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does not show a significant trend in changing (p 1 0.05). Conclusions: We verified that the relationship between the risk of Gleason upgrading and prostate volume does not become significant simply by increasing the number of laterally directed biopsies from 6 to 10

Long-term experience with an anatomical anterograde approach to radical prostatectomy: Results in terms of positive margin rate

Purpose: To evaluate the effect of an anterograde approach to radical retropubic prostatectomy ( RRP) in terms of positive surgical margins ( SM+). Methods: 323 untreated patients underwent anterograde RRP for clinically localized prostate adenocarcinoma. Spearman coefficients, logistic univariate and multivariate analysis were used. Results: The incidence of SM+ was 14.9% and, in particular, this was 4.5% for apical, 9.0% for lateral, 0.9% for other sites, and 2.8% for multiple SM+. Upon univariate analysis, prostate- specific antigen ( PSA; r = 0.2073, p = 0.0002), pathological stage ( r = 0.3777, p < 0.0001), and seminal vesicle invasion ( r = 0.1453, p = 0.0089) were found to be significantly associated with SM+. Upon multivariate analysis, only PSA ( p = 0.0090) and pathological stage ( p ! 0.0001) were significantly and independently associated with SM+ occurrence. Conclusion: In our experience, the anterograde approach to RRP is associated with low SM+ rates. Copyright (C) 2008 S. Karger AG, Basel

Biopsy-derived gleason artifact and prostate volume: Experience using ten samples in larger prostates

Purpose: To verify whether a significant relationship between the risk of Gleason upgrading and the prostate volume remains when the number of biopsies is increased for larger prostate volumes. Materials: A total of 281 biopsy-proven prostate adenocarcinoma cases who underwent radical prostatectomy ( RRP) formed the cohort for this study. Change in transrectal ultrasound of the prostate ( TRUS) biopsies number based on total gland volume was made simply by increasing the number of biopsies from 6 to 10 when prostate volume was 1 50 cc. The total number of cancers with Gleason pattern 4 or greater on biopsy and on RRP was tabulated over TRUS volume categories and tests for trend. Results: The proportion of Gleason score ( GS) 6 7 at biopsy was 44.5% whereas, at RRP, it was 68.3%. The rate of upgrading from Gleason = 7 at RRP was 46.8%. No significant difference in terms of age, serum PSA, prostate volume and pT stage was found between not upgraded and upgraded cases (p > 0.05). As prostate volume categories increase, the number of cancers upgraded at RRP slightly increases in particular from prostate volume 30 - 39 to 40 - 49 cc ( where only 6 biopsies were performed). However, either at biopsy or at RRP, the percentage of GS 6 7 tumors does not show a significant trend in changing (p > 0.05). Conclusions: We verified that the relationship between the risk of Gleason upgrading and prostate volume does not become significant simply by increasing the number of laterally directed biopsies from 6 to 10. Copyright (C) 2008 S. Karger AG, Basel

p53 Gene Mutational Rate, Gleason Score, and BK Virus Infection in Prostate Adenocarcinoma: Is There a Correlation?

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-em bedded 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. (C) 2008 Wiley-Liss, Inc