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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Animals
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Anticarcinogenic Agents* / metabolism
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Anticarcinogenic Agents* / pharmacology
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Apoptosis*
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Cadherins / metabolism
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Carcinogenesis / metabolism
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Carcinogens* / metabolism
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Carcinogens* / pharmacology
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Cell Proliferation*
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Cell Transformation, Neoplastic* / chemically induced
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Cell Transformation, Neoplastic* / metabolism
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Disease Progression
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Humans
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Neoplasms / chemically induced
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Neoplasms / metabolism*
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Neoplasms / prevention & control
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Neovascularization, Pathologic / chemically induced
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Neovascularization, Pathologic / prevention & control
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Protein Serine-Threonine Kinases / metabolism
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Receptor, Transforming Growth Factor-beta Type I
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Receptors, Transforming Growth Factor beta / metabolism
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Signal Transduction*
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Transforming Growth Factor beta / metabolism*
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Up-Regulation
Substances
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Anticarcinogenic Agents
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Cadherins
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Carcinogens
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Receptors, Transforming Growth Factor beta
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Transforming Growth Factor beta
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Protein Serine-Threonine Kinases
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Receptor, Transforming Growth Factor-beta Type I