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Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics

  • Authors:
    • Brenda Ivonn Rodríguez‑Romero
    • Nadia Mabel Pérez‑Vielma
    • Alejandro Corzo‑Cruz
    • Modesto Gómez‑López
    • María Olivia Medel‑Flores
    • Virginia Sánchez‑Monroy
  • View Affiliations / Copyright

    Affiliations: National Polytechnic Institute (Instituto Politécnico Nacional), ESM, Mexico City CP11340, Mexico, National Polytechnic Institute (Instituto Politécnico Nacional), CICS, UST, Mexico City CP11340, Mexico, National Polytechnic Institute (Instituto Politécnico Nacional), ENMH, Mexico City CP07320, Mexico
    Copyright: © Rodríguez‑Romero et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 85
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    Published online on: July 11, 2025
       https://doi.org/10.3892/mco.2025.2880
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Abstract

It has been demonstrated that there is an association between human papillomavirus (HPV) infection and prostate cancer (PCa). However, HPV infection in PCa and the causal role remains unclear, therefore the objective of the present study was to confirm this association and evaluate the clinical tumor characteristics to understand the underlying molecular mechanisms. HPV detection and genotyping were analyzed in 117 paraffin‑embedded prostate tissue from men diagnosed by histological analysis with adenocarcinoma, and a group including 60 men with benign prostatic hyperplasia (BPH). The clinical and histological characteristics in tissues with PCa were evaluated, comparing HPV‑infected vs. not infected, single vs. multiple HPV infection, and low‑risk (LR) HPV vs. high‑risk‑HPV (HR‑HPV). In 84.1% of all samples, HPV was detected, exhibiting a higher prevalence in tissues with PCa (109/117 or 93%) compared with tissues with BPH (40/60 or 67%), as evidenced by the association between the infection and PCa [odds ratio (OR); 6.8; 95% confidence interval (CI), 2.77‑16.69; P<0.0001]. The main viral genotypes detected in order of decreasing prevalence were 16, 11, 18 and 6. Detection of multiple HPV infection was significantly higher in PCa (78/117 or 66.7%) than in HPB (21/60 or 35%) (OR, 3.7; 95% CI, 1.929‑7.151; P=0.0001). Of note, co‑infections containing interactions of HPV 16‑18 types were associated with PCa (OR, 3.9079; CI, 1.2867‑11.8685; P=0.0162) which indicates new epidemiological data in PCa. Cribriform cells, prostatic atrophy and prostatitis were statistically less frequent in tissues with PCa HPV‑infected vs. not infected (P<0.05). Cribriform cells were also more frequent in single vs. multiple HPV infection (P<0.05), and in tissues with LR‑HPV vs. HR‑HPV (P<0.05). A worse prognosis was observed for HPV‑not infected, with a single HPV infection and LR‑HPV infection, suggesting that tumor progression could be attributed to the resistance of human PCa cells to tumor apoptosis in the presence of multiple HPV types to ensure cell survival. Studies evaluating differences in the tumor microenvironment are needed to clarify the association between viral infections and histopathological tumor characteristics.
View Figures

Figure 1

Representative histopathological
image derived of samples used in the present study. (A) Prostate
cancer and (B) Benign prostatic hyperplasia. Hematoxylin and eosin
staining at x200 magnification.

Figure 2

Frequency of multiple HPV patterns
detected in study groups. The figure describes 73 patterns of
multiple HPV infection detected (Y-axis), and the number of samples
(frequency for pattern (X-axis). *Coinfections
containing interactions of HPV16/18 genotypes were associated with
the PCa group (OR, 3.9079; CI, 1,2867-11,8685; P=0,0162).

Figure 3

Representative histological section
of (A-F) prostatic adenocarcinomas and (G-L) benign prostatic
hyperplasia used in the present study. (A and G) Samples without
HPV infection; (B and H) samples with single HPV infection; (C and
I) samples with multiple HPV infection; (D and J) samples with
single low-risk HPV infection; (E and K) samples with single
high-risk-HPV infectionl and (F and L) samples with multiple low
and risk HPV infection. Hematoxylin and eosin staining at x10
magnification.
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Copy and paste a formatted citation
Spandidos Publications style
Rodríguez‑Romero BI, Pérez‑Vielma NM, Corzo‑Cruz A, Gómez‑López M, Medel‑Flores MO and Sánchez‑Monroy V: Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics. Mol Clin Oncol 23: 85, 2025.
APA
Rodríguez‑Romero, B.I., Pérez‑Vielma, N.M., Corzo‑Cruz, A., Gómez‑López, M., Medel‑Flores, M.O., & Sánchez‑Monroy, V. (2025). Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics. Molecular and Clinical Oncology, 23, 85. https://doi.org/10.3892/mco.2025.2880
MLA
Rodríguez‑Romero, B. I., Pérez‑Vielma, N. M., Corzo‑Cruz, A., Gómez‑López, M., Medel‑Flores, M. O., Sánchez‑Monroy, V."Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics". Molecular and Clinical Oncology 23.3 (2025): 85.
Chicago
Rodríguez‑Romero, B. I., Pérez‑Vielma, N. M., Corzo‑Cruz, A., Gómez‑López, M., Medel‑Flores, M. O., Sánchez‑Monroy, V."Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics". Molecular and Clinical Oncology 23, no. 3 (2025): 85. https://doi.org/10.3892/mco.2025.2880
Copy and paste a formatted citation
x
Spandidos Publications style
Rodríguez‑Romero BI, Pérez‑Vielma NM, Corzo‑Cruz A, Gómez‑López M, Medel‑Flores MO and Sánchez‑Monroy V: Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics. Mol Clin Oncol 23: 85, 2025.
APA
Rodríguez‑Romero, B.I., Pérez‑Vielma, N.M., Corzo‑Cruz, A., Gómez‑López, M., Medel‑Flores, M.O., & Sánchez‑Monroy, V. (2025). Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics. Molecular and Clinical Oncology, 23, 85. https://doi.org/10.3892/mco.2025.2880
MLA
Rodríguez‑Romero, B. I., Pérez‑Vielma, N. M., Corzo‑Cruz, A., Gómez‑López, M., Medel‑Flores, M. O., Sánchez‑Monroy, V."Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics". Molecular and Clinical Oncology 23.3 (2025): 85.
Chicago
Rodríguez‑Romero, B. I., Pérez‑Vielma, N. M., Corzo‑Cruz, A., Gómez‑López, M., Medel‑Flores, M. O., Sánchez‑Monroy, V."Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics". Molecular and Clinical Oncology 23, no. 3 (2025): 85. https://doi.org/10.3892/mco.2025.2880
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