Angelo Cicalese

TL;DR: It is shown that senescence, triggered by the expression of an activated oncogene (H-RasV12) in normal human cells, is a consequence of the activation of a robust DDR, and proposed that OIS results from the enforcement of a DDR triggered by oncogen-induced DNA hyper-replication.

TL;DR: It is demonstrated that p53 regulates polarity of cell division in mammary SCs and suggested that loss of p53 favors symmetric divisions of cancer SCs, contributing to tumor growth.

TL;DR: It is proposed that steady-state levels of intracellular oxidants and oxidative damage are genetically determined and regulated by a stress-induced signal transduction pathway involving p53 and p66Shc.

TL;DR: It is found that mammary cancer stem cells (CSCs) possess increased levels of p63 expression compared with normal progenitors, and a link between p63 and the Sonic Hedgehog signaling pathway in the regulation of breast cancer stemness is provided.

TL;DR: It is shown that irradiation of hematopoietic and mammary stem cells up-regulates the cell cycle inhibitor p21, a known target of p53, which prevents p53 activation and inhibits p53 basal activity, impeding apoptosis and leading to cell cycle entry and symmetric self-renewing divisions.