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The focus of our research is the p53 family of tumor suppressor genes. The p53 family is activated by cellular stress, hyperproliferative signals and developmental stimuli. These inputs are integrated within the p53 family in crosstalk with other cellular signalling networks to reach an appropriate cell fate decision that is executed by the selective transactivation of distinct transcriptional programmes leading to reversible cell cycle arrest, irreversible cell cycle exit (differentiation or senescence) or apoptotic cell death.

We are interested in the following questions:
    ·     How do p53 and its family members suppress tumorigenesis?
    ·     How is the p53 tumor suppressor family inactivated in cancer cells?
    ·     How can tumor suppressive functions of the p53 family be reactivated for cancer therapy?

For background information and a more detailed description of our research interest please click the "Research" button!

Funding:
    ·     European Research Council
    ·     Deutsche Forschungsgemeinschaft DFG (TR17, TR81, KFO210)
    ·     Deutsche Krebshilfe - Dr. Mildred Scheel Stiftung
    ·     Bundesministerium für Bildung und Forschung (BMBF)
    ·     Deutsche José Carreras Leukämie-Stiftung
    ·     LandesOffensive zur Entwicklung Wissenschaftlich-ökonomischer Exzellenz (LOEWE)
    ·     von Behring-Röntgen-Stiftung
    ·     Rhön-Klinikum AG
    ·     Universitätsklinikum Gießen & Marburg

 

 

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Zuletzt aktualisiert: 03.08.2017 · mernberm

 
 
 
Fb. 20 - Medizin

Institut für molekulare Onkologie, Hans-Meerwein-Str. 3, 35043 Marburg
Tel. +49 6421/28-26280, Fax +49 6421/28-26769, E-Mail: thorsten.stiewe@staff.uni-marburg.de

URL dieser Seite: https://www.uni-marburg.de/fb20/imo

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