Wideroff L, Schottenfeld D, Carey T E, Beals T, Fu G, Sakr W, Sarkar F, Schork A, Grossman H B, Shaw M W
Department of Epidemiology, University of Michigan, Ann Arbor 48109-2029, USA.
Prostate. 1996 Feb;28(2):117-23. doi: 10.1002/(SICI)1097-0045(199602)28:2<117::AID-PROS7>3.0.CO;2-D.
This study hypothesized that human papillomavirus (HPV) infection is associated with increased prostate cancer risk, and that the 40% higher incidence rate in blacks is attributable to a greater prevalence of oncogenic viral DNA in prostatic tissues. Viral L1 and E6 gene sequences were polymerase chain reaction (PCR) amplified in archival tissues from 56 prostate cancer cases and 42 hyperplastic controls. L1 amplimers were hybridized by dot blot to HPV L1 generic probes, as were E6 amplimers to E6 probes specific for HPV 6, 11, 16, 18, 31, 33, and 45. 12.5% of cases and 9.5% of controls were HPV positive by L1 hybridization (age/race adjusted odds ratio = 1.66, 95% confidence interval = 0.33, 8.37). Four of 52 (7.7%) blacks were HPV positive compared to 7 of 46 (15.2%) whites. However, none of the L1-positive samples hybridized to the E6 type-specific probes, and positive results were not replicable using a broader spectrum of PCR primers and probes. These data suggest that HPV infection is not a significant risk factor for prostate cancer and does not explain the excess cancer risk in blacks.
本研究假设，人乳头瘤病毒（HPV）感染与前列腺癌风险增加相关，且黑人中高40%的发病率归因于前列腺组织中致癌病毒DNA的更高流行率。对来自56例前列腺癌病例和42例增生性对照的存档组织中的病毒L1和E6基因序列进行聚合酶链反应（PCR）扩增。L1扩增产物通过斑点印迹与HPV L1通用探针杂交，E6扩增产物与针对HPV 6、11、16、18、31、33和45的E6探针杂交。通过L1杂交，12.5%的病例和9.5%的对照为HPV阳性（年龄/种族调整比值比=1.66，95%置信区间=0.33，8.37）。52名黑人中有4名（7.7%）为HPV阳性，而46名白人中有7名（15.2%）为HPV阳性。然而，L1阳性样本中没有一个与E6型特异性探针杂交，并且使用更广泛的PCR引物和探针时，阳性结果无法重复。这些数据表明，HPV感染不是前列腺癌的重要风险因素，也无法解释黑人中额外的癌症风险。
