Deciphering the intricate regulatory mechanisms for the cellular choice between cell repair, apoptosis or senescence in response to damaging signals.

In response to various types of stress, cells can undergo significant phenotypic changes, ranging from an increased DNA repair to senescence and apoptosis. The mechanisms by which p53 manages the choice between three possible cell fates in response to damaging stress remain poorly understood. p53 is not a simple switch that determines cell fate single-handedly; but rather as a component, albeit an important one, of an intricate signal network and molecular interactions. Thus, in addition to p53, fine-tuned interactions between growth- and division-activator molecules such as TGFβ, cMyc and FOXO are important determinants of the cellular fate. The aim of the paper is to resolve the complex interactions between these molecules and to elicit clear and reasonable working mechanisms for these diverse cellular processes.