A senescence secretory switch mediated by PI3K/AKT/mTOR activation controls chemoprotective endothelial secretory responses

A senescence secretory switch mediated by PI3K/AKT/mTOR activation controls chemoprotective endothelial secretory responses

Cancer therapy targets malignant cells that are surrounded by a diverse complement of nonmalignant stromal cells. Therapy-induced damage of normal cells can alter the tumor microenvironment, causing cellular senescence and activating cancer-promoting inflammation. However, how these damage responses...

Full description

Bibliographic Details
Main Authors: Bent, Eric H, Gilbert, Luke Andrew, Hemann, Michael
Other Authors: Harvard University--MIT Division of Health Sciences and Technology
Format: Article
Language:en_US
Published: Cold Spring Harbor Laboratory Press 2017
Online Access:http://hdl.handle.net/1721.1/107125
https://orcid.org/0000-0002-6604-2129

Internet

http://hdl.handle.net/1721.1/107125
https://orcid.org/0000-0002-6604-2129

Similar Items