title: TGF-β: duality of function between tumor prevention and carcinogenesis.
abstract: 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.
authors: 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).
authors: Daniel R
authors: DR
authors: Principe
authors: Jennifer A
authors: JA
authors: Doll
authors: Jessica
authors: J
authors: Bauer
authors: Barbara
authors: B
authors: Jung
authors: Hidayatullah G
authors: HG
authors: Munshi
authors: Laurent
authors: L
authors: Bartholin
authors: Boris
authors: B
authors: Pasche
authors: Chung
authors: C
authors: Lee
authors: Paul J
authors: PJ
authors: Grippo
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000378:metabolism / Q000494:pharmacology; D017209:Apoptosis; D015820:Cadherins / Q000378:metabolism; D063646:Carcinogenesis / Q000378:metabolism; D002273:Carcinogens / Q000378:metabolism / Q000494:pharmacology; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced / Q000378:metabolism; D018450:Disease Progression; D006801:Humans; D009369:Neoplasms / Q000139:chemically induced / Q000378:metabolism* / Q000517:prevention & control; D009389:Neovascularization, Pathologic / Q000139:chemically induced / Q000517:prevention & control; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D000077293:Receptor, Transforming Growth Factor-beta Type I; D018125:Receptors, Transforming Growth Factor beta / Q000378:metabolism; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D016588:Anticarcinogenic Agents; D015820:Cadherins; D002273:Carcinogens; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D017346:Protein Serine-Threonine Kinases; D000077293:Receptor, Transforming Growth Factor-beta Type I