Shedding light on Testicular cancer

Zoltick, Barbara H.

doi:10.1097/01.npr.0000398870.16580.86

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…Testicular cancer (TC) is the most common solid tumor affecting males between 20 and 40 years old and accounting for approximately 1–1.5% of all cancers in men (1, 2). In the last decades, its incidence showed a progressive increase, particularly in some regions of Europe and Northern America (3–5). It is a real variegate cancer, characterized by several histological patterns, comprising germ-cell tumors and non-germ-cell tumors.…”

Section: Introductionmentioning

confidence: 99%

Role of Viral Infections in Testicular Cancer Etiology: Evidence From a Systematic Review and Meta-Analysis

et al. 2019

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The most represented histotype of testicular cancer is the testicular germ-cell tumor (TGCT), both seminoma and non-seminoma. The pathogenesis of this cancer is poorly known. A possible causal relationship between viral infections and TGCTs was firstly evoked almost 40 years ago and is still a subject of debate. In the recent past, different authors have argued about a possible role of specific viruses in the development of TGCTs including human papillomavirus (HPV), Epstein–Barr virus (EBV), cytomegalovirus (CMV), Parvovirus B-19, and human immunodeficiency virus (HIV). The aim of this present review was to summarize, for each virus considered, the available evidence on the impact of viral infections on the risk of developing TGCTs. The review was reported following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We included all observational studies reported in English evaluating the correlations between viral infections (HPV, CMV, EBV, Parvovirus B19, and HIV) and TGCTs. The methodological quality of studies included in the meta-analysis was evaluated using a modified version of the “Newcastle–Ottawa Scale.” Meta-analyses were conducted using the “Generic inverse variance” method, where a pooled odds ratio (OR) was determined from the natural logarithm (LN) of the studies' individual OR [LN (OR)] and the 95% CI. A total of 20 studies (on 265,057 patients) were included in the review. Meta-analysis showed an association with TGCTs only for some of the explored viruses. In particular, no association was found for HPV, CMV, and Parvovirus B-19 infection ( p = ns). Conversely, EBV and HIV infections were significantly associated with higher risk of developing TGCTs (OR 7.38, 95% CI 1.89–28.75, p = 0.004; OR 1.71, 95% CI 1.51–1.93, p < 0.00001). In conclusion, we found adequate evidence supporting an oncogenic effect of HIV and EBV on the human testis. Conversely, available data on HPV and TGCTs risk are conflicting and further studies are needed to draw firm conclusions. Finally, current evidence does not support an effect of CMV and Parvovirus B-19 on testicular carcinogenesis.

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Section: Introductionmentioning

confidence: 99%

Role of Viral Infections in Testicular Cancer Etiology: Evidence From a Systematic Review and Meta-Analysis

et al. 2019

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“…However, considering men aged 15–35, it becomes the most common solid malignancy (Siegel et al, 2012; Viatori, 2012). Moreover, many authors demonstrated an increasing secular trend especially in some regions of Europe and North America (Adami et al, 1994; Richiardi et al, 2004; Zoltick, 2011). Many risk factors have been studied as a pre-disposing factor in the development of this cancer, but only for some there is a high level of evidence (Senturia, 1987; Buetow, 1995).…”

Section: Introductionmentioning

confidence: 99%

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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Cisplatin-induced ototoxicity: Transporters playing a role in cisplatin toxicity

Waissbluth

Daniel

2013

Hearing Research

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Shedding light on Testicular cancer

Cited by 4 publications

References 32 publications

Role of Viral Infections in Testicular Cancer Etiology: Evidence From a Systematic Review and Meta-Analysis

Role of Viral Infections in Testicular Cancer Etiology: Evidence From a Systematic Review and Meta-Analysis

Testicular cancer and HPV semen infection

Cisplatin-induced ototoxicity: Transporters playing a role in cisplatin toxicity

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