Summary Forty-two oral squamous cell carcinomas (SCCs) were analysed for p53 mutations and human papillomavirus (HPV) (Regezi et al. 1993). W'hereas the epidemiology has been w-ell described so far. the molecular steps involsed in the pathogenesis of these common neoplasms are poorly understood. The role of human papillomas-irus (HPV) in the development of anogenital cancers has been widely studied. and current evidence shows that HPV infection is necessars for the desvelopment of most cervical cancers (zur Hausen. 1994). Approximately 80-90% of cervical carcinomas contain HPV DNA. and the predominant or high-risk types appear to be HPV-16. -18 and -33 (Yoshikawa et al. 1991). HPV E6 and E7 proteins. consistentlv expressed in HPV-transformed and HPVpositive tumours. can exert their oncogenic potential bv inactivating the products of the p53 tumour-suppressor cene (Lemine. 1990: zur Hausen. 1994) and the retimoblastoma (Rb) grene (Dy-son et al. 1989). In oral malignant lesions. the state of HPV infection has been reported to be as high as 76%c (Snijders et al. 1994). although there are still conflicting results in infection rate and role of HPV in oral carcinorenesis.

No abstract

No abstract