作者: Edward R. Sauter , Andres J. P. Klein-Szanto , Ercem Atillasoy , Kathleen T. Montone , Tamara Goodrow
DOI: 10.1002/(SICI)1098-2744(199811)23:3<168::AID-MC5>3.0.CO;2-E
关键词:
摘要: We previously demonstrated that precancers (actinic keratoses and dysplasias) squamous cell carcinomas (SCCs) develop in one quarter of human neonatal foreskins grafted onto recombinase-activating gene-1-knockout mice treated once with 7,12-dimethylbenz[a]anthracene (DMBA) followed by chronic intermediate-range ultraviolet (UV) B light irradiation. The goals this study were to determine if a longer UVB exposure further observation would increase the number invasive cancers evaluate whether model results changes p53 expression proliferation similar those seen sun-damaged normal skin, actinic keratoses, SCCs. treatment consisted single dose DMBA 500 J/m2 radiation administered three times weekly for at least 5 mo. Histologic (cysts, hyperplasias, precancers, and/or cancers) 24 25 xenografts but not controls. Ten grafts (40%) had two or more histological changes, SCCs developed. After seven months UV total time from killing 12-18 mo, 83% (15 18) specimens developed precancer SCC origin, 44% (eight melanocytic hyperplasia melanoma. change moderate dysplasias required (median, 11 mo), mo than did development mild (median exposure, 7 mo; median death time, 12 mo). There was direct correlation between both degree histologic alteration epithelial cells.