Liu Liwei1, Liu Chunyu, Han Ruifa. 1. Tianjin Institution of Urology, The 2nd. Hospital of Tianjin Medical University, Tianjin, China.
Abstract
OBJECTIVES: To examine the association between 2 mitochondrial manganese superoxide dismutase (MnSOD) genetic polymorphisms (Ala-9Val and Ala-16Val) and prostate cancer susceptibility. METHODS: A comprehensive search was conducted to identify all case-control studies of MnSOD polymorphisms and prostate cancer risk. Statistical analysis was performed with the software program Stata, version 8.0, and Review Manage, version 4.2. RESULTS: A total of 9 eligible studies, including 3268 cases and 5907 controls, relating the MnSOD polymorphism to the risk of prostate cancer were identified. For the Ala-9Val polymorphism, 5 studies, including 889 cases and 1841 controls, found no significant associations between MnSOD polymorphism and the risk of developing prostate cancer in the recessive, dominant, and co-dominant models. In the sensitivity analysis, exclusion of the study with the controls not in Hardy-Weinberg equilibrium, no significant associations were also found in the recessive (odds ratio [OR] 1.29, 95% confidence interval [CI] 0.66-2.50), dominant (OR 1.35, 95% CI 0.84-2.17), and co-dominant (OR 1.33, 95% CI 0.87-2.01) models. For the Ala-16Val polymorphism, 4 studies, including 2379 cases and 4066 controls, found no significant association between MnSOD polymorphism and the risk of developing prostate cancer in both co-dominant (OR 1.08, 95% CI 1.00-1.16), recessive (OR 1.06, 95% CI 0.94-1.20) and dominant (OR 1.14, 95% CI 1.00-1.28) models. CONCLUSIONS: No significant association was found between the Ala-9Val and Ala-16Val polymorphisms in MnSOD and prostate cancer susceptibility.
OBJECTIVES: To examine the association between 2 mitochondrial manganese superoxide dismutase (MnSOD) genetic polymorphisms (Ala-9Val and Ala-16Val) and prostate cancer susceptibility. METHODS: A comprehensive search was conducted to identify all case-control studies of MnSOD polymorphisms and prostate cancer risk. Statistical analysis was performed with the software program Stata, version 8.0, and Review Manage, version 4.2. RESULTS: A total of 9 eligible studies, including 3268 cases and 5907 controls, relating the MnSOD polymorphism to the risk of prostate cancer were identified. For the Ala-9Val polymorphism, 5 studies, including 889 cases and 1841 controls, found no significant associations between MnSOD polymorphism and the risk of developing prostate cancer in the recessive, dominant, and co-dominant models. In the sensitivity analysis, exclusion of the study with the controls not in Hardy-Weinberg equilibrium, no significant associations were also found in the recessive (odds ratio [OR] 1.29, 95% confidence interval [CI] 0.66-2.50), dominant (OR 1.35, 95% CI 0.84-2.17), and co-dominant (OR 1.33, 95% CI 0.87-2.01) models. For the Ala-16Val polymorphism, 4 studies, including 2379 cases and 4066 controls, found no significant association between MnSOD polymorphism and the risk of developing prostate cancer in both co-dominant (OR 1.08, 95% CI 1.00-1.16), recessive (OR 1.06, 95% CI 0.94-1.20) and dominant (OR 1.14, 95% CI 1.00-1.28) models. CONCLUSIONS: No significant association was found between the Ala-9Val and Ala-16Val polymorphisms in MnSOD and prostate cancer susceptibility.
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