The etiologic role of human papillomavirus in penile cancers: a study in Vietnam.

Penile cancer development is a multi-factorial process involving poor genital hygiene, phimosis, human papillomavirus (HPV), chronic inflammatory and premalignant conditions, and smoking (Misra et al, 2004). According to a systematic review, human papillomavirus (HPV) DNA was detected in 48%, on average, of penile squamous cell carcinomas (PSCCs) and the most frequent HPV-related histotype (66%) was basaloid PSCC (Backes et al, 2009). The integration of high-risk HPV genome into the host genome is suspected to be an important event for malignant transformation and cancer progression (Wentzensen et al, 2004; Williams et al, 2011). It usually disrupts the E2 gene, a suppressor of the E6/E7 promoter, leading to the overexpression of viral oncogenes E6 and E7. The high viral load, frequently observed in cervical cancer, is also a determinant of cancer development (Wu et al, 2006). The overexpression of p16INK4A is a useful biomarker for evaluating the aetiologic role of HPV because HPV-E7 disturbs the p16INK4A/cyclin D/Rb pathway, leading to the accumulation of p16INK4A (Narisawa-Saito and Kiyono, 2007). In PSCC, however, the association between p16INK4A overexpression and HPV presence is still unestablished (Ferreux et al, 2003; Poetsch et al, 2011; Stankiewicz et al, 2011a). To understand the aetiologic role of HPV in the development of PSCCs, we examined the presence, genotype, viral load and physical status of high-risk HPV, and p16INK4A expression in PSCCs in Vietnam.