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Updated: Jul 6, 2025

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Sexually and non-sexually transmitted infections and the risk of prostate cancer: Results from the EPICAP study
Melissa Sawaya1, Emilie Cordina-Duverger1, Pierre-Jean Lamy2,3
1Université Paris-Saclay, UVSQ, Inserm, Gustave Roussy, CESP, Villejuif, France.
Introduction:
Prostate cancer (PCa) is by far the most common type of cancer among men in western countries. However, relatively little is known about its etiology despite the high morbidity and mortality. It has been suggested that chronic inflammation may be involved in prostate carcinogenesis. We investigated the role of sexually and non-sexually transmitted infections in prostate cancer risk with a specific interest in the aggressive types.
Methods:
We used data from epidemiological study of prostate cancer (EPICAP), a population-based case-control study. A total of 819 incident cases and 879 controls were interviewed face-to-face using a standardized questionnaire gathering information on known or suspected risk factors of prostate cancer and personal history of specific sexually and non-sexually transmitted infections: gonorrhea, syphilis, trichomonas, herpes, mononucleosis, Epstein-Barr virus, varicella-zoster, and dengue. Odds ratios (OR) and their 95% confidence interval were estimated using multivariate unconditional logistic regression.
Results:
There was no significant association between gonorrhea (OR: 0.90, 95% CI: 0.61-1.33), trichomonas (OR: 0.74, 95% CI: 0.27-2.07), genital herpes (OR: 0.69, 95% CI: 0.38-1.27), and the risk of prostate cancer. No association emerged for overall sexually transmitted bacterial and viral infections (OR 1.05, 95% CI: 0.86-1.29) and overall non-sexually transmitted viral infections (OR 1.11, 95% CI: 0.90-1.35) and the risk of prostate cancer.
Conclusion:
Our results showed that sexually or non-sexually transmitted infections, either bacterial or viral, were not associated to prostate cancer. Therefore, further investigation is needed to help advance our understanding of the role of chronic inflammation in the etiology of prostate cancer, with a particular focus on its most aggressive types.
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