The MYC transcription factor network member MGA is a subunit of a non-canonical Polycomb complex, which, when inactivated, accelerates tumorigenesis in mouse models of cancer and proliferation in colon organoids.

Studies of organoid morphogenesis, combined with proteomics and molecular profiling, identify the THBS1-YAP axis as a signalling mechanism that mediates paracrine communication between tumour cells and their wildtype epithelial neighbours.

Libraries of patient-derived tumor organoids are a reliable and scalable model system that can help identify and optimize targeted therapies in a pre-clinical setting.

Human colonic organoid monolayers self organize into regularly spaced stem and differentiated cell compartments, which are maintained by waves of ERK activity originating from extruded/dying cells.

Novel human models of the lung and intestine are described and validated as preclinical in vitro tools for predictive profiling of T-cell-bispecific antibodies with expected on-target off-tumor risk.

Genetic analyses reveal how CDX2 and BRAF defects seen in serrated colorectal cancer (CRCs), a poor prognosis CRC subset, cooperate in tumorigenesis in humans and in a mouse cancer model.

DKK2 is crucial for the development of lysozyme-expressing cancer cells with Paneth cell characteristics necessary for liver metastasized colon cancer growth.

miR-34a prevents inflammation-induced colonic regeneration from oncogenesis by simultaneously targeting processes in both immune and epithelial cells, including T helper 17 cell differentiation, recruitment, and IL-17 induced epithelial proliferation.

miR-31 drives proliferation of intestinal stem cells, and protects intestinal stem cells against apoptosis both during homeostasis and regeneration in response to ionizing radiation injury, and promotes intestinal tumorigenesis through regulation of multiple signaling pathways.

Colon cancer cells disseminate and colonize distant organ sites along the invasion-metastasis cascade by transiently activating intermediate epithelial to mesenchymal transition states through distinct transcriptional trajectories.