Cancer represents a leading cause of death worldwide, with numbers projected to further rise to an estimated 13.1 million deaths in 2030. The transformation of normal into cancer cells is a stepwise process that generally involves activation of oncogenes and inactivation of tumor suppressors to undermine the normal biological contraints on growth control. Mutations in the small Ras GTPases are key drivers in 30% of all human cancers, making Ras GTPases the most prominent oncogenes in human disease. Ras mutation is critical for tumor initiation and progression as well as therapy response. However, the signaling and genetic networks that ultimately execute the oncogenic program and the mechanisms undelying their deregulation through altered Ras signaling remain incompletely understood. Despite immense research effort Ras GTPases remain refractory to therapeutic targeting. We are therefore interested in identifying and characterizing Ras downstream events that are critical for tumorigenesis with the goal to identify new potential targets for cancer therapy. To address these questions we are taking a multi-faceted approach combining mouse models with biochemical and cell biological techniques.
Undergraduate studies in Biochemistry at the Eberhard-Karls University, Tübingen, Germany
PhD studies with Dr. Daniel Krappmann at the Max-Delbrück-Center for Molecular Medicine and the Free University, Berlin, Germany
Postdoctoral fellow with Dr. Sankar Ghosh at Yale University, New Haven and Columbia University, New York, USA
Junior group leader at the IMTB