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

  1. 1Cancer Center, Nanjing Drum Tower Hospital, Nanjing Medical University, Nanjing, China
  2. 2Cancer Center, Affiliated Drum Tower Hospital, Medical School of Nanjing University & Clinical Cancer Institute of Nanjing University, Nanjing, China
  3. 3Nantong Cancer Research Institute, The Affiliated Cancer Hospital of Nantong University, Nantong, China
  4. 4Lung Cancer Research Institute & Cancer Center, Guangdong Provincial People's Hospital, Guangzhou, China
  5. 5Department of Epidemiology and Biostatistics, School of Public Health, Nanjing Medical University, Nanjing, China
  6. 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.

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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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