摘要
目的:研究前列腺病变中E-钙粘素、p16和雌激素受体(ER)基因启动子CpG岛甲基化状况及其与临床资料的关系,探讨基因过甲基化在前列腺癌(PCa)发生发展中的作用及其临床意义。方法:收集石蜡包埋前列腺全切术标本:良性前列腺增生(BPH)13例,高级别前列腺上皮内瘤(HGPIN)10例,有随访记录的PCa 20例。采用甲基化特异性PCR(MSP)技术对E-钙粘素、p16和ER基因CpG岛甲基化进行检测。结果:E-钙粘素、p16和ER基因过甲基化在PCa中的发生率分别为30%、25%和65%。非恶性病变(BPH和HGPIN)很少发生DNA过甲基化。结论:PCa的发生及进展与E-钙粘素、p16和ER基因过甲基化密切相关,检测甲基化状况对HGPIN与PCa的鉴别诊断可能有辅助作用。E-钙粘素和ER基因过甲基化可能提示预后差。
Objective: To investigate promotor hypermethylation of the CpG islands of E-Cadherin, p16 and estrogen receptor (ER) in prostate carcinoma and explore whether such methylation might play a role in the tumorigenesis and malignant progression of prostate carcinoma and their significance in the diagnosis, prognosis and treatment. Methods : Thirteen specimens of benign prostatic hypertrophy (BPH) , 10 specimens of high grade prostate intraepithelial neoplasia (HGPIN) and 20 specimens of prostate carcinoma (with follow-up records) were collected from the patients who underwent radical prostatectomy or transurethal resection. Methylation-specific PCR (MSP) was used to detect the promoter hypermethylation of E-Cadherin, p16 and ER genes. Results: Hypermethylation percentages in prostate carcinoma were: E-Cadherin, 30% ; p16, 25% ; and ER, 65%. Almost all nonmalignant tissues (BPH and HGPIN) lacked methylation of any genes. Conclusion: Detecting promotor hypermethylation of E-Cadherin, p16 and ER may be helpful to differentiate nonmalignant lesions from prostate carcinoma.
出处
《中华男科学杂志》
CAS
CSCD
2006年第1期28-31,共4页
National Journal of Andrology
基金
东南大学科研基金资助(9247341182)