Lack of evidence for an association between seminoma and human papillomavirus infection using GP5+/GP6+ consensus primers

Bertazzoni, Giorgia; Sgambato, Alessandro; Migaldi, Mario; Grottola, Antonella; Sabbatini, Anna Maria Teresa; Nanni, Nadia; Farinetti, Alberto; Iachetta, Francesco; Giacobazzi, Elisabetta; Pecorari, Monica; Bonetti, Luca Reggiani

doi:10.1002/jmv.23431

Cited by 14 publications

(16 citation statements)

References 25 publications

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“…By our findings we can conclude that HPV infection is more prevalent in affected patients than controls. However, as recently suggested by other authors (Bertazzoni et al, 2013), this infection seems not to be cause of testicular cancer, but rather the effect of a status of higher vulnerability induced by the tumor. More and larger studies of follow-up of HPV infected patients will clarify whether or not there is a cause-effect relationship between HPV and testicular cancer or vice versa .…”

Section: Discussionsupporting

confidence: 55%

Testicular cancer and HPV semen infection

et al. 2012

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Testicular cancer represents the more frequent solid tumor affecting males aged 15–35 years. In the last decades, its incidence showed a progressive increased probably due to genetic and environmental factors. Despite exposure to some viruses such as HIV, HCV, EBV, and HPV is frequently related to cancer development, there are no studies aimed to evaluate the possible implication of viral infections in the pathogenesis of testicular cancer. In this study, we analyzed sperm parameters and prevalence of HPV on sperm in 155 testicular cancer patients at diagnosis (T−1), after orchiectomy (T0) and after 12 months from surgery or from the end of adjuvant treatments (T12). All patients showed a significantly higher prevalence of semen infection than controls (9.5% and 2.4% respectively,) and altered sperm parameters both at T−1 and T0. Considering sperm parameters, at T−1 we observed a reduction of progressive motility, and after orchiectomy patients showed a reduction of sperm concentration and count and a further worsening of motility. Thereafter, patients were assigned to three groups on the basis of medical option after surgery: S = surveillance, R = radiotherapy, and C = chemotherapy +/− radiotherapy. At T12, untreated patients had an improvement of sperm parameters while R group and even more C group had a strong decrease of sperm number (p < 0.01 both vs. T0 and S group). Moreover, patients who received radio and/or chemotherapy had a very high prevalence of HPV semen infection (S = 7.7%, R = 30.8%, and C = 61.5%). In conclusion, patients with testicular cancer had frequently altered sperm parameters and higher prevalence of HPV semen infection that were worsened after radio and chemotherapy. Because HPV infection is a risk factor for cancer development and it may further reduce fertility, we suggest screening for HPV in testicular cancer patients at diagnosis and particularly after adjuvant treatments.

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Section: Discussionsupporting

confidence: 55%

Testicular cancer and HPV semen infection

et al. 2012

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“…In addition to the prostate, HPV are also discussed in the pathogenesis of anogenital and urinary cancers, including penis, anus, bladder, testis and renal cancer. HPV appears not to play a major causative role in renal 60 61 and testicular carcinogenesis 62 for the failure detection of HPV DNA in cancer cases. On the contrary, there is sufficient evidence in humans for the carcinogenicity of certain HPV types, (i.e.…”

Section: Discussionmentioning

confidence: 99%

Worldwide Prevalence of Human Papillomavirus and Relative Risk of Prostate Cancer: A Meta-analysis

Yang

Xie

Feng

et al. 2015

Sci Rep

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Despite the increasing number of studies conducted recently to evaluate the association between HPV infections and the risk of prostate cancer, the results remain inconclusive. Furthermore, the prevalence and distribution of overall and individual HPV types worldwide in prostate cancer has not been reported until now. Therefore, we estimated the prevalence of HPV in prostate cancer by pooling data of 46 studies with 4919 prostate cancer cases, taking into account the heterogeneity of major related parameters, including study region, specimen type, HPV DNA source, detection method, publication calendar period and Gleason score. Moreover, we tested the association of HPV infections with prostate cancer risks by a meta-analysis of 26 tissue-based case-control studies. We found that the prevalence of HPV infection was 18.93% (95% CI = 17.84–20.05%) in prostate cancer cases, and most of which were high-risk HPV types (17.73%, 95% CI = 16.52–18.99%). The prevalence varied by region, PCR primers used, publication calendar period and Gleason score. Our study also showed a significantly increased risk of prostate cancer with the positivity of overall HPV detected in prostate tissues (OR = 1.79, 95% CI = 1.29–2.49) and revealed the geographic variation of association strength (P < 0.001). In conclusion, HPV infections may contribute to the risk of prostate cancer.

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“…Recent reports have stated that HPV can bind to sperm heads (8,9) or is localized in exfoliated epithelial cells present in semen samples (10). Small studies have proposed the testes, seminal vesicles, and ductus deferens as reservoirs of HPV infection (11,12), but a more recent study could not confirm the presence of HPV-DNA in normal testicular tissue (13). Thus, the source of HPV in semen has remained elusive.…”

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confidence: 95%