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