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Enhanced lung tumor development in tobacco smoke-exposed p53 transgenic and Kras2 heterozygous deficient mice. Inhal Toxicol 2007;19 Suppl 1:183-7 PMID: 17886066

Pubmed ID

17886066

Abstract

A/J mice bearing either a mutation in the p53 gene or a Kras2 heterozygous deficiency were investigated for their susceptibility to tobacco smoke-induced lung tumorigenesis. Transgenic mice and their wild-type littermates were exposed to mainstream tobacco smoke (MS) for 5 mo, followed by 4 mo of recovery in filtered air. In sham (filtered air) groups, p53 transgenic mice did not exhibit a higher tumor multiplicity but did exhibit larger tumors, with tumor load increased 3.6-fold, when compared with wild-type mice. With exposure to MS, tumor multiplicity was increased 60% but there was a strikingly increased tumor load (15.9-fold) in p53 transgenic mice. Increased tumor load (5.3-fold) but not tumor multiplicity was seen in MS-exposed Kras2 heterozygous deficient mice. Interestingly, MS exposure did not increase benzo[a]pyrene-induced lung tumorigenesis when MS exposure was initiated after BaP treatment. These results indicate that a p53 mutation or loss of a Kras2 allele increases susceptibility to MS-induced lung tumor development.

Author List

Yan Y, Tan Q, Wang Y, Wang D, Jin M, Gordon T, Lubet RA, You M

Author

Ming You MD, PhD Associate Provost, Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin




Scopus

2-s2.0-34548852256   2 Citations

MESH terms used to index this publication - Major topics in bold

Animals
Carcinogenicity Tests
Genes, p53
Lung Neoplasms
Mice
Mice, Transgenic
Mutation
Proto-Oncogene Proteins p21(ras)
Smoke
Tobacco
Tobacco Smoke Pollution
jenkins-FCD Prod-353 9ccd8489072cb19f5b9f808bb23ed672c582f41e