Fabrizio D'Adda Di Fagagna
Fabrizio D'Adda Di Fagagna
e-mail:
affiliation: IFOM-FIRC Institute of Molecular Oncology
research area(s): Molecular Biology, Cell Biology
Course: Molecular Medicine: Molecular Oncology and Computational Biology
University/Istitution: Università di Milano, UNIMI-SEMM
1995 Doctor of Philosophy (PhD) awarded with full marks and Honours at the International School for Advanced Studies (ISAS-SISSA), Trieste, Italy, with a thesis entitled "Molecular and functional regulation of HIV-1 expression by the Long Terminal Repeat". Advisors: Prof. A. Falaschi and Prof. M. Giacca. External reviewer: Prof. N.J. Proudfoot, Oxford, UK. Experimental work carried out at the International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy.

1993 Magister of Philosophy (Master of Science degree) awarded with full marks and Honours at ISAS-SISSA with a thesis entitled "Interactions between the transcription factor USF/MLTF and the Long Terminal Repeat of Human Immunodeficiency Virus type 1".

1992 State registration exam passed with full marks.

1990 Graduated in Biological Sciences, with full marks and Honours (equivalent to BSc First Class Honours) at the University of Trieste, Italy, with an experimentally based thesis.
2009 – present Tenured Principal Investigator, FIRC Institute of Molecular Oncology (IFOM), Milan, Italy (http://www.ieo-ifom-campus.it).

2003 – 2009 Principal Investigator, FIRC Institute of Molecular Oncology (IFOM), Milan, Italy (http://www.ieo-ifom-campus.it).

1996 – 2003 Research Associate, laboratory of Prof. S.P. Jackson (http://www.gurdon.cam.ac.uk/~jacksonlab/) at Wellcome Trust/Cancer Research UK Gurdon Institute of Cancer and Developmental Biology, University of Cambridge, UK. Discovered a DNA damage response in senescence triggered by telomere shortening in human fibroblasts. Studied the control of chromosomal stability and telomere length regulation by the DNA repair and DNA damage checkpoint apparatus in mammals. Analysed the fate of DNA repair and checkpoint factors in apoptosis. Identified a novel family of prokaryotic orthologues of the human Ku DNA repair factor.

1991 – 1995 PhD student, laboratory of Prof. M. Giacca, Department of Molecular Medicine, ICGEB (http://www.icgeb.trieste.it/), Trieste, Italy. Studied the transcriptional control of Human Immunodeficiency Virus type 1 (HIV-1).
Interplay between oncogene-induced DNA Damage Response and heterochromatin in senescence and cancer. Raffaella Di Micco, Gabriele Sulli, Miryana Dobreva, Michalis Liontos, Oronza A. Botrugno, Roberto dal Zuffo, Giovanni d’Ario, Erica Montani, Ciro Mercurio, William C. Hahn, Vassilis Gorgoulis, Saverio Minucci and Fabrizio d'Adda di Fagagna. Nature Cell Biology, 13, 292–302 (2011)
Commentary by P Adams in NCB, T Halazonetis in Cell cycle.
Faculty of 1000: Highlighted as “Must read”. FFa = 8

SASPense and DDRama in cancer and ageing. Marzia Fumagalli and Fabrizio d’Adda di Fagagna. Nature Cell Biology, 2009 Aug;11(8):921-3.

Cellular senescence: hot or what? Gerard I. Evan and Fabrizio d’Adda di Fagagna. Current Opinion in Genetics and Development, 2009 Feb;19(1):25-31.

Living on a break: cellular senescence as a DNA damage response. d’Adda di Fagagna F. Nature Reviews Cancer, 2008 Jul;8(7):512-22.

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 and Jesús Gil. Cell, 2008 Jun 13; 133(6):1006-18.
Faculty of 1000: Highlighted as “Exceptional”. FFa = 9

Breaking news: high speed run away ends in arrest. How oncogenes induce senescence. Di Micco R., Fumagalli M. and d’Adda di Fagagna F. Trends in Cell Biology. 2007; 17 (11) 529-536.

Cellular senescence: When bad things happen to good cells. Campisi J. and d’Adda di Fagagna F. Nature Reviews Molecular Cell Biology. 2007; 8 (9): 729-740.

Complex engagement of DNA-damage response pathways in human cancer and in lung tumor progression. Nuciforo P., Luise C., Capra M., Pelosi G. and d'Adda di Fagagna F. Carcinogenesis. 2007; 28 (10): 2082-2088.

Oncogene-induced senescence is a DNA-damage checkpoint response triggered by DNA hyper-replication. Di Micco R., Fumagalli M., Cicalese A., Piccinin S. Gasparini P., Luise C., Schurra C., Garre’ M., Nuciforo P., Bensimon A., Maestro R., Pelicci P.G., and d'Adda di Fagagna F. Nature, 2006; 444: 638-642.
Faculty of 1000: Highlighted as “Must read”. FFa = 9

Telomere and telomerase modulation by the mammalian Rad9/Rad1/Hus1 DNA damage checkpoint complex. Francia S., Weiss R.S., Hande M.P., Freire R. and d'Adda di Fagagna F. Current Biology, 2006; 16: 1551-1558.

A DNA damage checkpoint response in telomere-initiated senescence. d'Adda di Fagagna F,Reaper P.M., Clay-Farrace L., Fiegler H., Carr P., von Zglinicki T., Saretzki G., Carter N.P. and Jackson S.P. Nature, 2003; 426: 194-198
Project Title:
DNA damage response regulation in mammals
There are a number of potential projects amenable to be developed by a talented student. They are best discussed in person.