Xiong Lan1, Tian Lan2, Qin Faxiang1. 1. Department of Respiratory Medicine, The Central Hospital of Enshi Autonomous Prefecture Enshi 445000, Hubei, China. 2. Medical School of Wuhan University Wuhan 430071, Hubei, China.
Abstract
BACKGROUND: Interleukin-10 (IL-10) is a multifunctional cytokine with both immunosuppressive and anti-angiogenic properties and it plays an important role in the pathogenesis of cancer. A number of studies have examined the association between its promoter -1082/-819/-592 polymorphism and risk of lung cancer. However, the results are inconsistent and inconclusive. The aim of this study was to explore whether the IL-10 gene polymorphism contribute to the susceptibility of lung cancer. METHOD: We searched in PubMed, EMBASE, Cochrane Library as well as Chinese databases including China National Knowledge Infrastructure (CNKI) and Wan Fang database for all the relevant studies up to May 15, 2015. The data were extracted by two independent authors. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) under co-dominant model, dominant model and recessive model were estimated. RESULTS: A total of 8 studies involving 2033 cases and 3100 controls were included in the meta-analysis. The results revealed that the IL-10 -592C/A polymorphism was related to lung cancer susceptibility under all models (C allele vs. A allele: OR=1.195, 95% CI=1.075-1.329; CC vs. AA: OR=1.651, 95%=1.290-2.113; CA vs. AA: OR=1.229, 95%=1.029-1.468; CA+AA vs. CC: OR=0.832, 95%=0.704-0.984; CC+CA vs. AA: OR=1.301, 95%=1.100-1.538) and IL-10 -819C/T polymorphism was associated with lung cancer susceptibility under three models (C allele vs. T allele: OR=1.441, 95% CI=1.228-1.691; CC vs. TT: OR=2.444, 95%=1.732-3.449; CC+CT vs. TT: OR=1.496, 95%=1.172-1.908). For IL-10 -1082G/A, there was no significant association between its polymorphism and lung cancer risk. CONCLUSIONS: This meta-analysis demonstrated that two polymorphisms (-592C/A and -819C/T) in the promoter region of IL-10 gene were significantly associated with the risk of lung cancer in general population, while -1082G/A polymorphism did not affect susceptibility to lung cancer.
BACKGROUND:Interleukin-10 (IL-10) is a multifunctional cytokine with both immunosuppressive and anti-angiogenic properties and it plays an important role in the pathogenesis of cancer. A number of studies have examined the association between its promoter -1082/-819/-592 polymorphism and risk of lung cancer. However, the results are inconsistent and inconclusive. The aim of this study was to explore whether the IL-10 gene polymorphism contribute to the susceptibility of lung cancer. METHOD: We searched in PubMed, EMBASE, Cochrane Library as well as Chinese databases including China National Knowledge Infrastructure (CNKI) and Wan Fang database for all the relevant studies up to May 15, 2015. The data were extracted by two independent authors. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) under co-dominant model, dominant model and recessive model were estimated. RESULTS: A total of 8 studies involving 2033 cases and 3100 controls were included in the meta-analysis. The results revealed that the IL-10-592C/A polymorphism was related to lung cancer susceptibility under all models (C allele vs. A allele: OR=1.195, 95% CI=1.075-1.329; CC vs. AA: OR=1.651, 95%=1.290-2.113; CA vs. AA: OR=1.229, 95%=1.029-1.468; CA+AA vs. CC: OR=0.832, 95%=0.704-0.984; CC+CA vs. AA: OR=1.301, 95%=1.100-1.538) and IL-10-819C/T polymorphism was associated with lung cancer susceptibility under three models (C allele vs. T allele: OR=1.441, 95% CI=1.228-1.691; CC vs. TT: OR=2.444, 95%=1.732-3.449; CC+CT vs. TT: OR=1.496, 95%=1.172-1.908). For IL-10-1082G/A, there was no significant association between its polymorphism and lung cancer risk. CONCLUSIONS: This meta-analysis demonstrated that two polymorphisms (-592C/A and -819C/T) in the promoter region of IL-10 gene were significantly associated with the risk of lung cancer in general population, while -1082G/A polymorphism did not affect susceptibility to lung cancer.
Authors: H Takizawa; M Tanaka; K Takami; T Ohtoshi; K Ito; M Satoh; Y Okada; F Yamasawa; A Umeda Journal: Am J Physiol Lung Cell Mol Physiol Date: 2000-05 Impact factor: 5.464