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Article
March 1990

cHa-ras Proto-oncogeneAmplification and Overexpression in UV-B-Induced Mouse Skin Papillomas and Carcinomas

Author Affiliations

From the Laboratory of Molecular Biology, Harvard School of Dental Medicine, Boston, Mass.

Arch Dermatol. 1990;126(3):324-330. doi:10.1001/archderm.1990.01670270056009
Abstract

• The role of cellular proto-oncogene activation in shortwave UV light in the B range (UV-B)-induced skin carcinogenesis was investigated. Epidermal papillomas and carcinomas were induced on the depilated skin surface of Sencar mice with single-dose UV-B irradiation (7 × 104 J/m2). The tumors thus initiated were present in 18.8% of treated animals and were primarily benign papillomas, while a few (6 of 17) progressed to form squamous cell carcinomas. A 5- to 10-fold stimulation of cHa-ras gene expression in both papillomas and carcinomas was observed. Other cellular proto-oncogenes such as cKi-ras, c-myc, or c-fos specific messenger RNAs were not detected in these UV-B-induced skin tumors. Subsequent Southern blot analysis revealed a threefold to fivefold amplification of cHa-ras gene in skin papillomas and carcinomas. However, only the carcinoma and not the papilloma DNA induced foci in the classic NIH-3T3 transformation assay, suggesting that activation of cHa-ras gene alone is not sufficient to exhibit this phenotypic expression of transformed cells. The NIH-3T3 transformants exhibited (1) anchorage independent growth on soft agar, (2) tumor induction in athymic mice, and (3) overexpression and amplification of the cHa-ras gene. We propose that overexpression of a ras gene by gene amplification plays a role in the UV-B-induced skin carcinogenesis process.

(Arch Dermatol. 1990;126:324-330)

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