Short-term gain, long-term pain: the senescence life cycle and cancer.
Accepted version
Peer-reviewed
Repository URI
Repository DOI
Change log
Authors
Chan, Adelyne Sue Li https://orcid.org/0000-0003-2214-0306
Narita, Masashi https://orcid.org/0000-0001-7764-577X
Abstract
Originally thought of as a stress response end point, the view of cellular senescence has since evolved into one encompassing a wide range of physiological and pathological functions, including both protumorignic and antitumorigenic features. It has also become evident that senescence is a highly dynamic and heterogenous process. Efforts to reconcile the beneficial and detrimental features of senescence suggest that physiological functions require the transient presence of senescent cells in the tissue microenvironment. Here, we propose the concept of a physiological "senescence life cycle," which has pathological consequences if not executed in its entirety.
Description
Keywords
cancer, epigenetics, inflammation, senescence, Cell Cycle, Cellular Microenvironment, Cellular Senescence, Epigenomics, Humans, Neoplasms, Precancerous Conditions, Telomere Shortening
Journal Title
Genes Dev
Conference Name
Journal ISSN
0890-9369
1549-5477
1549-5477
Volume Title
33
Publisher
Cold Spring Harbor Laboratory
Publisher DOI
Sponsorship
Cancer Research UK (CB4210)
Cancer Research UK (C14303/A17197)
Medical Research Council (MR/R010013/1)
Cancer Research UK (C20/A20976)
Cancer Research UK (24453)
Cancer Research UK (15890)
Cancer Research UK (C14303/A17197)
Medical Research Council (MR/R010013/1)
Cancer Research UK (C20/A20976)
Cancer Research UK (24453)
Cancer Research UK (15890)
The Narita laboratory is funded by a Cancer Research UK Cambridge Institute Core Grant (C14303/A17197). Masashi Narita is also supported by Cancer Research UK Early Detection Pump Priming award (C20/A20976), Medical Research Council (MR/R010013/1) and the Tokyo Tech World Research Hub Initiative (WRHI).