Raffaella Di Micco

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: The mechanisms and modulators of cellularsenescence establishment and induction of a senescence-associated secretory phenotype are discussed, and the potential of senolytic and senomorphic therapies in ageing and associated diseases is provided.

TL;DR: A microRNA analysis of human melanoma found that miR-30b/30d upregulation correlates with stage, metastatic potential, shorter time to recurrence, and reduced overall survival, and these data support a key role of miR/30D and GalNAc transferases in metastasis, by simultaneously promoting cellular invasion and immunosuppression.

TL;DR: It is shown that in human fibroblasts resistant to premature p16INK4a induction, SAHF are preferentially formed following oncogene activation but are not detected during replicative cellular senescence or on exposure to a variety ofsenescence-inducing stimuli.

TL;DR: The interplay between chromatin and DDR factors in the context of cellular senescence that is induced by oncogenes and in cancer is discussed.