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−160C/A polymorphism in the E‐cadherin gene promoter and risk of hereditary, familial and sporadic prostate cancer
Author(s) -
Jonsson BjörnAnders,
Adami HansOlov,
Hägglund Maria,
Bergh Anders,
Göransson Ingela,
Stattin Pär,
Wiklund Fredrik,
Grönberg Henrik
Publication year - 2004
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.11629
Subject(s) - prostate cancer , odds ratio , single nucleotide polymorphism , allele , prostate , heterozygote advantage , genotype , genetics , medicine , oncology , cancer , biology , gene
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.