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Brief Communication
Nature Medicine  9, 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)-bold gamma 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.


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Nature Medicine
ISSN: 1078-8956
EISSN: 1546-170X
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