Papillomaviruses: death-defying acts in skin cancer.
Ultraviolet (UV) radiation is an environmental agent that has a major impact on humans, and cumulative exposure poses a serious risk in terms of developing skin cancer. Acute doses of UV induce apoptotic cell death in the skin via signalling pathways that are, in part, dependent on the p53 tumour suppressor protein. However, p53-independent mechanisms have also been described. Recent findings show that a high proportion of non-melanoma skin cancers contain human papillomavirus. The viral E6 protein effectively blocks the epidermal apoptotic response to UV and might play a key role in promoting tumour development in cooperation with the mutagenic effects of UV.
Storey
Alan
A
Cancer Research UK, Skin Tumour Laboratory, 2 Newark Street, London, UK E1 2AT. alan.storey@cancer.org.uk
D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis / Q000528:radiation effects; D004195:Disease Models, Animal; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008969:Molecular Sequence Data; D009856:Oncogene Proteins, Viral / Q000737:chemistry / Q000378:metabolism; D027383:Papillomaviridae / Q000378:metabolism / Q000472:pathogenicity*; D017386:Sequence Homology, Amino Acid; D012878:Skin Neoplasms / Q000821:virology*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects; D050998:bcl-2 Homologous Antagonist-Killer Protein
C494772:BAK1 protein, human; C494773:Bak1 protein, mouse; C466080:E6 protein, human papillomavirus type 1; D008565:Membrane Proteins; D009856:Oncogene Proteins, Viral; D016159:Tumor Suppressor Protein p53; D050998:bcl-2 Homologous Antagonist-Killer Protein