Marzia Fumagalli

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 reported that knocking down the chemokine receptor CXCR2 (IL8RB) alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA-damage response and suggests that senescent cells activate a self-amplifying secretory network in which CX CR2-binding chemokines reinforce growth arrest.

TL;DR: It is proposed that linear genomes are not uniformly reparable and that telomeric DNA tracts, if damaged, are irreparable and trigger persistent DDR and cellular senescence.

TL;DR: It is shown that ROS are indeed mitogenic signaling molecules that fuel oncogene-driven aberrant cell proliferation, however, by their very same ability to mediate cell hyperproliferation, ROS eventually cause DDR activation.

TL;DR: It is demonstrated that multiple and distinct human cancer precursor lesions, but not corresponding malignant cancers, are comprised of cells that display hallmarks of TDIS, and it is shown that telomeric repeats indeed are hypersensitive to DNA replication stress.