Reference SummaryYou M, Proc Natl Acad Sci U S A 1989 May;86(9):3070-4

Title	Activation of the Ki-ras protooncogene in spontaneously occurring and chemically induced lung tumors of the strain A mouse.
Authors	You M; Candrian U; Maronpot RR; Stoner GD; Anderson MW
Journal	Proc Natl Acad Sci U S A
Volume	86
Issue	9
Year	1989
Pages	3070-4
Abstract	The strain A mouse has a high incidence of spontaneous lung tumors and is susceptible to lung tumor induction by chemical carcinogens. By utilizing transfection assay, Southern blot analysis, and DNA amplification techniques, we have detected an activated Ki-ras gene in the DNAs of both spontaneously occurring and chemically induced lung tumors of strain A mice. The point mutations in the spontaneous lung tumors were in both codon 12 (60%) and codon 61 (30%). In contrast, 100% of the mutations in the Ki-ras gene detected in methylnitrosourea-induced lung tumors and 93% of the mutations in the Ki-ras genes detected in benzo[a]pyrene-induced lung tumors were in codon 12, whereas 90% of the mutations in the Ki-ras genes detected in ethyl carbamate-induced lung tumors were in codon 61. The selectivity of mutations in the Ki-ras oncogene observed in chemically induced tumors, as compared to spontaneous tumors, suggests that these chemicals directly induce point mutations in the Ki-ras protooncogene. These data indicate that the strain A mouse lung tumor model is a very sensitive system to detect the ability of chemicals to activate the Ki-ras protooncogene in lung tissue.
Links	J:22773 – MGI References 2654935 – National Library of Medicine/PubMed

Models
Strain	Model Name	Treatment Agent(s)	Organ Affected	Frequency	Model Details
A/HeN	Lung adenocarcinoma		Lung	observed
A/J	Lung adenocarcinoma	urethane (ethyl carbamate)	Lung	observed
A/HeN	Lung adenoma		Lung	observed
A/J	Lung adenoma	benzo[a]pyrene (BP) (BaP) (B[a]P)	Lung	observed
A/J	Lung adenoma	urethane (ethyl carbamate)	Lung	observed
A/J	Lung adenoma	N-methyl-N-nitrosourea (MNU)	Lung	observed