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Amplification and Overexpression in UV-B-Induced Mouse Skin Papillomas and Carcinomas

Zaheed Husain, PhD; Qiuming Yang, MD; Debajit K. Biswas, DSc

Arch Dermatol. 1990;126(3):324-330.

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 x 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)

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

Footnotes
Accepted for publication August 29, 1989.

Reprint requests to Laboratory of Molecular Biology, Harvard School of Dental Medicine, 188 Longwood Ave, Boston, MA 02115 (Dr Biswas).

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