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.