# Human Papillomavirus Prevalence in the Prostate and Seminal Vesicles: Does This Virus Have an Etiological Role in the Development of Prostate Cancer?

## TL;DR

This study investigates whether human papillomavirus (HPV) is present in prostate cancer tissues and whether it might play a role in causing the disease.

## Contribution

The study provides evidence that HPV may be present in prostate cancer and suggests a potential, though not definitive, etiological role in some cases.

## Key findings

- HPV-DNA was detected in 9.6% of prostate cancer cases but not in seminal vesicles.
- High-risk HPV was found in 4.5% of samples, with HPV44 being the most common identifiable genotype.
- HPV-DNA was found in both cancerous and non-cancerous prostate lesions, suggesting a possible role in carcinogenesis.

## Abstract

Human papillomavirus (HPV) is common in both sexes and is also detected in male urine and semen. However, its exact origin and its etiological role in the male genital tract remain unclear. A total of 157 formalin-fixed paraffin-embedded tissues from 156 primary prostate cancer lesions and one metastatic lesion were analyzed. HPV-DNA was detected using a nested PCR, and HPV genotyping was performed using flow-through hybridization for positive cases. In situ hybridization (ISH) was used to localize HPV-DNA, whereas HPV-E6/E7 mRNA ISH and p16INK4a immunohistochemistry were conducted on high-risk (HR) HPV-positive samples. A nested PCR analysis demonstrated that HPV-DNA was detected in 9.6% of prostate cancers and 0% of seminal vesicles. HR-HPV was observed in 4.5% of the samples. Unknown type was the most common genotype. Of the genotypes which could be identified in the genotyping assay, HPV44 was the most prevalent. HPV prevalence was significantly higher in patients with high-grade groups. Among 15 HPV-positive cases, HPV-DNA was found in 9 cancerous and 10 non-cancerous lesions. E6/E7 mRNA was expressed in 6 of 7 HR-HPV-positive cases, while p16INK4a expression was weak or absent in all cases. HPV can infect prostate tissue and may contribute to carcinogenesis in some cases, but p16INK4a was not a consistent surrogate for E7 expression.