Human papillomaviruses in non-melanoma skin cancer.
Recent data suggest that additional factors, other than UV radiation, are involved in the etiology of non-melanoma skin cancer. These include alterations in the tumor suppressor genes, p53, p16$L*I*U$LINK4a$L*I$L/CDKN2A, p21$L*I*U$LWAF1/CIP1$L*I$L and the PTCH gene, as well as cytokines. Papillomavirus infections have been implicated in the etiology of non-melanoma skin cancer. The interaction of tumor suppressor genes and cytokines with the oncoproteins of high-risk mucosal HPV types have been studied in detail, but very little is known about the cutaneous HPV types. We have studied the effect of UV radiation on the URRs of HPV 1, 2, 3, 5, 7, 20, 23, 27, 38, 41, and 77. Neither the CAT-expression and promoter activity of these HPV types, nor presence or absence of wild-type or mutated p53 in the cell lines used, could be related to the DNA sequence homology between the different HPV types or their biological behavior.
de Villiers
E M
EM
Division for Tumour-virus Characterization, Research Programme Applied Tumour-virology, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 242, Heidelberg, 69120, Germany.
Ruhland
A
A
Sekarić
P
P
D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000235:genetics; D016207:Cytokines / Q000502:physiology; D019942:Genes, p16; D016158:Genes, p53; D006801:Humans; D027383:Papillomaviridae / Q000302:isolation & purification*; D012878:Skin Neoplasms / Q000209:etiology*; D014466:Ultraviolet Rays / Q000009:adverse effects*
C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D016207:Cytokines