In an investigation of 201 prostate tissue samples from patients with benign prostate hyperplasia that later progressed to prostate cancer and 201 matched controls that did not, there were no differences in the prevalence of adenovirus, herpesvirus, papilloma virus, polyoma virus and Candida albicans DNA. (Palapattu et al, 2005;Sun et al, 2005). Moreover, population studies have revealed an increased relative risk for development of prostate cancer in men with a prior history of sexually transmitted infections (Dennis and Dawson, 2002). These findings support the hypothesis that an infectious agent can be a potential cofactor in prostate cancer development. Human papilloma virus (HPV), Epstein -Barr virus (EBV) and the polyoma viruses JCV and BKV represent viruses with proven linkage to different human cancers and have been traced in prostate cancer tissues (Grinstein et al, 2002;Zambrano et al, 2002). To further evaluate if a viral infection could contribute to prostate cancer development, we conducted a case -control study of 402 patients with benign prostate hyperplasia (BPH), of which 201 later progressed to prostate cancer. We examined whether the presence of genetic traces of EBV, herpes simplex virus (HSV) 1 and 2, cytomegalovirus (CMV), adenovirus, HPV, polyoma viruses BKV and JCV and Candida albicans in the prostate correlate with histological inflammation and subsequent prostate cancer diagnosis.
MATERIALS AND METHODSA case -control study of 402 archival prostate tissue samples obtained during transurethral resection of the prostate (TURP) collected at the Department of Pathology at the University Hospital of Northern Sweden, Umeå was conducted as described previously Bergh et al, 2006). Briefly, tissues were obtained from men with BPH (median age 64, range 51 -71), fixed in formalin, paraffin-embedded and stored at room temperature until tested. A total of 201 men developed prostate cancer at least 6 months after the TURP. For each case, a control was randomly selected from a cohort of patients that did not develop prostate cancer. The case -control pairs were matched for year of birth, residence and year of TURP. Histological inflammation was graded as mild or severe as described . DNA from prostate tissue was purified and checked for integrity as described . Nested PCR assays were used for all the assays except HPV and C. albicans PCRs. Primers and PCR protocols for adenovirus (Allard et al, 2001), CMV (Brytting et al, 1991), EBV (Meyohas et al, 1996), HSV1 and 2 (Aurelius et al, 1991) and HPV (de Roda Husman et al, 1995) were used with minor modifications. Primers for the polyoma viruses JCV and BKV and C. albicans were designed according to published sequence information (Table 1). To verify the positive PCR findings, PCR products were purified with QIAquick Purification Kit protocol (Qiagen s , Hilden, Germany) and directly sequenced in the ABI PRISM 3700 DNA ANALYSER (AME Bioscience, Toroed, Norway) using the Big Dyet Terminator Cycle Sequencing kit 1.1 (Applied Biosystems, Forster City, CA, US...
