PhD-Program Inflammation and Immunity
Medizinische Universität Wien

Maria Sibilia, PhD

Institute for Cancer Research (Head)
Department of Medicine I
Medical University of Vienna
Borschkegasse 8a
A-1090 Vienna, Austria
Tel: +43-1-4277-65211
Fax: +43-1-4277-65193

Vienna Competence Center (VCC)
Tel: +43-1-40160-63011
 Fax: +43-1-40160-963005

Email:      Maria.Sibilia@meduniwien.ac.at
Website: http://www.meduniwien.ac.at/krebsforschung
               http://www.meduniwien.ac.at/typo3/?id=5688&L=1


Research interests
 

The major focus of our laboratory is to understand the molecular pathways leading to diseases such as cancer using the mouse as a model system. Specifically, we are focusing on tumor/tissue cell intrinsic mechanisms by analysing how signalling via the Epidermal Growth Factor Receptor (EGFR), a receptor tyrosine kinase frequently amplified and overexpressed in human tumors, affects the development of epithelial and glial cells and tumors. Moreover, we are also studying tumor/tissue cell extrinsic mechanisms focusing on the role of innate and adaptive immune cells in normal and diseased skin as well as in anti-tumor immune responses and inflammation. The ultimate goal is to translate this knowledge to patients to develop rational and effective therapies for disease treatment.

 

 

Selected publications

 
Lichtenberger BM, Tan PK, Niederleithner H, Ferrara N, Petzelbauer P, Sibilia M. “Autocrine VEGF signaling synergizes with EGFR in tumor cells to promote epithelial cancer development”. Cell, 140, 268-279, (2010).

Holcmann M, Stoitzner P, Drobits B, Luehrs P, Stingl G, Romani N, Maurer D, Sibilia M. “Skin inflammation is not sufficient to break tolerance induced against a novel antigen”, J. Immunology 183, 1133-43, (2009).

Natarajan A. Wagner B. and Sibilia M. “The EGF receptor is required for efficient liver regeneration”, PNAS 104, 17081-17086 (2007).

Palamara F, Meindl S, Holcmann M, Lührs P, Stingl G, Sibilia M. “Identification and characterization of ‘pDC-like cells’ in normal mouse skin and melanomas treated with Imiquimod”, J. Immunology 173, 3051-3061, (2004). 

 


 
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