Abstract
Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene may influence the risk of cancer, but the results are still debatable. Therefore, we performed a systematic review to provide a more complete picture and conducted a meta-analysis to derive a precise estimation. We searched PubMed, EMBASE, EBSCO, Google Scholar and China National Knowledge Infrastructure (CNKI) databases until April 2014 to identify eligible studies. Thirty-one studies with cancer patients and controls were included in the meta-analysis. Overall, the polled analysis revealed that the T-786C polymorphism was significantly associated with increased cancer risk under multiple genetic models (C vs T: OR=1.135, 95%CI=1.048-1.228; CC vs TT: OR=1.278, 95%CI=1.045- 1.562; TC vs TT: OR=1.136, 95%CI=1.023-1.261; CC+TC vs TT: OR=1.159, 95%CI=1.047-1.281; CC vs TC+TT: OR=1.204, 95%CI= 1.003-1.447). G894T was associated with significant risk for females (TT vs GG: OR=1.414, 95%CI=1.056-1.892; TT vs GT+GG: OR=1.356, 95%CI=1.108-1.661) and for breast cancer (T vs G: OR=1.097, 95%CI=1.001-1.203; TT vs GG: OR=1.346, 95%CI=1.012-1.789; TT vs GT+GG: OR=1.269, 95%CI=1.028-1.566). Increased susceptibility was revealed for prostate cancer with 4a/b (ba vs bb: OR=1.338, 95%CI=1.013-1.768; aa+ba vs bb: OR=1.474, 95%CI=1.002-2.170). This meta-analysis indicated that the eNOS T-786C polymorphism is associated with elevated cancer risk; the G894T polymorphism contributes to susceptibility to breast cancer and cancer generally in females; and the 4a/b polymorphism may be associated with prostate cancer risk.
Highlights
Cancer is a major public health problem and it is one of the leading causes of death worldwide (Jemal et al, 2011)
“NO synthase (NOS),” “Endothelial nitric oxide synthase (eNOS),” “NOS3,” “polymorphism (s),” “genotype,” “variant,” “carcinoma,” “cancer,” “tumor,” and “malignancy” in PubMed, EMBASE, EBSCO, Google Scholar and China National Knowledge Infrastructure (CNKI) databases without a language limitation, and the last search updated on 5 April 2014
Inclusion criteria Studies were included in the meta- analysis if (1) it investigated the association between eNOS polymorphism and cancer risk; (2) the design was case-control study or nested case-control study; (3) data regarding genotype distributions were sufficient to calculate the odds ratio (OR) and its corresponding 95% confidence interval (CI)
Summary
Cancer is a major public health problem and it is one of the leading causes of death worldwide (Jemal et al, 2011). The global burden of cancer is ever-increasing in both economically developed countries and developing countries (Are et al, 2013). Tremendous efforts have been made to unravel the underlying mechanism of cancer, with the aim to develop optimal prophylactic and therapeutic strategies. The mechanism of developing cancer is still unclear. People generally agree that complex environmental factors and interindividual genetic susceptibility may contribute to cancer development (Perera, 1997). Substantial evidence shows that genetic susceptibility has a significant role in an individual’s risk of developing cancer (Dong et al, 2008)
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