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Publication : Genetic selection for high acute inflammatory response confers resistance to lung carcinogenesis in the mouse.

First Author  Ribeiro OG Year  2005
Journal  Exp Lung Res Volume  31
Issue  1 Pages  105-16
PubMed ID  15765921 Mgi Jnum  J:97847
Mgi Id  MGI:3576524 Doi  10.1080/01902140490495237
Citation  Ribeiro OG, et al. (2005) Genetic selection for high acute inflammatory response confers resistance to lung carcinogenesis in the mouse. Exp Lung Res 31(1):105-16
abstractText  Mice selected for a high acute inflammatory response (AIRmax) are resistant to chemically induced lung tumorigenesis, whereas the low responders (AIRmin) are susceptible. In urethane-treated mice, anti-inflammatory drugs increased the tumor incidence in AIRmax but not AIRmin mice, and an inverse correlation (P<.001) between the degree of acute inflammatory response (AIR) and lung tumorigenesis was found in an F2 (AIRmax x AIRmin) intercross population. The results provide evidence for the involvement of lung tumor modifier loci in AIR regulation and implicate AIR quantitative trait loci in the inherited predisposition to lung cancer.
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