SKIN TUMOR-DEVELOPMENT AND KERATIN EXPRESSION IN DIFFERENT EXPERIMENTAL-MODELS - RELATION TO INDUCING AGENT AND TARGET TISSUE STRUCTURE

The applicability of the experimental skin carcinogenesis model for st udies of tumor development was examined by exposing the skin of variou s mouse strains to different chemical carcinogens and UV radiation reg imens, in order to analyze the development and progression of the neop lastic process and the role of differentiation markers such as keratin s. In tumor-sensitive hairy NMRI mouse skin, the chemical carcinogen, 7,12-dimethylbenz(a)-anthracene (DMBA) induced an abnormal epidermal c ell differentiation and structural irregularities associated with an a ltered keratin expression, as well as numerous papillomas and squamous cell carcinomas. A suboptimal dose of UVB irradiation increased the n umber of DMBA-induced benign squamous neoplasms. Low doses of benzo(a) pyrene resulted in mild epidermal alterations, but only in one tumor. High doses of UVB induced a large number of undifferentiated spindle c ell tumors with few keratinpositive cells in NMRI mice, similar though fewer tumors in hairy, heavily pigmented C57BL/6 mice, numerous papil lomas and squamous cell carcinomas in hairless hr/hr mice but only two papillomas in hairy, moderately pigmented DBA/2 mice while UVA exposu re produced only two papillomas in hairless SKH-1 mice. In conclusion, the extent and type of skin tumor development depended upon the induc tion regimen: physical, chemical, dose and duration, as well as on the skin structure: pigmentation and adnexal development, all of which ha ve to be taken into account when relating experimental results to huma n conditions.