Docenti

Erich Piovan

Assistant Professor

Telefono: +39 049 8215895

Phone lab: +39 049 8211198

E-mail: erich.piovan@unipd.it

Education
1992-1999: Medical Degree, University of Padova, 110/110 cum laude
1999-2003: Post graduate specialization in Oncology (Specializzazione in Oncologia), University of Padova, 70/70 cum laude
2003-2007: PhD in Oncology (Dottorato di Ricerca in Oncologia), University of Padova

Positions
September 2005-October 2008: Post-doctoral fellow at the Institute for Cancer Genetics (ICG), under the supervision of Prof. Riccardo Dalla-Favera (Columbia University, New York, USA)
November 2008-August 2011: Post-doctoral research scientist in Dr. Adolfo Ferrando’s laboratory (Columbia University, ICG)
December 2011-March 2012: Visiting Scientist in Dr. Adolfo Ferrando’s Laboratory (Columbia University)
October 2011-to date: Ricercatore Universitario (Associate Research Scientist), Lab Head

T-lineage acute lymphoblastic leukemia (T-ALL) accounts for 10% to 15% of pediatric and 25% of adult ALL cases.  Our research interest focuses particularly on those alterations which result still poorly understood.

1.The role of WT1 deletions and mutations in T-ALL is still not clear. Using the shRNA and the Cripsr-Cas9 technologies we are mimicking the role of WT1 deletions and mutations in T-ALL cells. In particular, mimicking WT1 mutations in T-ALL cells will allow the identification of a de-regulated WT1 signature  and its role in the pathogenesis of T-ALL.

2. NOTCH1 pathway results mutated in over 60% of cases of T-ALL cases, making NOTCH1 oncogene an appealing molecular target in T-ALL. In the last years, different attempts to target NOTCH signaling in T-ALL have been developed. In this scenario, the understanding of the molecular mechanisms downstream of NOTCH1 signaling is fundamental to design novel therapeutic strategies. The role microRNAs downstream NOTCH1 signaling have been recently explored, however their role is not completely clear. Our laboratory is currently studying few novel microRNAs downstream NOTCH1 and their roles in T-ALL pathogenesis.

3. The evolutionary conserved Hedgehog (Hh) signaling pathway plays a crucial role in patterning and organogenesis during early development, in adult tissue maintenance and repairing functions. Aberrant Hh signaling has been described in numerous tumors. Through gene knock-out studies complimented with gene expression profiling studies and quantitative proteomics we aim at elucidating the mechanistic role of Hh signaling in T-ALL.
I have contributed to elucidate the role of constitutive AKT activation in regulating glucocorticoid response in T-ALL patients. More specifically, we found that AKT1 is able to interact and phosphorylate the glucocorticoid receptor, leading to an alteration of its functional properties. Our findings, together with the availability of PI3K-AKT specific inhibitors in clinical trials for the treatment of human cancer support a role of PI3K-AKT pathway as therapeutic target for the reversal of glucocorticoid resistance in T-ALL. Also, thanks to the computational analysis developed in our study, numerous drivers of resistance in cancer can be potentially uncovered, and could ultimately lead to more effective and patient tailored therapies. 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.

1. Piovan E*., Tosello V., Amadori A. and Zanovello P*. Chemotactic Cues for NOTCH1-Dependent Leukemia. Front. Immunol., 03 April 2018 | https://doi.org/10.3389/fimmu.2018.00633. Review. * Co-last authors

2. Bordin F*, Piovan E*, Masiero E, Ambesi-Impiombato A, Minuzzo S, Bertorelle R, Sacchetto V, Pilotto G, Basso G, Zanovello P, Amadori A, Tosello V. (2017). WT1 loss attenuates the TP53-induced DNA damage response in T-cell acute lymphoblastic leukemia. PMID: 29170254 DOI: 10.3324/haematol.2017.170431. * Co-first authors

3. Bongiovanni D, Saccomani V, Piovan E. (2017). Aberrant Signaling Pathways in T-Cell Acute Lymphoblastic Leukemia. Int J Mol Sci. 2017 Sep 5;18(9). pii: E1904. doi: 10.3390/ijms18091904. Review.

4. Tosello V., Saccomani V., Yu J., Bordin F., Amadori A., Piovan E (2016). Calcineurin complex isolated from T-cell acute lymphoblastic leukemia (T-ALL) cells identifies new signaling pathways including mTOR/AKT/S6K whose inhibition synergize with Calcineurin inhibition to promote T-ALL cell death. ONCOTARGET, ISSN: 1949-2553, doi: 10.18632/oncotarget.9933 

5. Tosello V, Bordin F, Yu J, Agnusdei V, Indraccolo S, Basso G, Amadori A, Piovan E (2015). Calcineurin and GSK-3 inhibition sensitizes T-cell acute lymphoblastic leukemia cells to apoptosis through X-linked inhibitor of apoptosis protein degradation. LEUKEMIA, ISSN: 0887-6924, doi: 10.1038/leu.2015.335

6. Piovan E*, Yu J*, Tosello V, Herranz D, Ambesi-Impiombato A, Da Silva AC, Sanchez-Martin M, Perez-Garcia A, Rigo I, Castillo M, Indraccolo S, Cross JR, de Stanchina E, Paietta E, Racevskis J, Rowe JM, Tallman MS, Basso G, Meijerink JP, Cordon-Cardo C, Califano A, Ferrando AA. Direct reversal of glucocorticoid resistance by AKT inhibition in acute lymphoblastic leukemia. Cancer Cell. 2013 Dec 9;24(6):766-76. doi: 10.1016/j.ccr.2013.10.022. Epub 2013 Nov 27.

7. Piovan E, Tosello V, Indraccolo S, Masiero M, Persano L, Esposito G, Zamarchi R, Ponzoni M, Chieco-Bianchi L, Dalla-Favera R, Amadori A., Differential regulation of hypoxia-induced CXCR4 triggering during B-cell development and lymphomagenesis. Cancer Res. 2007 Sep 15;67(18):8605-14.

8. Piovan, E., Tosello, V., Indraccolo, S., Cabrelle, A., Baesso, I., Trentin, L., Zamarchi, R., Tamamura, H., Fujii, N., Semenzato, G., Chieco-Bianchi, L. and Amadori, A., Chemokine receptor expression in EBV-associated lymphoproliferation in hu/SCID mice: implications for CXCL12/CXCR4 axis in lymphoma generation. Blood 2005 Feb 1;105(3):931-939.

9. Stievano, L.*, Piovan, E*. and Amadori, A., C and CX3C Chemokines: Cell sources and physiopathological implications. Crit Rev immunol 2004;24(3):205-28. * Co-authors

10. Piovan, E., Bonaldi, L., Indraccolo, S., Tosello, V., Menin, C., Comacchio, F., Chieco-Bianchi, L. and Amadori, A., Tumor outgrowth in peripheral blood mononuclear cell-injected SCID mice is not associated with early Epstein-Barr virus reactivation. Leukemia 2003. 17: 1643-1649.

Collaborator in the following Grants: AIRC MFAG #13053 with title-“Mechanisms of leukemogenesis induced by loss of function of WT1”  (2012-2015) and AIRC IG#14256 with title “Role of microRNAs and their targets downstream of NOTCH1 activation in T-ALL: implications for therapeutic strategies” (2015-2017).