Allele-specific activation and expression of the k-ras gene in hybrid mouse lung tumors induced by chemical carcinogens

Bin Chen, Liang You, Yian Wang, Gary D. Stoner, Ming You

Research output: Contribution to journalArticlepeer-review

43 Scopus citations

Abstract

A mouse hybrid, (C3H × A/J)F1 or C3A, was developed by crossing male A/J mice (high lung tumor susceptibility) with female C3H mice (low lung tumor susceptibility). The lung tumor responses of the C3A mice to dimethylnitrosamine (DMN) or benzo[a]pyrene (B[a]P) were found to be intermediate between those of the two parental strains. Mutational activation of the K-ras gene was found at a high frequency in both the B[a]P-and DMN-induced C3A lung tumors. To explore the genetic basis of the K-ras gene involvement in mouse lung tumor susceptibility, the parental origin of the K-ras oncogene in the chemically induced C3A lung tumors was determined. K-ras oncogenes were found on the allele inherited from the susceptible A/J parent in 14/16 of DMN-induced tumors and 15/17 of B[a]P-induced tumors from C3A mice. Furthermore, the K-ras mRNA transcribed from the A/J allele was 5-20 times more than C3H K-ras transcripts in 10/10 DMN-induced and 10/10 B[a]P-induced C3A lung tumors. These data suggest that an activated A/J K-ras allele could be more tumorigenic than an activated C3H allele due to the differential expression of the two alleles in lung cells.

Original languageEnglish (US)
Pages (from-to)2031-2035
Number of pages5
JournalCarcinogenesis
Volume15
Issue number9
DOIs
StatePublished - Sep 1994

ASJC Scopus subject areas

  • Cancer Research

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