Carcinogenesis of cutaneous malignancies.
BACKGROUND
Over the past several years significant progress has been made in identifying the cellular and biochemical mechanisms underlying carcinogenesis.


OBJECTIVE
This review summarizes recent advances that have helped clarify the process of malignant transformation in cutaneous tumors.


RESULTS
Ultraviolet radiation-induced mutations in the p53 tumor suppressor gene and human papilloma virus inhibition of the p53 and retinoblastoma tumor suppressor gene products appear to play significant roles in the development of many cutaneous squamous cell carcinomas. Studies of patients with the nevoid basal cell carcinoma syndrome suggest the existence of an additional regulatory gene that may be involved in the development of basal cell carcinomas.


CONCLUSIONS
Carcinogenesis is multistep process involving genetic and epigenetic alterations to specific proto-oncogene and tumor suppressor gene products that progressively release the cell from normal controlled growth and replication.
Buzzell
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Division of Dermatology, Southern Illinois University School of Medicine, Springfield 62794-9230, USA.
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D004195:Disease Models, Animal; D016147:Genes, Tumor Suppressor / Q000235:genetics; D006801:Humans; D009154:Mutation; D009381:Neoplasms, Radiation-Induced / Q000209:etiology; D000090063:Proto-Oncogene Mas; D012878:Skin Neoplasms / Q000209:etiology* / Q000235:genetics; D014466:Ultraviolet Rays / Q000009:adverse effects