Recent data suggest that additional factors, other than UV radiation, are i
nvolved in the etiology of non-melanoma skin cancer. These include alterati
ons in the tumor suppressor genes, p53, p16(INK4a)/CDKN2A, p21(WAF1)/(CIP1)
and the PTCH gene, as well as cytokines. Papillomavirus infections have be
en 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 abo
ut the cutaneous HPV types. We have studied the effect of UV radiation on t
he URRs of HPV 1, 2, 3, 5, 7, 20, 23, 27, 38, 41, and 77. Neither the CAT-e
xpression 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 th
e DNA sequence homology between the different HPV types or their biological
behavior.