Source: https://medtriennalito.campusnet.unito.it/do/docenti.pl/Show?_id=sdeaglio
Timestamp: 2019-04-21 18:13:52+00:00

Document:
Deaglio, S., K.M. Dwyer, W. Gao, D. Friedman, A. Usheva, A. Erat, J.F. Chen, K. Enjyoji, J. Linden, M. Oukka, V.K. Kuchroo, T.B. Strom, and S.C. Robson. 2007. Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression. J Exp Med 204:1257-1265.
Malavasi, F., S. Deaglio, A. Funaro, E. Ferrero, A.L. Horenstein, E. Ortolan, T. Vaisitti, and S. Aydin. 2008. Evolution and function of the ADP ribosyl cyclase/CD38 gene family in physiology and pathology. Physiol Rev 88:841-886.
Serra, S., A.L. Horenstein, T. Vaisitti, D. Brusa, D. Rossi, L. Laurenti, G. D'Arena, M. Coscia, C. Tripodo, G. Inghirami, S.C. Robson, G. Gaidano, F. Malavasi, and S. Deaglio. 2011. CD73-generated extracellular adenosine in chronic lymphocytic leukemia creates local conditions counteracting drug-induced cell death. Blood 118:6141-6152.
Saborit-Villarroya, I., T. Vaisitti, D. Rossi, G. D'Arena, G. Gaidano, F. Malavasi, and S. Deaglio. 2011. E2A is a transcriptional regulator of CD38 expression in chronic lymphocytic leukemia. Leukemia 25:479-488.
Rossi, D., V. Trifonov, M. Fangazio, A. Bruscaggin, S. Rasi, V. Spina, S. Monti, T. Vaisitti, F. Arruga, R. Fama, C. Ciardullo, M. Greco, S. Cresta, D. Piranda, A. Holmes, G. Fabbri, M. Messina, A. Rinaldi, J. Wang, C. Agostinelli, P.P. Piccaluga, M. Lucioni, F. Tabbo, R. Serra, S. Franceschetti, C. Deambrogi, G. Daniele, V. Gattei, R. Marasca, F. Facchetti, L. Arcaini, G. Inghirami, F. Bertoni, S.A. Pileri, S. Deaglio, R. Foa, R. Dalla-Favera, L. Pasqualucci, R. Rabadan, and G. Gaidano. 2012. The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development. J Exp Med 209:1537-1551.
Arruga, F., B. Gizdic, S. Serra, T. Vaisitti, C. Ciardullo, M. Coscia, L. Laurenti, G. D'Arena, O. Jaksic, G. Inghirami, D. Rossi, G. Gaidano, and S. Deaglio. 2014. Functional impact of NOTCH1 mutations in chronic lymphocytic leukemia. Leukemia 28:1060-1070.
Audrito, V., S. Serra, D. Brusa, F. Mazzola, F. Arruga, T. Vaisitti, M. Coscia, R. Maffei, D. Rossi, T. Wang, G. Inghirami, M. Rizzi, G. Gaidano, J.G. Garcia, C. Wolberger, N. Raffaelli, and S. Deaglio. 2015. Extracellular nicotinamide phosphoribosyltransferase (NAMPT) promotes M2 macrophage polarization in chronic lymphocytic leukemia. Blood 125:111-123.
Vaisitti, T., V. Audrito, S. Serra, R. Buonincontri, G. Sociali, E. Mannino, A. Pagnani, A. Zucchetto, E. Tissino, C. Vitale, M. Coscia, C. Usai, C. Pepper, V. Gattei, S. Bruzzone, and S. Deaglio. 2015. The enzymatic activities of CD38 enhance CLL growth and trafficking: implications for therapeutic targeting. Leukemia 29:356-368.
Bologna, C., R. Buonincontri, S. Serra, T. Vaisitti, V. Audrito, D. Brusa, A. Pagnani, M. Coscia, G. D'Arena, E. Mereu, R. Piva, R.R. Furman, D. Rossi, G. Gaidano, C. Terhorst, and S. Deaglio. 2016. SLAMF1 regulation of chemotaxis and autophagy determines CLL patient response. The Journal of clinical investigation 126:181-194.
After obtaining an MD degree and training as a medical oncologist, I started a PhD program in Genetics at the University of Turin. My research interests were focused on enzymes that can synthesize and metabolize nucleotides, such as ATP and NAD, in the extracellular environment. During the PhD, I trained at the Beth Israel Deaconess Medical Center of Harvard University with Drs. Simon Robson and Terry Strom, where we identified an ATP-degrading pathway as an integral component of the suppressive machinery of regulatory T cells. After going back to Italy at the end of 2005, I obtained my first two grants as an independent investigator and studied nucleotide-nucleoside balance in the tumor microenvironment. In 2010 I started my own research group in the Laboratories of the Human Genetics Foundation in Turin, Italy. This group now comprises 12 researchers. In the past few years we have focused on NAD metabolism as a critical step in the regulation of leukemic cell homing and in the skewing of bystander cells towards a pro-survival phenotype. Furthermore, we participated in a joint effort to identify recurrently mutated genes in patients with chronic lymphocytic leukemia and splenic marginal zone lymphoma. Current studies are dedicated to the understanding of the role of these genes and their mutations in the biology of the disease. To do this, there is an urgent need of xenograft models that will allow expansion of genetically-typed primary cells. In order to implement these models in the lab, I spent two years as a visiting professor at Weill Cornell Medical College. Upon returning to Turin in September 2016, I obtained a clinical position in the Transplant Immunology Unit of the local University Hospital to work on immune-mediated transplant rejection.

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