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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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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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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DOI: https://doi.org/10.1038/nm928
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