Rate My Professor Jonas Fuxe

The research of Jonas Fuxe focuses on cellular plasticity as a key driver linking chronic inflammation and cancer progression, particularly epithelial-mesenchymal transition (EMT), tumor cell invasion, metastasis, and interactions within the tumor microenvironment. Major themes include remodeling of blood and lymphatic vessels, phenotypic switches in endothelial and epithelial cells, TGF-β signaling, immune escape mechanisms, and chemotactic factors such as IL7 and IL15 that promote breast cancer cell migration through lymphatic systems. The Jonas Fuxe Group utilizes in vitro studies and mouse models of chronic airway inflammation and cancer to dissect intercellular junctions, growth factor-induced tissue remodeling, and monocyte/macrophage properties in tumor cells. Key publications include "TGF-β-induced epithelial-mesenchymal transition: a link between cancer and inflammation" (Seminars in Cancer Biology, 2012), "A SNAIL1-SMAD3/4 transcriptional repressor complex promotes TGF-β mediated epithelial-mesenchymal transition" (Nature Cell Biology, 2009), "Epithelial-mesenchymal transition in cancer metastasis through the lymphatic system" (Molecular Oncology, 2017), "Reprogramming Tumor-Associated Macrophages by Antibody Targeting Inhibits Cancer Progression and Metastasis" (Cell Reports, 2016), "CXADR-Mediated Formation of an AKT Inhibitory Signalosome at Tight Junctions Controls Epithelial-Mesenchymal Plasticity in Breast Cancer" (Cancer Research, 2019), and "Guidelines and definitions for research on epithelial-mesenchymal transition" (Nature Reviews Molecular Cell Biology, 2020). These studies have elucidated molecular mechanisms underlying tumor invasiveness, vascular barrier functions, and potential therapeutic targets for preventing metastasis.