Jonas Fuxe Group

A major research theme in the lab is remodeling of blood and lymphatic vessels.

Research Project

Photo of Jonas Fuxe, Senior researcher, Department of Laboratory Medicine, Division of Pathology
Jonas Fuxe, Senior researcher, Department of Laboratory Medicine, Division of Pathology Photo: Filippa Fuxe

Mechanisms of Tissue Remodeling in Inflammation and Cancer

A fundamental principle of multi-cellular organisms is the ability of cells to interact and communicate. Tubular organs are lined by epithelial and endothelial cells that form selective barriers allowing the formation of different tissue compartments. This function is dependent on the ability of cells to polarize and establish specialized intercellular junctions that regulate flux of ions, solutes and cells across the barrier. The assembly and disassembly of these junctions is tightly regulated during development and in normal physiology, but is disturbed in pathological conditions of tissue remodeling, such as in chronic inflammation and cancer. We use a combination of in vitro studies and mouse models of chronic airway inflammation and cancer to study the role of specific growth factors and cytokines in mediating tissue remodeling and junction reorganization in endothelial and epithelial cell layers.

A major research theme in the lab is remodeling of blood and lymphatic vessels. While VEGF is a major angiogenic factor, less is known about the mechanisms that drive other types of vascular remodeling including phenotypic switches of endothelial cells leading to excessive infiltration of inflammatory cells. We are particularly interested in the role of angiopoietins and the Tie2 signaling pathway in modulating the inflammatory response by acting on blood and lymphatic vessels.

Another theme is the role of epithelial-mesenchymal transition (EMT) in tumor cell invasion and epithelial remodeling in chronic inflammation. EMT is characterized by loss of cell-cell adhesion and polarity accompanied by cytoskeletal rearrangements and increased cell motility. TGF-b is a major inducer of EMT but the molecular mechanisms involved are not clear. We are interested in transcriptional regulation of target genes downstream of the TGF-b/Smad signaling pathway.

Group Members


Mei-Fong Pang, PhD. PhD student in Fuxe group 2009-2012. Current position: postdoc at Princeton University, US.

Jill Johnson, PhD. Postdoc in Fuxe group 2008-2011. Current position: Research Fellow at the National Heart and Lung Institute, Imperial College London

Tove Berg, PhD. Postdoc in Fuxe group 2009-2012.

Vedrana Tabor, PhD. Postdoc in Fuxe group 2012-2014.

Sandra Travica, PhD. Postdoc in Fuxe group 2013-2014. Current position: Medical Scientific Advisor for Oncology Business at Pfizer Inc.


Guidelines and definitions for research on epithelial-mesenchymal transition.
Yang J, Antin P, Berx G, Blanpain C, Brabletz T, Bronner M, et al
Nat. Rev. Mol. Cell Biol. 2020 Jun;21(6):341-352

CXADR-Mediated Formation of an AKT Inhibitory Signalosome at Tight Junctions Controls Epithelial-Mesenchymal Plasticity in Breast Cancer.
Nilchian A, Johansson J, Ghalali A, Asanin ST, Santiago A, Rosencrantz O, et al
Cancer Res. 2019 01;79(1):47-60

EMT, inflammation and metastasis.
Vincent CT, Fuxe J
Semin. Cancer Biol. 2017 12;47():168-169

Epithelial-mesenchymal transition in cancer metastasis through the lymphatic system.
Karlsson MC, Gonzalez SF, Welin J, Fuxe J
Mol Oncol 2017 07;11(7):781-791

Reprogramming Tumor-Associated Macrophages by Antibody Targeting Inhibits Cancer Progression and Metastasis.
Georgoudaki AM, Prokopec KE, Boura VF, Hellqvist E, Sohn S, Östling J, et al
Cell Rep 2016 05;15(9):2000-11

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