During my research career I have contributed to determining the role of Epstein Barr virus reactivation and de novo infection of B lymphocytes to tumor outgrowth in Severe Combined Immunodeficient (SCID) mice injected with human peripheral blood mononuclear cells (hu/SCID), a relevant B lymphomagenesis model (Leukemia 2003). I subsequently went on to study the role of chemokines and chemokine receptors in the pathogenesis of human B cell lymphomas which arise in immunodeficient mice (hu/SCID lymphomas), demonstrating the importance of the CXCL12/CXCR4 axis in lymphoma generation in this experimental model (Blood 2005). Stemming from these observations, I went on to dissect the role of hypoxia in the regulation of the CXCL12/CXCR4 axis in malignant B cells (Cancer Res 2007). Following my experience in Adolfo Ferrando’s Laboratory (New York) and my return to Padua University, I have contributed to elucidate the role of constitutive AKT activation (often due to PTEN alterations) in regulating glucocorticoid response in T-cell acute lymphoblastic leukemia (T-ALL) patients. More specifically, we found that AKT1 is able to interact and modify (phosphorylate) the glucocorticoid receptor, leading to an alteration of its functional properties (Cancer Cell 2013). Recently, we have investigated the role of constitutive calcineurin activation in the pathogenesis of T-ALL and executed a proteomics approach to identify core interacting proteins and signaling pathways associated with Calcineurin complex (Oncotarget 2016). With this comprehensive analysis of proteomic data, we have identified novel combination therapies including Calcineurin and GSK-3 inhibition for treatment of T-ALL (Leukemia 2015).
Immunology and Molecular Oncology Unit
– Department of Translational Oncology and Health Services, IOV-IRCCS
– Section of Oncology and Immunology-DiSCOG, University of Padova
- Curriculum Vitae
- [email protected]
- phone: ++39 049 821 5895
- fax: ++39 049 807 2854
- ORCID: 0000-0002-4241-563X