Vienna ImmunoLectures

Dr. Sabine Taschner-Mandl serves as Scientific and Managing Director at St. Anna Children's Cancer Research Institute and leads an interdisciplinary research group focusing on high-risk pediatric tumors, cancer metastasis, and the development of diagnostic and prognostic markers for precision oncology. Her team uses advanced single-cell, imaging and AI technologies to explore tumor cell plasticity and the microenvironment. She earned her PhD at the University of Vienna (Austria) and completed postdoctoral training at the Medical University of Vienna (Austria) and at several leading international institutions. She holds leadership roles in major pediatric oncology networks, including the Executive Board and Biology Committee of the European Society for Pediatric Oncology Neuroblastoma (SIOPEN) and the International Neuroblastoma Risk Group (INRG).

Dietmar Herndler-Brandstetter studied pharmacy at the University of Innsbruck, and obtained his PhD in Immunology at the Medical University Innsbruck. As a FLARE postdoctoral fellow, he continued his research on human T cell biology and aging at the Institute for Biomedical Aging Research in Innsbruck and the University of Birmingham, UK. In 2011 he joined the Richard Flavell lab at Yale University as an Erwin Schrödinger postdoctoral fellow. There he generated fate reporter mouse models to describe the plasticity of effector T cells and humanized mouse models to study novel cancer immunotherapies. In 2018 he joined the Center for Cancer Research in Vienna as a principal investigator. His lab is using humanized mouse models and patient-derived colorectal cancers (PDX) to reconstruct the patient’s tumor-immune microenvironment and to identify effective combination cancer immunotherapies.

About Dietmar’s research: Colorectal cancer (CRC) is the third most commonly diagnosed malignancy and the second leading cause of cancer-related deaths worldwide. The clinical benefit of currently available immune checkpoint inhibitors (anti-PD-1 and anti-CTLA-4) is limited to only 15% of CRC patients who have heavily mutated tumors (microsatellite instable). One of the reasons for the treatment failure is that available immunotherapies target only a fraction of tumor-infiltrating immune cells, such as T cells. Using multi-omics single cell and spatial profiling, we show that we can recapitulate patient tumor heterogeneity and immunosuppressive myeloid cell landscapes in our CRC-PDX MISTRG-6 humanized mice. Myeloid cells are highly abundant in CRC and play a key role in promoting angiogenesis, metastasis and resistance to PD-1/CTLA-4 immunotherapy. By reprogramming myeloid cells using first-in-class therapeutics and epigenetic modifiers in our CRC-PDX MISTRG-6 humanized mice we aim to understand and break immunosuppressive interaction networks in human CRC.