Role of human papillomavirus in cutaneous oncogenesis.

Abstract

There is a strong association between the human papillomavirus and cutaneous squamous cell carcinoma. If this association was merely random, one would expect an equal distribution of human papillomavirus types among affected individuals. However, only specific types of human papillomavirus are consistently found in cutaneous and genital squamous cell carcinomas. Immunosuppressed individuals clearly have a much higher incidence of cutaneous carcinomas. Immunosuppression, either local or systemic, not only decreases immune surveillance but may also dictate the amount and type of virus each individual may carry. Epidermodysplasia verruciformis and other rare hereditary disorders that combine specific immune defects and an increased incidence of malignancy are very useful models that clearly fulfill a multistep theory of oncogenesis. The precise mechanism of oncogenesis in these select human papillomavirus types is not yet fully understood. Intracellular interactions with the recently described tumor suppressor proteins may prove to be the primary site of action of these oncogenic viruses. Environmental cocarcinogens and activation of oncogenes are clearly important if not essential factors in human papillomavirus-associated tumors. As our knowledge and understanding of malignant transformation grows, it becomes apparent that this is a complex multistep process.