Anita De Rossi

Career/Employment

Education
1986-Post Graduate Degree in Microbiology and Virology, University of Padova
1976-Biological Sciences Degree, University of Padova;

Positions
2004-Present: Full Professor of Pathology, Medical School, University of Padova
2005-Present: Head of Viral Oncology Unit, Istituto Oncologico Veneto (IOV)-IRCCS, Padova
1992-2004: Associate Professor of Pathology, Medical School, University of Padova
1981-1992: Assistant Professor of Pathology, Medical School, University of Padova
1977-1981: Fellow, Oncology Section, Medical School, University of Padova

Foreign working experiences
National Cancer Institute, NIH, Bethesda, USA, Laboratory of Viral Carcinogenesis (Prof. P Fischinger Head) in 1980, and Laboratory of Tumor Cell Biology (Prof. R Gallo, Head) in 1984,1985,1988

Research interests and career highlights

Anita De Rossi has long been involved in oncogenic retroviruses research. Her early efforts were directed towards investigating virus-host interactions in the murine system, including the role of endogenous retroviruses on leukemia development. Since 1983, her research has shifted from murine to human retroviruses (HTLV/HIV) in both experimental models and clinical settings. In the experimental model, she demonstrated that CD4 T cells are not the only target of HIV infection (PNAS 1986). She has been involved in several European projects concerning pediatric HIV/AIDS; her studies in this field addressed the virological and immunological correlates of pediatric disease outcome and are some of the first to indicate that HIV infection from mother-to-child HIV mainly occurs during intrapartum period (AIDS 1992; J Clin Invest 1996) and that host factors may restrict HIV infection (AIDS 1995; J Inf Dis 2001). Her interest has expanded to studying tumors in immunocompromised patients, with particular regard to EBV-related lymphomagenesis in HIV-infected or transplant patients, and more recently to studying cellular replicative potential driven by telomere/telomerase in virus-driven and virus-independent malignancies. Her studies are some of the first demonstrating that LMP1 of EBV activates at transcriptional level the expression of TERT, the catalytic component of telomerase, which in turn contributes to preserving the expression of EBV latency proteins, a prerequisite for EBV-driven transformation (J Virol 2008). The consequence is that inhibition of TERT triggers the activation of the viral lytic cycle with death of the infected cells (Clin Cancer Res 2013).

Lastly, her studies demonstrated that quantification of TERT in plasma may represent a minimally invasive tool for monitoring malignancies (Clin Cancer Res 2008) and response to therapy (Br J Cancer 2018). In addition, her studies provide the rationale for considering inhibition of TERT a useful approach for setting up new therapeutic strategies for virus-dependent and virus-independent malignancies (Clin Cancer Res 2013; Cell Death Dis 2016).

Key publications

1. Rampazzo E, Del Bianco P, Bertorelle R, Boso C, Perin A, Spiro G, Bergamo F, Belluco C, Buonadonna A, Palazzari E, Lonardi S, De Paoli S, Pucciarelli S, De Rossi A. The predictive and prognostic potential of plasma Telomerase Reverse Transcriptase (TERT) RNA in Rectal Cancer. Brit J Cancer 2018;118:878-886.

2. Celeghin A, Giunco S, Freguja R, Zangrossi M, Nalio S, Dolcetti R, De Rossi A. Short-term inhibition of TERT induces telomere length-independent cell cycle arrest and apoptotic response in EBV-immortalized and transformed B cells. Cell Death Dis 2016; 12:e2562. doi: 10.1038/cddis.2016.425.

3. Giunco S, Dolcetti R, Keppel S, Celeghin A, Indraccolo S, Dal Col J, Mastorci K, De Rossi A. hTERT inhibition triggers Epstein-Barr virus lytic cycle and apoptosis in immortalized and transformed B cells: a basis for new therapies. Clin Cancer Res 2013; 19: 2036-2047.

4. Terrin L, Rampazzo E, Pucciarelli S, Agostini M, Bertorelle R, Esposito G, Del Bianco P, Nitti D, De Rossi A. Relationship betwen tumor and plasma levels of hTERT mRNA in patients with colorectal cancer: implications for monitoring of neoplastic disease. Clin Cancer Res 2008; 14, 7444-7451.

5. Terrin L, Dal Col J, Rampazzo E, Zancai P, Pedrotti M, Ammirabile G, Bergamin S, Rizzo S, Dolcetti R, De Rossi A. The latent Membrane Protein-1 of Epstein Barr virus activates hTERT promoter and enhances telomerase activity in B lymphocytes. J Virol 2008; 82, 10175-10187.

6. Ometto L, Bertorelle R, Mainardi M, Zanchetta M, Tognazzo S, Rampon O, Ruga E, Chieco-Bianchi L, De Rossi A. Polymorphisms in the CCR5 promoter region influence disease progression in perinatally human immunodeficiency virus type 1-infected children. J Infect Dis 2001; 183: 814-818.

7. De Rossi A, Masiero S, Giaquinto C, Ruga E, Comar M, Giacca M, Chieco-Bianchi L. Dynamics of viral replication in infants with vertically acquired human immunodeficiency virus type 1 infection. J Clin Invest 1996; 97: 323-330.

8. Ometto L, Zanotto C, Maccabruni A, Caselli D, Truscia D, Giaquinto C, Ruga E, Chieco-Bianchi L, De Rossi A. Viral phenotype and host cell susceptibility to HIV-1 infection as risk factors for mother-to-child HIV-1 transmission. AIDS 1995; 9: 427-434.

9. De Rossi A, Ometto L, Mammano F, Zanotto C, Giaquinto C, Chieco-Bianchi L. Vertical transmission of HIV-1: lack of detectable virus in peripheral blood cells of infected children at birth. AIDS 1992; 6: 1117-1120.

10. De Rossi A, Franchini G, Aldovini A, Del Mistro A, Chieco-Bianchi L, Gallo RC, Wong-Staal F. Differential response to the cytopathic effects of human T-cell lymphotropic virus type III (HTLV-III) superinfection in T4+ (helper) and T8+ (suppressor) T-cell clones transformed by HTLV-I.Proc Natl Acad Sci USA 1986; 83: 4297-4301.