Tumor growth fueled by spurious senescence phenotypes

Abstract

Cancer treatments can induce a form of senescence that halts cellular division while allowing continued secretion of tumor-promoting proteins. We recently found that antiangiogenic treatment resistance can lead to a transient hijacking of the senescence-controlled secretory machinery that, when therapeutically targeted during treatment cessation, can blunt rebound tumor growth.

Keywords

• angiogenesis
• resistance
• senescence
• vegfr tki
• rebound