Advanced Disease Models


Research Interests

Stem cells; Metabolic liver diseases; Cancer; Obesity; Bioengineering; Drug repositioning; Tissue regeneration; Organoids

Description of Research

Our research is centered on unraveling the intricate interplay between metabolic diseases and tumour development, particularly within the context of the tumour microenvironment and stem cell niches. We leverage our multi-disciplinary expertise in the fields of cancer, stem cells, and bioengineering to explore and comprehend the fundamental mechanisms that underlie tumour initiation and progression in chronic liver diseases. Furthermore, we are keenly interested in investigating the biology of tissue-resident epithelial stem cells to pave the way for innovative regenerative medicine strategies. To address our basic biomedical questions, we adopt an integrative approach combining dietary-induced and genetically-engineered mouse models, tissue engineering techniques, as well as 3D organotypic cultures. Our work involves meticulously designing of sophisticated disease models, which provide a close representation of the intricate interplay of biological factors and signalling pathways found within human and mouse tissues. This allows us to simulate disease processes with a high degree of fidelity, enabling us to investigate the underlying factors and discover novel insights into disease progression and treatment.

Recent Publications

Ece, Y. et al. Hepatic lipid overload potentiates biliary epithelial cell activation via E2Fs. eLife 11, (2022) PubMed

Sorrentino, G. et al. Bile Acids Signal via TGR5 to Activate Intestinal Stem Cells and Epithelial Regeneration. Gastroenterology 159, 956-968.e8 (2020) PubMed

Sorrentino, G. et al. Mechano-modulatory synthetic niches for liver organoid derivation. Nat Commun 11, 3416 (2020) PubMed

Lund, M. L. et al. L-Cell Differentiation Is Induced by Bile Acids Through GPBAR1 and Paracrine GLP-1 and Serotonin Signaling. Diabetes 69, 614–623 (2020). PubMed

Sorrentino, G. et al. Glucocorticoid receptor signalling activates YAP in breast cancer. Nat Commun 8, 14073 (2017) PubMed

Sorrentino, G. et al. Metabolic control of YAP and TAZ by the mevalonate pathway. Nat Cell Biol 16, 357–366 (2014) PubMed