p53 mutations are common in human papillomavirus type 38-positive non-melanoma skin cancers.
In cervical cells, the E6 protein of the oncogenic human papillomavirus (HPV) types inactivates p53, promoting its degradation. Consequently, mutations of the p53 gene are rarely seen in these cancers. Our recent data indicate that the cutaneous HPV38 is involved in skin carcinogenesis. In this study, we have determined the presence of HPV38 and the status of p53 gene in 32 non-melanoma skin cancers. We found that p53 gene is frequently mutated in HPV38-positive skin cancers and that HPV38 E6 does not promote p53 degradation. Thus, different mechanisms appear to be involved in the development of HPV-positive cervical and skin cancers.
Caldeira
Sandra
S
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal.
Filotico
Raffaele
R
Accardi
Rosita
R
Zehbe
Ingeborg
I
Franceschi
Silvia
S
Tommasino
Massimo
M
D000818:Animals; D002478:Cells, Cultured; D018920:Coculture Techniques; D003062:Codon; D004247:DNA / Q000378:metabolism; D005091:Exons; D005347:Fibroblasts / Q000378:metabolism; D016158:Genes, p53; D015151:Immunoblotting; D015603:Keratinocytes / Q000378:metabolism; D009154:Mutation; D027383:Papillomaviridae / Q000235:genetics*; D016133:Polymerase Chain Reaction; D051381:Rats; D012190:Retroviridae / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012878:Skin Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000821:virology*
D003062:Codon; D004247:DNA