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.
Saez
Enrique
E
The Salk Institute for Biological Studies and Howard Hughes Medical Institute, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.
Olson
Peter
P
Evans
Ronald M
RM
D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D008297:Male; D051379:Mice; D009374:Neoplasms, Experimental / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics* / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism*; D019076:Transgenes
D018160:Receptors, Cytoplasmic and Nuclear; D014157:Transcription Factors