Basaloid squamous cell carcinoma is a variant of squamous cell carcinoma, preferentially arising in the head and neck region. Current reports point to an association of basaloid squamous cell carcinoma (BSCC) and human papilloma virus (HPV) infection. This virus is supposed to be an aetiological factor in this entity. The aim of this study was to analyse the HPV infection status in different entities of oral neoplasms or dysplasias with basaloid differentiation of epithelial cells.
Materials and methods: The study comprised data from 34 oral lesions of squamous epithelial origin: 17 BSCCs, 10 papillomas and 7 hyperplasias/dysplasias of oral epithelia. HPV DNA was detected by means of a hybrid capture technique. HPV types were identified by direct sequencing. Immunohistochemical investigation of the specimens with anti-p16 antibody was performed in order to elucidate the putative role of p16 as a surrogate marker of HPV infection.
Results: The rate of HPV-infected BSCC was extraordinarily high. About two thirds of the cases (61%, 11/17) were infected with HPV high-risk types, predominantly with HPV genotype 16 (>90%, 10/11). The infection status differed significantly between BSCC and other oral lesions in terms of frequency of HPV infection and HPV genotypes. p16 expression proved not to be a suitable surrogate marker of HPV high-risk infection in oral lesions, in particular in BSCC. This was an essential difference of this collective compared to genital carcinomas with HPV high-risk infections.
Conclusion: This study revealed a high association between BSCC and HPV type 16. This close phenotype-genotype correlation could be of diagnostic value. Type-specific analysis of HPV infection in head and neck cancer may be important in the differential diagnosis of malignancies in the head and neck region with a basaloid growth pattern. However, the investigation is technically demanding, including hybridisation and sequencing techniques. A simplified test for HPV in BSCC of the oral cavity using the immunohistochemical proof of p16 expression as a surrogate marker is non-effective.