Abstract

Cervical dysplasias and cancers associated with high-risk human papilloma virus (HPV) have shown overexpression of the p16 protein. This cyclin-dependent kinase inhibitor is a cell cycle regulator and its overexpression in anogenital neoplasia depends on the physical status (episomal or integrated) of HPV. Low-risk HPV mostly stays in its episomal form and causes cellular atypism, mild dysplasia and condyloma. Integration of high-risk HPV in host cellular DNA is associated with neoplastic progression, resulting in overexpression of its oncoproteins, and further in the compensatory overexpression of p16. Screening for p16  overexpression allows discrimination between the lesions associated with integrated HPV and the lesions associated with episomal HPV or without HPV. However, in a few cases there is no overexpresson of the p16 protein in lesions harbouring high-risk episomal HPV. At the Pathology Centre of East Tallinn Central Hospital, p16 immunohistochemistry is used as diagnostic support in the case of a limited or unclear pathohistological finding. We enclosed some of our cases for illustrative purposes.