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Mol Cell Biol. 1988 February; 8(2): 786-793

H-ras activation in benign and self-regressing skin tumors (keratoacanthomas) in both humans and an animal model system.

Department of Pathology, New York University Medical Center, New York 10016.

ABSTRACT

The involvement of the ras oncogenes in tumorigenesis was investigated in keratoacanthomas, which are benign and self-regressing skin tumors, both in humans and in a corresponding animal model system. Keratoacanthomas were induced on rabbit ears by repeated applications of 7,12-dimethylbenz(a)anthracene. About 60% of the tumor DNAs produced transformed foci after transfection into NIH 3T3 cells, and in all of them the transforming gene was identified as H-ras by Southern and Northern (RNA) hybridization. Immunoprecipitation experiments suggested that the transforming rabbit H-ras protein carried a mutation in codon 61. In addition, an activated H-ras gene was detected in a human keratoacanthoma by using a nude mouse tumorigenesis assay after transfection of tumor DNA into NIH 3T3 cells. This is the first report of ras activation in a benign human tumor. The transforming human H-ras gene showed a point mutation in codon 61 that would result in leucine instead of the glutamine present in the normal gene product. The finding of ras activation in tumors that are not only benign but also self-regressing indicates that activated ras genes are not sufficient to maintain a neoplastic phenotype, although they likely play a role in early stages of tumorigenesis.

This article has been cited by other articles:

• Peng, X., Griffith, J. W., Han, R., Lang, C. M., Kreider, J. W. (1999). Development of Keratoacanthomas and Squamous Cell Carcinomas in Transgenic Rabbits with Targeted Expression of EJras Oncogene in Epidermis. Am. J. Pathol. 155: 315-324 [Abstract] [Full Text]  
• Kumar, R, Sukumar, S, Barbacid, M (1990). Activation of ras oncogenes preceding the onset of neoplasia. Science 248: 1101-1104 [Abstract]