Curzio Ruegg

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University of Fribourg
The main research interest of the laboratory is the study of tumor-host interactions. We are particularly interested in understanding how the growing tumor modify normal tissue to its advantage, how this modify tissue contribute to tumorigenesis and how therapeutic interventions modify this cross-talk, and what are the consequences. More specifically we are investigating the following aspects of tumor - host interaction: - Tumor microenvironment: How do cells of the microenvironment, in particular bone marrow-derived cells, promote tumor growth and metastasis? How do therapeutic interventions modify the tumor microenvironment and how do these modifications impact tumor behavior? - Tumor angiogenesis: how does tumor angiogenesis modulate tumor dormancy, tumor growth and metastasis? How can we therapeutically exploit this tumor cell - endothelial cell interaction? - Tumor metastasis: How does the cross-talk between tumor cells and the microenvironment evolve during tumor metastasis ? - Understanding how tumors adapt and evade anticancer therapies. How do tumors and the microenvironment react to anticancer therapies and what are the consequences to tumor progression ?
C. Rüegg, A. Yilmaz, G. Bieler, J. Bamat, P. Chaubert, and F. J. Lejeune (1998). Evidence for the involvement of endothelial cell integrin alphaVbeta3 in the disruption of the tumor vasculature induced by TNF and IFNgamma. Nature Med., 4:408-414 O. Dormond, A. Foletti, C. Paroz, and C. Rüegg (2001). Nonsteroidal anti-inflammatory drugs inhibit αVβ3 integrin-mediated and Cdc42/Rac-dependent endothelial cell spreading, migration and angiogenesis. Nature Med., 9:1041-1047 J. Laurent, E. Faes-van't Hull, C. Touvrey, F. Kuonen, Q. Lan, N. G. Lorusso, Imaizumi, L. Ciarloni, , M.A. Doucey, G. Alghisi, E. Fagiani, K. Zaman, R. Stupp, M. Shibuya, J. F. Delaloye, G. Christofori, and C. Rüegg. PlGF promotes angiogenic education of CD11b+ monocytes in breast cancer during differentiation from CD34+ hematopoietic progenitors. Cancer Res, 2011, 71:3781-3791 J Zaric, S. Tercier, J-M. Joseph, T. Sengstag, M. Delorenzi, L. Ponsonnet, and C. Rüegg. Identification of MAGI1 as a tumor suppressor protein induced by COX-2 inhibitors in colon cancer cells. Oncogene, 2012, 31, 48–59 G. Xue, D. F. Restuccia, Q. Lan, D. Hynx, S. Dirnhofer, D. Hess, C. Ruegg and B. A. Hemmings. Akt/PKB-mediated phosphorylation of Twist1 is crucial for tumor metastasis. Cancer Discovery, 2012, 2(3):248-59. F. Kuonen, J Laurent, J-C Stehle, T. Rausch, E. Faes-van't Hull, G. Biéler, G.C. Alghisi, R. Schwendener, G. Lorusso, S. Andrejevic-Blant, R-O. Mirimanoff, and C. Ruegg KITL-dependent mobilization of CD11b+cKit+ myelomonocytic cells promotes post-radiation metastasis. Clin Cancer Res, 2012;18(16):4365-74 D. Barras, G. Lorusso, C. Rüegg, Widmann Inhibition of cell migration and invasion mediated by the TAT-RasGAP317-326 peptide requires the DLC1 tumor suppressor. Oncogene. 2014;33(44):5163-72 N. Guex, I. Crespo, S. Bron, A. Ifticene-Treboux, E. Faes van’t Hul, S. Kharoubi, R. Liechti1, P. Werffeli, M. Ibberson, F. Majo, M. Nicolas, J. Laurent, A. Garg, K. Zaman, H-A. Lehr, B. J. Stevenson1, C. Rüegg, G. Coukos, J.-F. Delaloye, I. Xenarios and M.-A. Doucey. Angiogenic activity of breast cancer patients' monocytes reverted by combined use of systems modeling and experimental approaches (2014) Plos Comput Biol, 2015;11(3):e1004050