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It is known that human papillomavirus(HPV) infection can cause squamous cell neoplasms at several sites, such as cervix uteri carcinoma and oral squamous carcinoma. There is little information on the expression of HPV and its predictive markers in tumours of the major and minor salivary glands of the head and neck. We therefore assessed oral salivary gland neoplasms to identify associations between HPV and infection-related epidermal growth factor receptor(EGFR), cyclin-dependent kinase inhibitor 2A(CDKN2A/p16) and tumour protein p53(TP53). Formalin-fixed, paraffin-embedded tissue samples from oral salivary gland carcinomas(n551) and benign tumours(n526) were analysed by polymerase chain reaction(PCR) analysis for several HPV species, including high-risk types16 and 18. Evaluation of EGFR, CDKN2 A, TP53 and cytomegalovirus(CMV) was performed by immunohistochemistry. Epstein–Barr virus(EBV) was evaluated by EBV-encoded RNA in situ hybridisation. We demonstrated that salivary gland tumours are not associated with HPV infection. The expression of EGFR, CDKN2 A and TP53 may be associated with tumour pathology but is not induced by HPV.CMV and EBV were not detectable. In contrast to oral squamous cell carcinomas, HPV, CMV and EBV infections are not associated with malignant or benign neoplastic lesions of the salivary glands.
It is known that human papillomavirus (HPV) infection can cause squamous cell neoplasms at several sites, such as cervix uteri carcinoma and oral squamous carcinoma. There is little information on the expression of HPV and its predictive markers in tumors of the major and minor salivary glands of the head and neck. We therefore assessed oral salivary gland neoplasms to identify associations between HPV and infection-related epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitor 2A (CDKN2A / p16) and tumor protein p53 (TP53). Formalin-fixed, paraffin-embedded tissue samples from oral salivary gland carcinomas (n551) and benign tumors (n526) were analyzed by polymerase chain reaction (PCR) analysis for several HPV species, including high-risk types 16 and 18. Evaluation of EGFR, CDKN2 A, TP53 and cytomegalovirus (CMV) was performed by immunohistochemistry. Epstein-Barr virus (EBV) was evaluated by EBV-encoded RNA in situ hybridization. We demonstrated that salivary gland tum The expression of EGFR, CDKN2 A and TP53 may be associated with tumor pathology but is not induced by HPV. CMV and EBV were not detectable. In contrast to oral squamous cell carcinomas, HPV, CMV and EBV infections are not associated with malignant or benign neoplastic lesions of the salivary glands.