Latest News

MSCA 2017 Presidency conference ‘Mobility takes research further’

13 March 2017

Read more ...

aDDRess and CodeAge Final ITN Conference: Abstract book now online!

03 November 2016

Read more ...

Björn Schumacher presentation on BR alpha Campus

7 October 2016

Read more ...

Gallery

gallery prev2

(Click image to open the gallery)

Contact

Let us hear from you.
This email address is being protected from spambots. You need JavaScript enabled to view it. or complete our contact form.

Thanks to

sponsors1sponsors2sponsors3


Dr. Fabrizio d’Adda di Fagagna
IFOM Fondazione Istituto Firc di Oncologia Molecolare, Italy

Image

IFOM Fondazione Istituto Firc di Oncologia Molecolare

Via Adamello 16

20139 Milan, Italy
fabrizio.dadda@ifom.eu
Tel: +39 0257 430 3221
www.ifom-ieo-campus.it/research/dadda.php

Image

Fabrizio d’Adda di Fagagna obtained his PhD at the International School for Advanced Studies (ISAS-SISSA) in Trieste (Italy). He was then postdoc and Research Associate in the group of Steve Jackson at the Gurdon Institute of the University of Cambridge (UK). He is now a tenured Principal Investigator at IFOM Foundation (FIRC Institute of Molecular Oncology) in Milan (Italy) and a group leader at Istituto di Genetica Molecolare (IGM) of the National Research Council in Pavia (Italy). He is an EMBO member since 2012.

Research Interests:

Fabrizio d’Adda di Fagagna established the involvement of the DNA damage Response (DDR) machinery in mammalian telomere maintenance (Nature Genetics 1999) and demonstrated that replicative cellular senescence is the outcome of the direct recognition of critically-short telomeres by the DDR apparatus (Nature 2003). He also showed that oncogene activation is an intrinsically genotoxic event that, by altering DNA replication, causes DDR activation and cellular senescence (Nature 2006) and this is associated with profound chromatin changes that impact on DDR signaling itself (Nature Cell Biology 2011).
Recently he proposed a unifying model involving the generation of irreparable DNA damage at telomeres to explain the establishment of different types of cellular senescence (Nature Cell Biol 2012; EMBO J. 2012). Finally, he discovered a previously unanticipated role of non coding RNAs in the direct activation of the DDR at DNA damage sites (Nature 2012).