•  
  •  
 

Abstract

Dysregulation of mammalian target of rapamycin (mTOR) signaling has been found in many human tumors, including endometrial cancer, and mTOR inhibitors have been utilized in clinical trials as targeted therapies with only limited success. Herein we identify a viable treatment alternative that overcomes temsirolimus-induced AKT phosphorylation in endometrial cancer. Our data suggest temsirolimus and BEZ235 inhibit different components of the AKT/mTOR signaling pathway to accomplish synergistic pathway inhibition, which is necessary for therapeutic efficacy to abrogate the increased signaling through AKT that occurs with mTOR inhibition alone

Keywords

PI3K, Akt, mammalian target of rapamycin, temsirolimus, BEZ235, endometrial cancer

Submission Type

Article

Rights

Copyright © Shujie Yang, Xue Xiao, Xiangbinb Meng, and Kimberly K. Leslie, 2011.

Creative Commons License


This work is licensed under a Creative Commons Attribution 3.0 License.