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Peroxisome Proliferator-Activated Receptor Pathway Targeting in Carcinogenesis: Implications for Chemoprevention

Authors' Affiliation: Department of Otolaryngology and University of Minnesota Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota

Requests for reprints: Frank Ondrey, Department of Otolaryngology and University of Minnesota Masonic Cancer Center, University of Minnesota, 410 Delaware Street Southeast, MMC396, Minneapolis, MN 55455. Phone: 612-625-9449; Fax: 612-625-2101; E-mail: ondre002{at}umn.edu.

Abstract

The peroxisome proliferator-activated receptor (PPAR) is one member of the nuclear receptor superfamily that contains in excess of 80 described receptors. PPAR activators are a diverse group of agents that range from endogenous fatty acids or derivatives (linolenic, linoleic, and 15-deoxy-^12,14-prostaglandin J₂) to Food and Drug Administration-approved thiazolidinedione drugs [pioglitazone (Actos) and rosiglitazone (Avandia)] for the treatment of diabetes. Once activated, PPAR will preferentially bind with retinoid X receptor and signal antiproliferative, antiangiogenic, and prodifferentiation pathways in several tissue types, thus making it a highly useful target for down-regulation of carcinogenesis. Although PPAR- activators show many anticancer effects on cell lines, their advancement into human advanced cancer clinical trials has met with limited success. This article will review translational findings in PPAR activation and targeting in carcinogenesis prevention as they relate to the potential use of PPAR activators clinically as cancer chemoprevention strategies.

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