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. 1989 May;81:33–37. doi: 10.1289/ehp.898133

Radiation and chemical activation of ras oncogenes in different mouse strains.

E W Newcomb 1, L E Diamond 1, S R Sloan 1, M Corominas 1, I Guerrerro 1, A Pellicer 1
PMCID: PMC1567548  PMID: 2667982

Abstract

A survey of a large series of radiation- or chemically induced thymic lymphomas in (AKR X RF)F1, RF/J, 129/J, and C57BL/6J mouse strains for activated ras oncogenes showed that of the tumors containing transforming activity, in more than 75% of the cases this activity segregated with either K-ras or the N-ras gene. H-ras activity was never detected. The genetic background of the host influenced susceptibility to tumor induction and oncogene activation. The K-ras gene was preferentially activated over the N-ras gene (approximately 2:1) whether the inducing agent was radiation or the chemical N-nitrosomethylurea. The activating mutation for the K-ras gene was consistently identified as a GGT to GAT transition in codon 12. In contrast, several different mutations of the N-ras gene were identified and localized to codons 12, 13, or 61. Assessment of the allelic composition of the ras locus shows that some proportion of the tumors lost the normal ras allele.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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