Parisotto et al. demonstrate that ablation of the tumor suppressor gene PTEN in prostatic luminal epithelial cells of adult mice stimulates their proliferation, induces replication stress and a DNA damage response, followed by growth arrest with characteristics of cell senescence.

We report that Pten (phosphatase and tensin homologue) ablation in prostatic epithelial cells of adult mice promotes cell proliferation to generate prostatic intraepithelial neoplasia. Moreover, our results demonstrate that proliferating Pten-deficient cells undergo replication stress and exhibit a DNA damage response, leading to cell senescence, as seen in oncogene-induced senescence. ARTICLE HISTORY