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Stiewe Lab
Molecular Oncology

The tumor suppressor p53 is the most commonly mutated gene in cancer patients. p53 is activated in response to cellular stress and oncogenes and acts as a transcription factor regulating effector programs designed to prevent the development or clonal expansion of cancer cells. It is the research focus of our group to better understand how these inputs are integrated by p53 in crosstalk with other cellular signaling networks to reach an appropriate cell fate decision involving, for example, reversible cell cycle arrest, irreversible cell cycle exit (differentiation or senescence) or apoptotic cell death. The ultimate goal are therapeutic strategies to reactivate and stimulate p53's anti-tumor activity in cancer patients.