-160C/A polymorphism in the E-cadherin gene promoter and risk of hereditary, familial and sporadic prostate cancer
-160C/A polymorphism in the E-cadherin gene promoter and risk of hereditary, familial and sporadic prostate cancer
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DOI：
10.1002/ijc.11629
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发表时间：
2004-04-10
影响因子：
6.4
通讯作者：
Grönberg, H
中科院分区：
文献类型：
--
作者：
Jonsson, BA;Adami, HO;Grönberg, H
e -钙粘蛋白（CDH1）基因与前列腺癌的发生有关。相对于转录起始位点-160碱基对的CIA多态性已被证明会降低基因转录。我们分析了这种多态性与散发性、家族性（2个近亲）和遗传性（3个或更多近亲）前列腺癌风险之间的关系。我们结合了瑞典3项基于人群的流行病学研究的数据，其中包括1036例前列腺癌病例和669例对照，对短核苷酸多态性进行了基因分型。通过无条件逻辑回归估计95%置信区间的比值比。我们发现a等位基因与散发性（OR = 1.0; 95% CI = 0.8-1.2）或家族性（OR = 1.4; 95% CI = 0.9-2.2）前列腺癌之间无显著关联。相比之下，杂合子CA携带者（OR = 1.7; 95% CI = 1.0-2.7），特别是纯合子AA携带者（OR = 2.6; 95% CI = 1.4-4.9），遗传性癌症的风险增加。我们的数据表明，CDH1的-160单核苷酸多态性是一种低渗透的前列腺癌易感基因，可能解释了家族性和遗传性前列腺癌的一部分。(C) 2004 Wiley-Liss, Inc。
The E-cadherin (CDH1) gene has been associated with prostate carcinogenesis. The CIA 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. (C) 2004 Wiley-Liss, Inc.