Molecular pathways underlying an EMT, cancer cell plasticity and metastasis
Gerhard Christofori studied Biology at the University of Heidelberg and obtained his PhD in 1988 in the laboratory of Walter Keller at the German Cancer Research Center in Heidelberg and at the Biocenter of the University Basel on the biochemistry of 3’ processing and polyadenylation of eukaryotic mRNA. He did postdoctoral training with Douglas Hanahan at the University of California San Francisco, USA, where he began to study the molecular mechanisms of
multistage tumor development. In 1994 he became a group leader at the Institute of Molecular Pathology (IMP) in Vienna, Austria. Since Sept. 2001 he is professor and Chair of Biochemistry at the Department of Biomedicine of the University of Basel.
Using cultured tumor cell lines in vitro and transgenic mouse models of tumorigenesis in vivo, Gerhard Christofori contributed in several ways to the understanding of how tumor cells evolve on their way to tumor malignancy and metastasis. For example, he demonstrated that tumor cells use survival factors to overcome apoptosis that accompanies their hyperproliferation. Studying the molecular mechanisms of tumor angiogenesis, Gerhard Christofori revealed the detailed functions of several angiogenic growth factors in tumor hemangiogenesis and lymphangiogenesis and their contribution to the metastatic dissemination of tumor cells. Finally, he unraveled several aspects of the molecular pathways underlying malignant tumor cell invasion and metastatic dissemination: for example, his group emonstrated
that changes in cell adhesion and in transcriptional and epigenetic control are causally involved in epithelial-mesenchymal transition and malignant tumor progression and in the metastatic dissemination of tumor cells. More recently, his group reported a novel molecular pathway of collective tumor cell invasion. A major focus of the laboratory is based on the observation that metastatic dissemination of tumor cells is not only induced by genotypic or phenotypic changes within the tumor cells themselves but also by the tumor microenvironment.