ArticleFrontiers in oncology2025
Prostate cancer evolution after COVID-19-related prostatitis in a TMPRSS2-altered patient: a case report and review of the molecular interface between SARS-CoV-2 and prostate oncogenesis.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: SARS-CoV-2 exploits TMPRSS2, an androgen-regulated protease highly expressed in prostate tissue, to enter host cells. While inflammation is a recognized promoter of oncogenesis, the possibility that viral prostatitis could precede prostate cancer has not been previously reported. Case presentation: We describe the case of a 55-year-old male with no family history of prostate or breast cancer and no germline pathogenic variants on next-generation sequencing (NGS), who developed lower urinary tract symptoms (LUTS) and PSA elevation shortly after a second COVID-19 infection. Multiparametric MRI initially demonstrated diffuse PI-RADS 4 changes compatible with prostatitis. Although symptoms improved with antibiotics, LUTS persisted and were managed with finasteride and doxazosin. Over the following two years, serial imaging revealed progression to a long, poorly demarcated PI-RADS 5 lesion extending from apex to base in the right posterior peripheral zone, and a smaller PI-RADS 4 lesion on the left. Targeted biopsy confirmed acinar adenocarcinoma (Gleason 7 and 6 in 16 of 26 cores). PET-PSMA showed disease confined to the prostate. The patient underwent neoadjuvant therapy with androgen deprivation therapy (ADT) plus a novel hormonal agent (NHA) from April 14 to October 15, 2024, resulting in significant tumor reduction. Radical prostatectomy on November 1, 2024 revealed a small residual acinar adenocarcinoma focus with perineural invasion, negative surgical margins, and molecular evidence of TMPRSS2::ERG gene fusion and PTEN loss. Conclusion: This is the first documented case suggesting a potential link between COVID-19-related prostatitis and subsequent prostate cancer in a TMPRSS2::ERG-altered patient without hereditary predisposition. Although causality cannot be established, the findings highlight a hypothesis-generating interface between viral infection, inflammation, and oncogenesis that warrants further study.
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