Strickler H D, Burk R, Shah K, Viscidi R, Jackson A, Pizza G, Bertoni F, Schiller J T, Manns A, Metcalf R, Qu W, Goedert J J
Viral Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Cancer. 1998 Mar 15;82(6):1118-25.
The presence of human papillomavirus (HPV) in the prostate and its role in prostate carcinoma are in dispute. To address these issues, two laboratories with extensive HPV experience were selected to test specimens from two populations at different risk for prostate carcinoma, using three different polymerase chain reaction (PCR) assays and two serologic assays for HPV.
The cases were comprised of 51 African-American (men at high risk for prostate carcinoma) and 15 Italian (men at intermediate risk for prostate carcinoma) men with prostate carcinoma. Controls were 108 African-American men and 40 Italian men with histologically proven benign prostate hypertrophy (BPH). Prostate tissue was obtained from each patient at surgery and immediately frozen in liquid nitrogen. The PCR primer sets included two (MY09/MY11 and GP5+/ GP6+) that amplify different regions of L1 and a third (WD66,67,154/WD72,76) targeted to E6. Sensitivity in the 2 L1 PCR assays was shown to be 1 HPV DNA genome per 100 cells. Serum antibodies to HPV-16 and HPV-11 virus-like particles (VLPs) were detected using enzyme-linked immunosorbent assays.
All available prostate carcinoma tissue specimens (n = 63) and BPH specimens from selected controls (n = 61) were tested by PCR. Human beta-globin DNA could be amplified from all specimens except three carcinomas, but no HPV DNA was detected in any case or control specimens by MY09/MY11 or E6 PCR. Microdissection of 27 carcinoma specimens was conducted to minimize nontumor DNA, but results remained negative by MY09/MY11 and GP5+/GP6+ PCR. In addition, serum specimens in cases (n = 63) and controls (n = 144) showed no differences in their responses against HPV-16 (P = 0.54) or HPV-11 VLPs (P = 0.64).
The findings suggest that HPV is not associated with prostate carcinoma, and that HPV DNA is not at all common in the prostate glands of older men.
前列腺中人类乳头瘤病毒（HPV）的存在及其在前列腺癌中的作用存在争议。为解决这些问题，选择了两个在HPV检测方面经验丰富的实验室，使用三种不同的聚合酶链反应（PCR）检测方法和两种HPV血清学检测方法，对来自前列腺癌不同风险的两个人群的标本进行检测。
病例包括51名非裔美国男性（前列腺癌高风险男性）和15名意大利男性（前列腺癌中等风险男性），均患有前列腺癌。对照组为108名非裔美国男性和40名意大利男性，经组织学证实患有良性前列腺增生（BPH）。在手术时从每位患者获取前列腺组织，并立即液氮冷冻。PCR引物组包括两组（MY09/MY11和GP5+/GP6+），用于扩增L1的不同区域，第三组（WD66,67,154/WD72,76）靶向E6。两种L1 PCR检测方法的灵敏度显示为每100个细胞中有1个HPV DNA基因组。使用酶联免疫吸附测定法检测针对HPV-16和HPV-11病毒样颗粒（VLP）的血清抗体。
所有可用的前列腺癌组织标本（n = 63）和选定对照组的BPH标本（n = 61）均通过PCR检测。除了三个癌组织标本外，所有标本均可扩增出人β-珠蛋白DNA，但在任何病例或对照标本中，通过MY09/MY11或E6 PCR均未检测到HPV DNA。对27个癌组织标本进行显微切割以尽量减少非肿瘤DNA，但MY09/MY11和GP5+/GP6+ PCR结果仍为阴性。此外，病例组（n = 63）和对照组（n = 144）的血清标本对HPV-16（P = 0.54）或HPV-11 VLP（P = 0.64）的反应无差异。
研究结果表明HPV与前列腺癌无关，且在老年男性的前列腺中HPV DNA根本不常见。
