The p53 tumour suppressor protein can be rendered ineffective by mutations in the p53 gene or by interactions with proteins of DNA-transforming viruses, including Human Papillomaviruses (HPVs). Our aim was to determine whether the inactivation of p53, caused by a mutation of gene itself or by HPV is involved in anogenital carcinogenesis. We studied p53 overexpression by immunohistochemical methods, and HPV/DNA by non isotopic in situ hybridization method in 137 anogenital lesions. Immunoreactivity for p53 was seen in 5% of condylomata acuminata, in 12% of low-grade CINs, in 3.5% of high-grade CINs, and in 17% of invasive cervical carcinomas. Two (67%) of three condylomata acuminate p53+ harboured HPV/DNA. The concomitant presence of p53 and HPV was not detected in intraepithelial and invasive cervical lesions. Our findings suggest that p53 inactivation does not seem to play an important role in anogenital carcinogenesis. Further investigation of the concomitant presence of p53 and HPV in condylomata acuminate and its role in recurrences or progression of these lesions is needed.