Oral cancer provides a unique model system for the study Of the multistep n
ature of cancer. The influence of viruses and tumor suppressor gene inactiv
ation are of major importance in this HPVs are small oncogenic viruses whic
h are implicated in epithelial carcinogenesis, and p53 is a tumor suppresso
r gene with a central role in the prevention of genomic injury. p53 protein
defection is usually a synonym for p53 mutation. This study was designed t
o determine the immunohistochemical detection of p53 protein in HPV positiv
e oral squamous cell carcinomas and hyperplastic oral lesions. p53 was dete
cted in 50% (5/10) of HPV positive hyperplastic oral lesions and in 59.41%
(22/39) of oral squamous cell carcinomas. These results indicate that HPV a
nd p53 protein alterations frequently coexist in the lesions of our study a
nd suggest that p53 mutation may be an early generic event in oral carcinog
enesis. Moreover, this coexistance reveals that other environmental carcino
gens have a more prominent role in oral carcinogenesis, one that overrides
the action of HPV.