Targeting the PI3K/Akt/mTOR pathway in castration-resistant prostate cancer
- Divisions of Medical Oncology and Urology , Duke Cancer Institute, Duke University, DUMC Box 102002, Durham, North Carolina 27710, USA
- (Correspondence should be addressed to A J Armstrong; Email: andrew.armstrong{at}duke.edu)
Abstract
The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is a key signaling pathway that has been linked to both tumorigenesis and resistance to therapy in prostate cancer and other solid tumors. Given the significance of the PI3K/Akt/mTOR pathway in integrating cell survival signals and the high prevalence of activating PI3K/Akt/mTOR pathway alterations in prostate cancer, inhibitors of this pathway have great potential for clinical benefit. Here, we review the role of the PI3K/Akt/mTOR pathway in prostate cancer and discuss the potential use of pathway inhibitors as single agents or in combination in the evolving treatment landscape of castration-resistant prostate cancer.
- castration-resistant prostate cancer (CRPC)
- PI3K inhibitors
- mTOR
- PI3K pathway
- Akt
- androgen receptor signaling
- combination therapy
- Revision received 22 February 2013
- Accepted 1 March 2013
- Made available online as an Accepted Preprint 1 March 2013
- © 2013 Society for Endocrinology