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Exploring anti-TGF-β therapies in cancer and fibrosis
Department of Molecular Cell Biology and Centre for Biomedical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwig Institute for Cancer Research.
2011 (English)In: Growth Factors, ISSN 0897-7194, E-ISSN 1029-2292, Vol. 29, no 4, 140-152 p.Article in journal (Refereed) Published
Abstract [en]

Transforming growth factor-β (TGF-β) is a multifunctional cytokine, with important roles in maintaining tissue homeostasis. TGF-β signals via transmembrane serine/threonine kinase receptors and intracellular Smad transcriptional regulators. Perturbed TGF-β signaling has been implicated in a large variety of pathological conditions. Increased TGF-β levels have been found in patients with cancer, fibrosis, and systemic sclerosis, and were correlated with disease severity. In cancer, TGF-β mediates tumor invasion and metastasis by affecting both tumor cells and the tumor microenvironment including fibroblast activation and immune suppression. Furthermore, TGF-β is a strong stimulator of extracellular matrix deposition. On the basis of these observations, small molecule inhibitors of the TGF-β receptor kinases, neutralizing antibodies that interfere with ligand?receptor interactions, antisense oligonucleotides reducing TGF-β expression, and soluble receptor ectodomains that sequester TGF-β have been developed to intervene with excessive TGF-β signaling activity in the aforementioned disorders. Here, we review the current state of anti-TGF-β therapy in clinical trials.

Place, publisher, year, edition, pages
2011. Vol. 29, no 4, 140-152 p.
National Category
Endocrinology and Diabetes Cell and Molecular Biology
URN: urn:nbn:se:uu:diva-168730DOI: 10.3109/08977194.2011.595411ISI: 000292706200004PubMedID: 21718111OAI: oai:DiVA.org:uu-168730DiVA: diva2:503299
Available from: 2012-02-15 Created: 2012-02-15 Last updated: 2015-08-12Bibliographically approved

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