title: A novel role for DNA single-strand breaks in senescence and neoplastic escape of epithelial cells.
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.
authors.affiliation: The Salk Institute for Biological Studies, Molecular and Cell Biology Laboratory , La Jolla, CA, USA.
authors.forename: Joe
authors.initials: J
authors.lastname: Nassour
authors.affiliation: University of Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Targeted Therapies , F-59000 Lille, France.
authors.forename: Corinne
authors.initials: C
authors.lastname: Abbadie
keywords: Cancerogenesis; DNA single-strand breaks; XRCC1; keratincytes; oxidative stress; p16; p38MAPK; senescence