Tumor growth fueled by spurious senescence phenotypes

Michalis Mastri; John M L Ebos

doi:10.1080/23723556.2019.1575707

Tumor growth fueled by spurious senescence phenotypes

Mol Cell Oncol. 2019 Feb 20;6(2):1575707. doi: 10.1080/23723556.2019.1575707. eCollection 2019.

Authors

Michalis Mastri¹, John M L Ebos^{1

2}

Affiliations

¹ Department of Cancer Genetics and Genomics, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA.
² Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA.

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; VEGFR TKI; rebound; resistance; senescence.

Grants and funding

This work was supported by grants to JMLE from the Roswell Park Alliance Foundation (RPAF); the American Cancer Society (ACS) via a Research Scholar Grant (RSG-18-064-01-TBG) and via an Institutional Research Grant (IRG-14-194-11SUB); and the Department of Defense (DoD) through the Peer Reviewed Cancer Research Program (Award No. W81XWH-14-1-0210). Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the RPAF, ACS, or DoD.