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Genetic deficiency in Pparg does not alter development of experimental prostate cancer

Nature Medicine volume 9, pages 1265–1266 (2003)Cite this article

Abstract

The role of the nuclear peroxisome proliferator–activated receptor (PPAR)-γ 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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Figure 1: Gene expression analysis and pathology of Pparg hemizygous tumors.

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Acknowledgements

This work was supported by CaP CURE and the Howard Hughes Medical Institute. The experiments were conducted in accordance with National Institutes of Health guidelines, with the approval of The Salk Institute's animal care committee. R.M.E. is an Investigator of the Howard Hughes Medical Institute for Biological Studies and March of Dimes Chair in Molecular and Developmental Biology.

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Author notes

  1. Enrique Saez

    Present address: Genomics Institute of the Novartis Research Foundation, 10675 John J. Hopkins Drive, San Diego, California, 92121, USA

Authors and Affiliations

  1. The Salk Institute for Biological Studies and Howard Hughes Medical Institute, 10010 North Torrey Pines Road, La Jolla, 92037, California, USA

    Enrique Saez, Peter Olson & Ronald M Evans

  2. Department of Biology, University of California, San Diego, La Jolla, 92037, California

    Peter Olson

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  1. Enrique Saez
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  2. Peter Olson
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  3. Ronald M Evans
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Correspondence to Ronald M Evans.

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The authors declare no competing financial interests.

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Saez, E., Olson, P. & Evans, R. Genetic deficiency in Pparg does not alter development of experimental prostate cancer. Nat Med 9, 1265–1266 (2003). https://doi.org/10.1038/nm928

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