Abstract
Obesity is a well-recognized risk factor for postmenopausal breast cancer. Although the underlying mechanisms are not clearly defined, aromatase is thought to play a pivotal role in connecting obesity-associated inflammation with postmenopausal breast cancer. It has been well established that both the proinflammatory prostaglandin E2 (PGE2) and the BRCA1 tumor-suppressor gene regulate aromatase expression. In this issue of the journal (beginning on p. 1183), Subbaramaiah and colleagues improve our understanding of the molecular mechanisms by which PPARγ inhibits aromatase expression. They found that pioglitazone, a PPARγ agonist, inhibited aromatase expression by inhibition of PGE2 signaling and upregulation of BRCA1. Their findings provide potential targets for preventing or treating obesity-related breast cancer. Cancer Prev Res; 5(10); 1169–72. ©2012 AACR.
Perspective on Subbaramaiah et al., p. 1183
- Received August 23, 2012.
- Revision received August 27, 2012.
- Accepted August 31, 2012.
- ©2012 American Association for Cancer Research.
Volume 5, Issue 10
