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p53 gene mutational rate, Gleason score, and BK virus infection in prostate adenocarcinoma: Is there a correlation?
Author(s) -
Russo Giuseppe,
Anzivino Elena,
Fioriti Daniela,
Mischitelli Monica,
Bellizzi Anna,
Giordano Antonio,
AutranGomez Anamaria,
Di Monaco Franco,
Di Silverio Franco,
Sale Patrizio,
Di Prospero Laura,
Pietropaolo Valeria
Publication year - 2008
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.21312
Subject(s) - prostate cancer , carcinogenesis , prostate , biology , immunohistochemistry , pca3 , cancer research , cancer , gene , virology , virus , exon , adenocarcinoma , pathology , medicine , immunology , genetics
Prostate cancer represents the second leading cause of cancer deaths in Western countries. Viral infections could play a role in prostate carcinogenesis. Human polyomavirus BK (BKV) is a possible candidate because of its transforming properties. In this study, BKV sequences in urine, blood, fresh, and paraffin‐embedded prostate cancer samples from 26 patients were searched using Q‐PCR analysis. T antigen (TAg) and p53 localization in neoplastic cells were evaluated by immunohistochemical analysis. Also, the presence of mutations in 5–9 exons of p53 gene was analyzed. Results showed that BKV‐DNA was found in urine (54%), plasma (31%), and in fresh prostate cancer specimens (85%). The analysis of p53 gene evidenced several mutations in high Gleason patients, according to tumor advanced stage. Immunohistochemical analysis results evidenced the localization of p53 and TAg into cytoplasm, whereas in TAg‐negative tumors, p53 was nuclear. This study suggests that BKV acts as cofactor in the pathogenesis of prostate cancer. These observations emphasize previous studies regarding the cellular pathways that may be deregulated by BKV. J. Med. Virol. 80:2100–2107, 2008. © 2008 Wiley‐Liss, Inc.