Cardillo M R, Stamp G W, Pignatelli M N, Lalani E N
Royal Postgraduate Medical School, Department of Histopathology, London, UK.
Eur J Gynaecol Oncol. 1993;14(6):484-90.
Recent data suggest an inverse correlation between human papillomavirus (HPV) infection and p53 tumor-suppressor gene mutation. In an attempt to elucidate the role of p53 mutations in cervical neoplasias, 65 cervical lesions, ranging from normal to malignant, were examined for overexpression of p53 protein by immunohistochemistry in paraffin-embedded tissue, and correlated with proliferating cell nuclear antigen (PCNA). An overexpression was seen in 35% of well-differentiated and 32.5% of poorly-differentiated squamous carcinomas, in 43.33% of microinvasive and 21.66% of CIS. More than 50% of neoplastic cells were immunoreactive for p53 protein in 10% of well-differentiated squamous carcinomas. Other positive specimens showed reactivity in < 24% of tumor cells. No staining was found in adenocarcinoma, dysplastic tissue, condylomas and normal tissue (83.07%). In contrast PCNA was detected in all cases of invasive squamous carcinomas, adenocarcinoma, CIS, CIN III, in 32.5% of CIN II, in 29.54% CIN I, and in 53.52% of wart. More than 50% of tumor cells showed nuclear staining for PCNA protein in 61.17% of invasive squamous carcinomas, in 21.66% of CIS, in 39% CIN III, in 32.5% CIN II and in 7.64% of wart. In the remain cases the positivity of nuclear staining was < 24%. No staining was present in 20% of cases including in normal cervix. Our data suggest that the viral-host protein interactions result in loss of the negative growth control normally exerted by p53. The consequence of HPV infection is a loss of functional wild-type p53 protein within the cells.(ABSTRACT TRUNCATED AT 250 WORDS)
