Human papillomavirus (HPV) infections of the high-risk types are strongly linked to the development of cervical carcinoma. The HPV oncoproteins E6 and E7 are thought to play a crucial role in this process through their interactions with the P53 protein. E6 binds to P53 protein promoting its degradation. This is considered to contribute to the oncogenesis of HPV-associated anogenital cancer. On the other hand, in HPVnegative cervical carcinoma, P53 mutations are thought to have a role in the transformation process. In 25 formaldehyde-fixed paraffin embedded cervical carcinoma tissue samples were evaluated for the presence of HPV-DNA and mutations in exons 5-8 of the P53 gene by single-stranded conformation polymorphism analysis. Fourteen samples were HPV positive and only 3 missense point mutations were detected. These findings suggest that other mechanisms independent of P53 inactivation may play a role in the genesis of cervical carcinomas