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Carcinogenesis Advance Access originally published online on June 13, 2006
Carcinogenesis 2006 27(8):1517-1525; doi:10.1093/carcin/bgl080
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Inverse genetic predisposition to colon versus lung carcinogenesis in mouse lines selected based on acute inflammatory responsiveness

Roberto Francisco Di Pace, Solange Massa, Orlando Garcia Ribeiro, Wafa Hanna Koury Cabrera, Marcelo De Franco, Nancy Starobinas, Michel Seman and Olga Célia Martinez Ibañez*

Laboratório de Imunogenética, Instituto Butantan São Paulo, SP, Brazil
1 INSERM U519 - Faculté de Médecine et de Pharmacie Rouen, France

*To whom correspondence should be addressed at: Laboratório de Imunogenética, Instituto Butantan, Avenida Vital Brazil 1500, São Paulo, CEP 05503-900, Brasil. Tel: +55 11 3726 7222; Fax: +55 11 3726 1505; Email: olgaibanez{at}butantan.gov.br

Mouse lines produced by bidirectional selection on the basis of maximum (AIRmax) or minimum (AIRmin) acute inflammatory reactions were examined for the development of chemically induced acute colitis and colon tumors and the development of lung tumors. AIRmax mice were more susceptible than AIRmin to acute colitis induced by ingestion of dextran sodium sulfate showing a 3-fold higher disease activity index and presenting an intense inflammatory infiltrate in the base of colon crypts as well as elevated expression of IL-1ß, TNF{alpha}, IFN{gamma} and IL-6 mRNA in colon tissue. AIRmax were also more susceptible than AIRmin to colon cancer induced by 2 or 7 weekly doses of 1,2-dimethylhydrazine (DMH), showing significantly higher numbers of colonic aberrant crypt foci (ACF) at 150 days after DMH treatment (P = 0.01) and significantly higher numbers of tumors affecting larger intestinal areas at 300–475 days. At the latter time point, however, multiple lung adenomas and large adenocarcinomas were found in AIRmin but not in AIRmax mice. Treatment of mice with nimesulide for 60 days beginning 24 h before the first of two DMH doses almost completely inhibited the appearance of ACF in both lines. Furthermore, ACF numbers and the degree of acute inflammation directly co-segregated in an F2 (AIRmax x AIRmin) intercross population. The results demonstrate that genetic determinants of the inflammatory response differentially influence susceptibility to colon and lung carcinogenesis in the AIRmax and AIRmin mouse model.


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