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−160C/A polymorphism in the E-cadherin gene promoter and risk of hereditary, familial and sporadic prostate cancer

✍ Scribed by Björn-Anders Jonsson; Hans-Olov Adami; Maria Hägglund; Anders Bergh; Ingela Göransson; Pär Stattin; Fredrik Wiklund; Henrik Grönberg

Publisher
John Wiley and Sons
Year
2004
Tongue
French
Weight
167 KB
Volume
109
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

The E‐cadherin (CDH1) gene has been associated with prostate carcinogenesis. The C/A polymorphism −160 base pairs relative to the transcription start site has been shown to decrease gene transcription. We analyzed the association between this polymorphism and the risk of sporadic, familial (2 close relatives) and hereditary (3 or more close relatives) prostate cancer. We combined data from 3 population‐based epidemiologic studies in Sweden encompassing altogether 1,036 prostate cancer cases and 669 controls that were genotyped for the short nucleotide polymorphism. Odds ratios with 95% confidence intervals were estimated through unconditional logistic regression. We found no significant association between the A‐allele and sporadic (OR = 1.0; 95% CI = 0.8–1.2) or familial (OR = 1.4; 95% CI = 0.9–2.2) prostate cancer. In contrast, risk of hereditary cancer was increased among heterozygote CA carriers (OR = 1.7; 95% CI = 1.0–2.7) and particularly among homozygote AA carriers (OR = 2.6; 95% CI = 1.4–4.9). Our data indicate that the −160 single nucleotide polymorphism in CDH1 is a low‐penetrant prostate cancer susceptibility gene that might explain a proportion of familial and notably hereditary prostate cancer. © 2004 Wiley‐Liss, Inc.

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