J Egypt Natl Canc Inst. 2025 Sep 1;37(1):63. doi: 10.1186/s43046-025-00313-y.
ABSTRACT
BACKGROUND: The potential involvement of JC polyomavirus (JCPyV) in prostate cancer (PCa) remains a subject of debate, as existing in vitro studies have produced conflicting results. Understanding the viral oncogenic mechanisms underlying prostate cancer could offer valuable insights into its etiology. This study aimed to explore the association between JCPyV infection and prostate cancer by detecting the viral large T-antigen gene in prostate tissue specimens.
METHODS: A case-control study was conducted from February 2022 to March 2023, including 100 participants: 50 diagnosed with prostate cancer (cases) and 50 with benign prostatic hyperplasia (BPH) as controls. Formalin-fixed paraffin-embedded (FFPE) prostate tissue samples were collected from all participants. Nested polymerase chain reaction (PCR) was employed to detect JCPyV large T-antigen DNA using specific primers. Demographic and clinical data were obtained via a structured questionnaire. Statistical analysis was carried out using SPSS version 20, and associations between JCPyV presence and prostate cancer were analyzed using logistic regression.
RESULTS: The mean age of the prostate cancer group was 67.5 ± 10.9 years, compared to 70.9 ± 8.9 years in the control group. JCPyV large T-antigen DNA was detected in 29 out of 50 (58%) prostate cancer cases, compared to 19 out of 50 (38%) controls (P = 0.045; odds ratio = 1.45; 95% confidence interval: 1.011 to 5.019). Within the prostate cancer group, patients testing positive for the JCPyV T-antigen had a mean age of 73.3 ± 8.7 years, significantly higher than T-antigen-negative patients, whose mean age was 67.0 ± 8.3 years (P = 0.029).
CONCLUSION: The prevalence of JCPyV large T-antigen gene was significantly higher in prostate cancer patients than in individuals with benign prostatic hyperplasia. These findings suggest that JCPyV infection may be linked to an increased risk of prostate cancer, reinforcing prior studies that imply a potential oncogenic role for the virus in prostate carcinogenesis. Further investigations are necessary to elucidate the molecular mechanisms driving this association and its potential clinical implications.
PMID:40888995 | DOI:10.1186/s43046-025-00313-y
