Everything Old is Neu Again: Cellular Senescence in HER2-Positive Breast Cancer

An irreversible cell proliferation arrest, senescence can be trig-gered by a variety of stressors, including oncogenes. In onco-gene-induced senescence (OIS), senescent cells are capable of releasing a wealth of factors, collectively termed senescence-associated secretory phenotype (1,2). In addition to including components necessary to establish and maintain the senes-cence program, the secretome not infrequently includes pro-tumorigenic factors, which have been proposed to contribute to tumor progression in a cell nonautonomous manner (1–3). In this issue of the Journal, Zacarias-Fluc and colleagues at the Vall d’Hebron Institute of Oncology in Barcelona look at a previously unstudied aspect of the biology of human epidermal growth factor receptor 2 (HER2)–positive breast cancer, namely the role played by cellular senescence in the disease (4). Their study is interesting for the new light shed on the disease an