Nahand · BMC cancer 2021 · case-control study · n=107

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer.

Cited 62 times in the scientific literature.

Level 4 - case-series / case-control

Case-control study evaluating viral coinfection in human tissue samples.

PubMed 34399719 · doi:10.1186/s12885-021-08658-y · record verified 2026-08-28

What was done

This case-control study analyzed 67 patients with prostate cancer (PCa) and 40 control subjects to assess the role of human papillomavirus (HPV) and Epstein-Barr virus (EBV) coinfection. Expression levels of viral and cellular factors related to inflammation, tumor progression, and metastasis were quantified using enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR).

What was found

EBV/HPV coinfection was detected in 14.9% of PCa cases and 7.5% of controls, which was not a statistically significant difference (OR = 2.9, 95% CI: 0.18-45.2, P = 0.31). Among the 10 coinfected PCa cases, HPV 16 and HPV 18 accounted for 50% and 30% of infections, respectively, and 80% (8/10) demonstrated HPV genome integration. Compared to non-coinfected PCa cases, coinfected PCa cases had significantly higher mean expression of inflammatory markers (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin), along with significant downregulation of p53, pRb, and E-cadherin.

Why it matters

The study suggests that while HPV/EBV coinfection was not statistically associated with prostate cancer occurrence in this cohort, viral coinfection may influence tumor molecular phenotype by altering apoptotic and anoikis resistance pathways.

Limits

The study is constrained by a small sample size (n = 107 total; only 10 coinfected PCa cases), resulting in extremely wide confidence intervals for odds ratio estimates. As an observational case-control design, it cannot establish causality or determine the temporal sequence of infection and carcinogenesis, and the abstract does not provide exact numerical expression values or control group characteristics.

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