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J Natl Cancer Inst. 2014 Feb;106(2):djt369. doi: 10.1093/jnci/djt369.

TGF-β: duality of function between tumor prevention and carcinogenesis.

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Affiliations of authors: Department of Medicine, Division of Gastroenterology (DRP, JB, BJ) and Division of Hematology/Oncology (HGM), Department of Surgery, Division of GI Surgical Oncology (DRP, PJG), and Department of Urology (CL), Northwestern University Feinberg School of Medicine, Chicago, IL; Department of Biomedical Engineering. McCormick School of Engineering, Northwestern University, Evanston, IL (DRP); Department of Biomedical Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI (JAD); UMR INSERM U1052, CNRS 5286, Université Lyon 1, Centre de Recherche en Cancérologie de Lyon, Lyon, France (LB); Division of Hematology/Oncology, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL (BP); Department of Pathology and Laboratory Medicine, University of California-Irvine, Irvine, CA (CL).


Several mechanisms underlying tumor progression have remained elusive, particularly in relation to transforming growth factor beta (TGF-β). Although TGF-β initially inhibits epithelial growth, it appears to promote the progression of advanced tumors. Defects in normal TGF-β pathways partially explain this paradox, which can lead to a cascade of downstream events that drive multiple oncogenic pathways, manifesting as several key features of tumorigenesis (uncontrolled proliferation, loss of apoptosis, epithelial-to-mesenchymal transition, sustained angiogenesis, evasion of immune surveillance, and metastasis). Understanding the mechanisms of TGF-β dysregulation will likely reveal novel points of convergence between TGF-β and other pathways that can be specifically targeted for therapy.

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