Pathogenic bacteria have evolved sophisticated strategies to manipulate fundamental and often vital functions of the infected human host. Investigation of the molecular basis of the underlying bacterial virulence mechanisms may lead to new concepts for therapeutic intervention of bacterial infection, but should also increase our knowledge about basic pathological processes in humans, such as chronic inflammation and cancer.  Similar to cancer-inducing viruses (e.g. papilloma virus, HHV8), some pathogenic bacteria can cause the formation of tumors in humans. Prominent examples are stomach cancer induced by Helicobacter and vascular tumor formation triggered by the emerging pathogen Bartonella. Vascular tumor formation by Bartonella results from the massive and uncontrolled stimulation of blood vessel growth, a pathological process which represents also an essential step in tumorigenesis in most forms of human cancer. We are thus using Bartonella as a model for studying cancer tumorigenesis. Our previous work has shown that the stimulation of blood vessel growth by Bartonella critically depends on two fundamental aspects of vascular cell biology: (i) the triggering of cell proliferation and (ii) the inhibition of cell death. While the bacterial factor triggering cell proliferation is still unknown, we have recently identified the factor inhibiting cell death as the bacterial protein BepA, which is injected by the pathogen into infected vascular cells. The Ph.D. project proposed for a Misrock-fellow would focus on the molecular analysis of cell death inhibition by BepA. The project would further include the identification and initial characterization of the bacterial factor triggering cell proliferation factor. Together, this work is expected to significantly advance our understanding of tumorigenesis in human cancer.