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Toxicologic Pathology, Vol. 32, No. 1, 58-63 (2004)
DOI: 10.1080/01926230490261320

Promotion of Colon Tumors in C57BL/6J-APCmin/+ Mice by Thiazolidinedione PPAR{gamma} Agonists and a Structurally Unrelated PPAR{gamma} Agonist

Michael V. Pino

Aventis Inc, Drug Safety Evaluation, Bridgewater, New Jersey, USA, michael. pino{at}aventis.com

Michael F. Kelley

Aventis Inc, Drug Safety Evaluation, Bridgewater, New Jersey, USA

Zaid Jayyosi

Aventis Inc, Drug Safety Evaluation, Bridgewater, New Jersey, USA

Thiazolidinedione PPAR{gamma} agonists (troglitazone and rosiglitazone) were previously shown to promote colon tumor formation in C57BL/6JAPC min/+ mice, a model for human familial adenomatous polyposis. This study was conducted to determine if another thiazolidinedione PPAR{gamma} agonist, pioglitazone, and a PPAR{gamma} agonist structurally unrelated to the thiazolidinedione family, NID525, (a tetrazole-substituted phenoxymethylquinolone), would also promote colon tumors in this mouse model. Mice were treated in-feed with the thiazolidinediones troglitazone (150 mg/kg/day), rosiglitazone (20 mg/kg/day), or pioglitazone (150 mg/kg/day), or with NID525 (150 mg/kg/day) for 8 weeks. An increased incidence in colon tumors compared to controls was observed for all of the thiazolidinedione-treated groups as well as the NID525-treated group. These results indicate that the tumor-promoting effect of PPAR {gamma} agonists in the colon of C57BL/6J-APCmin/+ mice is likely related to the pharmacological activity of this group of drugs and not the thiazolidinedione structure.

Key Words: Thiazolidinedione • PPAR gamma agonist • colon tumors • APC min mouse • adenomatous polyposis coli gene.


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