Studying the (epigenetic) processes driving tumor initiation and progression

We are particularly interested in the epigenome changes occurring in pediatric tumors uniquely defined by mutations in SWI/SNF complex members. By using tumor organoids in combination with gene editing technologies and (single-cell) omics read-outs, we aim to pinpoint the tumor-driving signaling pathways that could serve as therapeutic targets. Furthermore, we have developed orthotopic organoid xenograft models and barcode lineage tracing strategies that allow us to study clonal dynamics during the different steps of tumorigenesis (such as primary tumor growth, metastasis formation, and therapy resistance) in great detail.

Besides tumor organoids, we use healthy tissue-derived organoids for the generation of tumor models. We apply different genome editing technologies (such as CRISPR/Cas9 technology) to healthy organoids to generate tumor progression models. Such engineered tumor organoids provide genetically defined models that allow for studying the contribution of specific genetic alterations to tumorigenesis.