Abstract

Tumor-specific combinations of oncogenic mutations often free cancer cells from their reliance on growth factors. One important example comprises the epidermal growth factor receptor (EGFR) and its kin, HER2 . In tumours, both EGFR and HER2 frequently display overexpression, internal deletions and point mutations. Accordingly, monoclonal antibodies and kinase inhibitors specific to these receptors have been approved for clinical application. My lecture will introduce our efforts to develop novel agents able to intercept growth factor signalling in tumours. Examples include aptamers, antibody combinations and decoy receptors. Alongside, my laboratory is interested in molecular mechanisms underlying the ability of EGFR and HER2 to enhance cell proliferation and promote invasive growth. I will focus on a model that portrays growth factor signalling as a pulsatile mechanism that eliminates noise and commits cells to consistent extracellular ques. In addition, I will describe several transcription-based mechanisms that explain the invasive behavior of HER2 and EGF -driven cancer cells.