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

The role of the nuclear peroxisome proliferator-activated receptor (PPAR)-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.