Isabel Garcia-Cao

TL;DR: The generation and characterization of mice carrying supernumerary copies of the p53 gene in the form of large genomic transgenes are reported, proving that cancer resistance can be enhanced by a simple genetic modification and in the absence of undesirable effects.

TL;DR: It is shown that genetically manipulated mice with increased, but otherwise normally regulated, levels of Arf and p53 present strong cancer resistance and have decreased levels of ageing-associated damage, revealing a previously unknown anti-ageing mechanism and providing a rationale for the co-evolution ofcancer resistance and longevity.

TL;DR: It is suggested that p27Kip1 is an important mediator of the permanent cell cycle arrest induced by PI3K inhibitors, and the first description that p130 may have a role in inhibiting CDK activity during senescence is described.

TL;DR: It is shown that p53-dependent protection against cancer is lost in mice that have been genetically manipulated so that their p53 is activated in response to DNA damage but not to oncogenic signalling.

TL;DR: It is concluded that p53 has an active role in eliminating telomere‐damaged cells, and the possibility of an age‐promoting effect of p53 on telomerase‐driven ageing is excluded.