Christopher K. Patil

TL;DR: A cell-nonautonomous mechanism by which p53 can restrain, and oncogenic RAS can promote, the development of age-related cancer by altering the tissue microenvironment is suggested.

TL;DR: In addition to orchestrating cell-cycle checkpoints and DNA repair, a new and important role of the DDR is to allow damaged cells to communicate their compromised state to the surrounding tissue.

TL;DR: It is shown that diverse senescence‐inducing stimuli activate the stress‐inducible kinase p38MAPK in normal human fibroblasts and assign p38 MAPK a novel role in SASP regulation—one that is necessary, sufficient, and independent of previously described pathways.

TL;DR: It is shown that “senescent” mouse fibroblasts, which arrested growth after repeated passage under standard culture conditions, do not express a human-like SASP, and differ from similarly cultured human cells in other respects, but when cultured in physiological oxygen and induced to senesce by radiation, mouse cells more closely resemble human cells, including expression of a robust SASP.

TL;DR: It is shown that ectopic expression of p16INK4a and another cyclin-dependent kinase inhibitor, p21CIP1/WAF1, induces senescence without a SASP, even though they induced other features of senescENCE, including a stable growth arrest, and that the SASP is a damage response that is separable from the growth arrest.