Nature Medicine9, 1265 - 1266 (2003)
Published online: 7 September 2003; | doi:10.1038/nm928
Genetic deficiency in Pparg does not alter development of experimental prostate cancer
Enrique Saez1, 3, Peter Olson1, 2
& Ronald M Evans1
1
The Salk Institute for Biological Studies and Howard Hughes Medical Institute, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.
2
Department of Biology, University of California, San Diego, La Jolla, California 92037.
3
Present address: Genomics Institute of the Novartis Research Foundation, 10675 John J. Hopkins Drive, San Diego, California 92121, USA.
Correspondence should be addressed to Ronald M Evans evans@salk.edu
The role of the nuclear peroxisome proliferator−activated receptor (PPAR)- in cancer has been a subject of debate. The identification of loss-of-function mutations in PPARG in colon and prostate tumors has led to the idea that this gene may function as a tumor suppressor. We have directly tested this notion using a mouse model of prostate cancer. Neither hemizygous deletion of Pparg nor complete ablation of Ppara influenced the development of prostate cancer in our experimental context.
in cancer has been a subject of debate. The identification of loss-of-function mutations in PPARG in colon and prostate tumors has led to the idea that this gene may function as a tumor suppressor. We have directly tested this notion using a mouse model of prostate cancer. Neither hemizygous deletion of Pparg nor complete ablation of Ppara influenced the development of prostate cancer in our experimental context.
