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italianoActivity Report IFOM 2008
In 2008 IFOM scientists published 110 research articles in international scientific journals, with an average impact factor of 8,664.
Highlights from the 2008 IFOM publications include:- A new prognostic biomarker for breast cancer
- The molecular switch that regulates metastatic invasion
- When stability runs through your veins
- Sox18: the source of "well-being" for the lymphatic system
- The cellular task force that safeguards genome stability
A new prognostic biomarker for breast cancer
Pier Paolo Di Fiore published his group's research on breast cancer in the January issue of the journal Nature.
Colaluca IN, Tosoni D, Nuciforo P, Senic-Matuglia F, Galimberti V, Viale G, Pece S, Di Fiore PP. NUMB controls p53 tumour suppressor activity. Nature. 2008, Jan 3;451(7174); 76-80. IF: 28,751.
The research group discovered a new prognostic biomarker for breast cancer, NUMB, through experiments performed on human breast cancer cells. The group also uncovered a novel "molecular circuitry" involving Numb that regulates p53, a key tumour suppressor gene that preserves genome integrity and protects against cancer-causing genetic mutations.
The molecular switch that regulates metastatic invasion
Pier Paolo Di Fiore and Giorgio Scita published their research related to metastasis in the July issue of the journal Cell.
Palamidessi A, Frittoli E, Garré M, Faretta M, Mione M, Testa I, Diaspro A, Lanzetti L, Scita G, Di Fiore PP. Endocytic trafficking of rac is required for the spatial restriction of signaling in cell migration. Cell. 2008, Jul 11;134(1); 135-47. IF: 29,887
The study identified a molecular switch (a protein complex involving RAB5 and RAC) that regulates metastatic invasion. The discovery opens new avenues in the development of anti-metastatic drugs for cancer treatment.
When stability runs through your veins
Elisabetta Dejana published her group's research on angiogenesis in the July issue of the journal Nature Cell Biology.
Taddei A, Giampietro C, Conti A, Orsenigo F, Breviario F, Pirazzoli V, Potente M, Daly C, Dimmeler S, Dejana E. Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5. Nat Cell Biol. 2008, Aug;10(8); 923-34. IF: 17,623.
The study unveils, through in vitro and in vivo experiments, an important mechanism for the stabilization of the vascular system that involves the protein VE-Cadherin. The group identified the pathway by which VE-Cadherin induces the production of Claudin-5, a protein that seals blood vessels from external infiltrations. These findings are relevant not only to cancer, but also other conditions such as heart attacks, stroke and inflammatory diseases.
Sox18: the source of "well-being" for the lymphatic system
Elisabetta Dejana published her group's research on the lymphatic system in the December issue of the journal Nature.
François M, Caprini A, Hosking B, Orsenigo F, Wilhelm D, Browne C, Paavonen K, Karnezis T, Shayan R, Downes M, Davidson T, Tutt D, Cheah KS, Stacker SA, Muscat GE, Achen MG, Dejana E, Koopman P. Sox18 induces development of the lymphatic vasculature in mice. Nature. 2008, Dec 4;456(7222); 643-7. IF: 28,751
The study uncovers a critical role of Sox18 in the formation, organization and maintenance of the lymphatic system. Indeed, inactivation of Sox18 causes defects in the lymphatic system as observed in the hypotrichosis-lymphoedema-telangiectasia syndrome, a rare disorder of the lymphatic system.
The cellular task force that safeguards genome stability
Dana Branzei published her group's research on DNA repair in the December issue of the journal Nature.
Branzei D, Vanoli F, Foiani M. SUMOylation regulates Rad18-mediated template switch. Nature. 2008, Dec 18;456(7224); 915-20. IF: 28,751
The study uncovers a complex network of regulatory processes (based on sumoylation and ubiquitination) that acts as an "emergency task force" to safeguard genome stability and protect against cancer-causing DNA damage. The discovery represents a significant step forward in cancer research and offers promising prospects for the identification of novel therapeutic targets for cancer treatment. In particular, the identification of DNA repair enzymes activated by these regulatory processes might lead to the development of anti-cancer drugs that specifically target tumour cells, without damaging the genomes of healthy cells.
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