 8 case-control studies involving 1,293 cases and 2,647 controls were included in the meta-analysis. Overall, the results showed no evidence of significant association between the COMT rs4680 polymorphism and ovarian cancer risk in any of the assessed genetic models. Subgroup analyses by ethnicity also did not reveal any significant association in any genetic model (p>0.05). In conclusion, our findings suggest that the COMT rs4680 polymorphism may not contribute to the risk of ovarian cancer.
Highlights
There has been considerable academic focus on the etiology of ovarian carcinoma, which has poor recurrencefree survival and overall survival and which is the third most common gynecological cancer worldwide (Schuler et al, 2014b; Schuler et al, 2014a)
The results showed no evidence of significant association between the COMT rs4680 polymorphism and ovarian cancer risk in any of the assessed genetic models
Study characteristics Initially, 27 potentially relevant publications related to the association between the COMT rs4680 polymorphism and ovarian cancer risk were retrieved in the database search
Summary
There has been considerable academic focus on the etiology of ovarian carcinoma, which has poor recurrencefree survival and overall survival and which is the third most common gynecological cancer worldwide (Schuler et al, 2014b; Schuler et al, 2014a). There is substantial evidence supporting the hormonal influence on female tumors, such as breast and ovarian cancer, thereby underlining the importance of mechanisms underlying steroid biosynthesis in the pathogenesis of this disease (Jakubowska et al, 2010; Chan et al, 2014). Variations in the genes involved in the biosynthesis and metabolism of estrogen may contribute to altered levels of estrogen and thereby contribute to the risk of ovarian cancer (Holt et al, 2007)
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