Article
European Journal of Human Genetics (2009) 17, 244–249; doi:10.1038/ejhg.2008.157; published online 10 September 2008
The E-cadherin (CDH1) -160 C/A polymorphism and prostate cancer risk: a meta-analysis
Li-Xin Qiu1,2, Ru-Tian Li2, Jian-Bing Zhang3, Wen-Zhao Zhong4, Jian-Ling Bai5, Bao-Rui Liu1,2, Ming-Hua Zheng6 and Xiao-Ping Qian1,2
- 1Cancer Center, Nanjing Drum Tower Hospital, Nanjing Medical University, Nanjing, China
- 2Cancer Center, Affiliated Drum Tower Hospital, Medical School of Nanjing University & Clinical Cancer Institute of Nanjing University, Nanjing, China
- 3Nantong Cancer Research Institute, The Affiliated Cancer Hospital of Nantong University, Nantong, China
- 4Lung Cancer Research Institute & Cancer Center, Guangdong Provincial People's Hospital, Guangzhou, China
- 5Department of Epidemiology and Biostatistics, School of Public Health, Nanjing Medical University, Nanjing, China
- 6Department of Infection and Liver Diseases, The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, China
Correspondence: Dr M-H Zheng, Department of Infection and Liver Diseases, The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, China. E-mail: conquerpkc@126.com; Dr X-P Qian, Cancer Center, Nanjing Drum Tower Hospital, Nanjing Medical University, Nanjing, China. Tel: +86 25 83107081; Fax: +86 25 83317016; E-mail: mdqiulixin@hotmail.com
Received 21 February 2008; Revised 29 July 2008; Accepted 30 July 2008; Published online 10 September 2008.
Abstract
Published data on the association between E-cadherin (CDH1) -160 C/A polymorphism and prostate cancer (PCA) risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. A logistic regression approach proposed for molecular association studies was used to estimate a biological model of the gene effect. A total of 11 studies including 2637 cases and 2673 controls were involved in this meta-analysis. Logistic regression analysis indicated that the CDH1 -160 C/A genotypes were associated with PCA risk. The genetic model test indicated that the genetic model was most likely to be dominant (CA+AA vs CC). Overall, meta-analysis indicated that the -160A allele carriers (CA+AA) had a 21% elevated risk of PCA, when compared with the homozygotes (CC) (odds ratio (OR)=1.21; 95% confidence interval (CI): 0.97–1.51; P=0.090, Pheterogeneity=0.001). In the subgroup analyses by ethnicity, significantly elevated risks were associated with -160 variant genotypes (CA+AA) in both European and Asian populations (OR=1.24; 95% CI: 1.08–1.43; P=0.003, Pheterogeneity=0.220 and OR=1.54; 95% CI: 1.23–1.93; P<0.001, Pheterogeneity=0.200). However, no significant associations were found in Africans (OR=0.59; 95% CI: 0.32–1.09; P=0.090, Pheterogeneity=0.070). Although some modest bias could not be eliminated, this meta-analysis suggests that the CDH1 -160A allele is a low-penetrant risk factor for developing PCA, especially in Europeans and Asians.
Keywords:
E-cadherin (CDH1) polymorphism, prostate cancer susceptibility, meta-analysis
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