Molecular mechanisms controlling self-renewal of stem and progenitor cells have to be under stringent control to ensure live long tissue homeostasis. Genetic alterations that dysregulate these mechanisms can lead to the development of Cancer stem cells (CSCs) that play important roles in tumor development, relapse, metastasis and resistance to anti-cancer therapy. CSCs originate from non-malignant stem or progenitor cells, which are often regulated by developmental signaling pathways like the Notch and Wnt cascades. These pathways ensure proper stem and progenitor cell homeostasis and function.

We perform basic and translational cancer research with a particular focus how dysregulation of these developmental pathways drives tumorigenesis and cancer progression. Using state-of-the art technologies, including omics analysis (transcriptomic, epigenetic, single cell analysis, proteomics), genetical engineered mouse models (GEMMs), organoids, patient derived xenografts (PDX) as well as primary human clinical samples, we aim to unravel molecular and mechanistic events driving the initiation and progression of blood borne cancers and solid tumors.

Current ongoing research seeks to understand the influence of inflammation in tumor progression addition, we optimize and validate potential drug candidates that target developmental signaling pathways to assess their mode-of-action and their efficacy in pre-clinical cancer models and in primary human tumor samples. The goal is to develop these drug development candidates further for clinical proof of concept in human clinical studies.