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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
Abstract
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.
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