HPV and skin carcinogenesis

Oxidative Stress and HPV Carcinogenesis

Extensive experimental work has conclusively demonstrated that infection with certain types of human papillomaviruses, the so-called high-risk human papillomavirus (HR-HPV), represent a most powerful human carcinogen. However, neoplastic growth is a rare and inappropriate outcome in the natural history of HPV, and a number of other events have to concur in order to induce the viral infection i...

HPV infection and oral carcinogenesis.

Deletion of epidermal Rac1 inhibits HPV-8 induced skin papilloma formation and facilitates HPV-8- and UV-light induced skin carcinogenesis

Overexpression and increased activity of the small Rho GTPase Rac1 has been linked to squamous cell carcinoma of the epidermis and mucosa in humans. Targeted deletion of Rac1 or inhibition of Rac1 activity in epidermal keratinocytes reduced papilloma formation in a chemical skin carcinogenesis mouse model. However, a potential role of Rac1 in HPV- and UV-light induced skin carcinogenesis has no...

Somatic Host Cell Alterations in HPV Carcinogenesis

High-risk human papilloma virus (HPV) infections cause cancers in different organ sites, most commonly cervical and head and neck cancers. While carcinogenesis is initiated by two viral oncoproteins, E6 and E7, increasing evidence shows the importance of specific somatic events in host cells for malignant transformation. HPV-driven cancers share characteristic somatic changes, including apolipo...

Environmental co-factors in HPV carcinogenesis.

Epidemiological studies have shown that only a small fraction of women infected with oncogenic HPV types will eventually progress to high-grade intraepithelial lesions (HSIL) and cervical cancer (CC). Because infection by oncogenic HPVs is a necessary but not a sufficient cause of CC, it has been assumed that other factors, acting in conjunction with HPV, influence the risk of transition from c...