F
Fabrizio d'Adda di Fagagna
Researcher at University of Cambridge
Publications - 85
Citations - 17497
Fabrizio d'Adda di Fagagna is an academic researcher from University of Cambridge. The author has contributed to research in topics: DNA damage & DNA repair. The author has an hindex of 44, co-authored 85 publications receiving 14874 citations. Previous affiliations of Fabrizio d'Adda di Fagagna include International Centre for Genetic Engineering and Biotechnology.
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Cellular senescence: when bad things happen to good cells
TL;DR: Understanding the causes and consequences of cellular senescence has provided novel insights into how cells react to stress, especially genotoxic stress, and how this cellular response can affect complex organismal processes such as the development of cancer and ageing.
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A DNA damage checkpoint response in telomere-initiated senescence
Fabrizio d'Adda di Fagagna,Philip Michael Reaper,Lorena Clay-Farrace,Heike Fiegler,Philippa Carr,Thomas von Zglinicki,Gabriele Saretzki,Nigel P. Carter,Stephen P. Jackson +8 more
TL;DR: It is proposed that telomere-initiated senescence reflects a DNA damage checkpoint response that is activated with a direct contribution from dysfunctional telomeres.
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Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication
Raffaella Di Micco,Marzia Fumagalli,Angelo Cicalese,Sara Piccinin,Patrizia Gasparini,Chiara Luise,Catherine Schurra,Massimiliano Garrè,Paolo Nuciforo,Aaron Bensimon,Roberta Maestro,Pier Giuseppe Pelicci,Fabrizio d'Adda di Fagagna +12 more
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.
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Chemokine Signaling via the CXCR2 Receptor Reinforces Senescence
Juan C. Acosta,Ana O'Loghlen,Ana Banito,Maria V. Guijarro,Arnaud Augert,Selina Raguz,Marzia Fumagalli,Marco Da Costa,Celia Brown,Nikolay Popov,Yoshihiro Takatsu,Jonathan Melamed,Fabrizio d'Adda di Fagagna,David Bernard,Eva Hernando,Jesús Gil +15 more
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.
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Living on a break: cellular senescence as a DNA-damage response.
TL;DR: The diverse mechanisms that lead to DNA-damage generation and the activation of DNA- damage-response signalling pathways are discussed, together with the evidence for their contribution to the establishment and maintenance of cellular senescence in the context of organismal ageing and cancer development.