Reinhardt, H Christian / Schumacher, Björn - A 8

Differential modulation of the p53 network in cancer therapy

Genome instability contributes to cancer development, while radiation and chemotherapy routinely rely on inflicting genotoxic stress to trigger apoptotic demise of cancer cells. DNA damage response (DDR) pathways that are mediated through the tumor suppressor p53 play an important role in the cell intrinsic responses to genome instability, including a transient cell cycle arrest, senescence and apoptosis.

Also non-cell autonomous interactions of the p53 network with the innate immune system and the systemic adjustments during the aging process comprise important aspects of p53-mediated tumor suppression. The network of p53 target genes thus functions as an important regulator of cancer prevention, tumor therapy responses and also the physiological adjustments during aging.

To gain a better understanding of the mechanisms of the differential outcomes of p53 activity, we aim to investigate by in vitro and in vivo live imaging of key effectors of the p53-mediated DDR.

Former Funding Period 01/2014 - 12/2016

Information from this funding period will not be updated anymore. New research related information is available here.

Prof. Dr. med. H Christian Reinhardt

Dept. I of Internal Medicine

Prof. Dr. med. H Reinhardt

Co-Principal Investigator A 9
Executive Board Member

Work +49 221 478 96701

Fax (Work) +49 221 478 97835

Cologne Center of Genomincs (CCG)
Weyertal 115 b
50931 Cologne


Link to PubMed

Prof. Dr. rer. nat. Björn Schumacher

Institute for Genome Stability in Ageing and Disease, CECAD Cologne

Prof. Dr. rer. nat. Björn Schumacher

Work +49 221 478 84202

CECAD Research Center
Joseph-Stelzmann-Str. 26
50931 Cologne


Link to PubMed