Over the past 7 years, my main research interest has focussed on furthering our understanding of the early molecular events associated with the initiation of Colorectal carcinoma (CRC) and how we could manipulate these signals to identify new therapeutic markers against CRC. By establishing and extensively characterising novel mouse models, I could discover the essential role for the anti-apoptotic factor MCL1 in maintaining intestinal homeostasis. Furthermore, the loss of MCL1 from intestinal epithelial cells is sufficient to trigger CRC formation in mice. Strikingly, by re-deriving these knockout mice under germ free conditions, I could demonstrate that MCL1-deficiency related tumorigenesis was completely independent of chronic inflammation. MCL1-deficiency associated carcinoma also shared cardinal histological, molecular and genetic features of human CRC. More recently, I have conceptualised and initiated an independent project which is designed to identify and characterise novel therapeutic targets against tumors of different etiologies. In order to discover previously uncharacterised therapeutic targets, I have designed an experimental workflow which combines ribosome profiling and CRISPR-Cas9 mediated gene silencing on patient-derived tumor samples.In addition to my primary research focus, I have also been integral to a number of very successful collaborative projects with collaborators throughout Europe and the US.In my position at USZ, I have been responsible for managing a number of projects. As well as playing an integral part to the conception of these projects, I have also written a number of successful grant applications and been involved in producing and adhering to the relevant budgets. I have been responsible for overseeing the project of numerous Ph.D. and MSc students and hold the position of Study director and Local Animal Welfare Officer (LAWO) for 6 project licenses certified by Schweizerische Eidgenossenschaft (Kanton Zürich).

During my PhD, my main interest was to elucidate the mechanisms by which Mesenchymal Stromal Cells (MSC) interact with the human immune system. I approached this topic in a number of ways. Firstly, I investigated the direct interaction between human MSC and primary human B cells. In order to do so, I isolated primary human B cells from patient samples and co-cultured them with primary human MSC. Through this work, I was able to discover a novel, cell-contact dependent mechanism by which MSC supported the survival and proliferation of human B cells via VEGF up-regulation.In addition to this work, I established a number of murine models of acute and chronic Graft versus Host Disease (GvHD) to investigate the molecular mechanisms by which MSC suppress T cell activation and proliferation. By using a humanized mouse model of GvHD, I could demonstrate human MSC protect against GvHD by inducing regulatory T cell populations and reducing TNF production by T cells. FACS-based analysis of human immune cells isolated from the essential organs of GvHD mice allowed the characterisation of human T cell populations and activation state with or without MSC therapy.