| Literature DB >> 27857969 |
Joe Nassour1, Corinne Abbadie2.
Abstract
In contrast to fibroblasts, epithelial cells spontaneously escape from senescence and develop clones of mutated, transformed, and tumorigenic cells. Recently, we revealed that accumulation of unrepaired DNA single-strand breaks is a trigger of the p16 (CDKN2)-dependent cell cycle arrest pathway in senescent epithelial cells and also the mutagenic motor of post-senescence neoplastic escape.Entities:
Keywords: Cancerogenesis; DNA single-strand breaks; XRCC1; keratincytes; oxidative stress; p16; p38MAPK; senescence
Year: 2016 PMID: 27857969 PMCID: PMC5068179 DOI: 10.1080/23723556.2016.1190885
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556