Tumorgenetik und zelluläre Stressantworten
Gruppenleiter
Prof. Dr. Clemens Schmitt
Our research program is driven by our interest in cellular stress responses (so called ‘failsafe mechanisms’) that may serve as anti-tumor barriers when challenged by transforming oncogenes, and, in turn, must be bypassed or inactivated before a full-blown malignancy can actually form. Importantly, ultimate stress responses such as apoptosis or cellular senescence – both terminal ‘cell-cycle exit’ programs – do not only counter tumorigenesis, but are utilized as chemotherapy- induced stress responses as well. Hence, principles of oncogenesis and mechanisms of treatment sensitivity seem to critically overlap and impinge on each other during tumor formation, cancer therapy and relapsed or progressive disease conditions. To test the impact of genetic lesions in cellular stress response programs on tumor development and treatment outcome under most physiological conditions in vivo, we generate mouse models harboring lymphomas (and other tumor entities) with defined genetic lesions.