Journal
INTERNATIONAL JOURNAL OF CANCER
Volume 116, Issue 4, Pages 495-499Publisher
WILEY
DOI: 10.1002/ijc.21018
Keywords
small intestine; colon; tumors; PPAR-gamma; Apc; Mlh1; troglitazone; thiazolidinediones
Categories
Funding
- NCI NIH HHS [N01-CN-15116, U01-CA-84301] Funding Source: Medline
- NIEHS NIH HHS [U01-ES-11040] Funding Source: Medline
Ask authors/readers for more resources
The role of the nuclear peroxisome proliferator-activated receptor-gamma (PPAR-gamma) in colon tumorigenesis remains controversial. Notwithstanding evidence that PPAR-gamma ligands impede murine colorectal carcinogenesis, PPAR-gamma agonists have been shown to enhance in vivo tumor formation in mouse models of human colon cancer. Our study was designed to determine whether troglitazone (TGZ) induces colonic tumor formation in normal C57BL/6J mice and enhances colorectal carcinogenesis in double mutant Apc(1638N/+) Mlh1(+/-) mice fed a standard AIN-76A diet. We report herein that not only does TGZ enhance carcinogenesis in the large intestine of mutant mice predisposed to intestinal carcinogenesis but TGZ also induces colonic tumors in normal mice without gene targeting or carcinogen administration. This observation indicates that preexisting mutational events are not necessary for induction of colonic tumors by activated PPAR-gamma in vivo. (c) 2005 Wiley-Liss, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available