摘要
The tumor suppressor gene p53 appears to be important in the development of many human cancers, such as prostate cancer. The association of p53 codon72 polymorphism with prostate cancer has been widely reported; however, the results are inconsistent. To derive a more precise estimation of this relationship, we performed an updated meta-analysis from 10 case-control studies. We conducted a search in the PubMed database without a language limitation, covering all papers published until July 2010. Risk ratios （RR） with 95% confidence intervals （CIs） were used to assess the strength of the association. Ten studies including 1,196 cases and 1,704 controls were selected. Overall, no significant differences of total prostate cancer risk and p53 codon polymorphism was found （Pro/Pro vs Arg/Arg, RR = 1.12, 95%CI=0.74-1.70, P heterogeneity = 0.016, I 2 = 55.8%; Pro/Pro＋Pro/Arg vs Arg/ Arg, RR = 1.05, 95%CI=1.00-1.11, P heterogeneity = 0.077, I 2 = 51.1%）. In the stratified analysis by ethnicity, the same results were found. However, in the control subgroup, there was a modest decreased association between prostate cancer risk and population-based control subjects under the recessive genetic model （RR = 0.31, 95%CI=0.10- 0.91, P heterogeneity = 0.110, I 2 =60.8%）. This meta-analysis suggested that p53 codon Pro72Arg polymorphism could be weakly associated with prostate cancer risk.
The tumor suppressor gene p53 appears to be important in the development of many human cancers, such as prostate cancer. The association of p53 codon72 polymorphism with prostate cancer has been widely reported; however, the results are inconsistent. To derive a more precise estimation of this relationship, we performed an updated meta-analysis from 10 case-control studies. We conducted a search in the PubMed database without a language limitation, covering all papers published until July 2010. Risk ratios （RR） with 95% confidence intervals （CIs） were used to assess the strength of the association. Ten studies including 1,196 cases and 1,704 controls were selected. Overall, no significant differences of total prostate cancer risk and p53 codon polymorphism was found （Pro/Pro vs Arg/Arg, RR = 1.12, 95%CI=0.74-1.70, P heterogeneity = 0.016, I 2 = 55.8%; Pro/Pro＋Pro/Arg vs Arg/ Arg, RR = 1.05, 95%CI=1.00-1.11, P heterogeneity = 0.077, I 2 = 51.1%）. In the stratified analysis by ethnicity, the same results were found. However, in the control subgroup, there was a modest decreased association between prostate cancer risk and population-based control subjects under the recessive genetic model （RR = 0.31, 95%CI=0.10- 0.91, P heterogeneity = 0.110, I 2 =60.8%）. This meta-analysis suggested that p53 codon Pro72Arg polymorphism could be weakly associated with prostate cancer risk.
