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Michael B. Sporn

Researcher at Dartmouth College

Publications -  561
Citations -  96644

Michael B. Sporn is an academic researcher from Dartmouth College. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 157, co-authored 559 publications receiving 94605 citations. Previous affiliations of Michael B. Sporn include Cornell University & Reata Pharmaceuticals.

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Isolation from murine sarcoma cells of novel transforming growth factors potentiated by EGF

TL;DR: The ability to enhance the growth-stimulating effects of the TGFs is specific to EGF, as insulin, the insulin-like growth factors, platelet-derived growth factor and nerve growth factor do not show this property.
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Loss of expression of transforming growth factor beta in skin and skin tumors is associated with hyperproliferation and a high risk for malignant conversion

TL;DR: TGF- beta expression and function are compartmentalized in epidermis and epidermal tumors and that loss of TGF-beta is an early, biologically relevant risk factor for malignant progression is shown.
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A Synthetic Triterpenoid, 2-Cyano-3,12-dioxooleana-1,9-dien-28-oic Acid (CDDO), Is a Ligand for the Peroxisome Proliferator-Activated Receptor γ

TL;DR: The triterpenoid CDDO is established as a member of a new class of PPARgamma ligands, and synergizes with a retinoid X receptor (RXR)-specific ligand to induce 3T3-L1 differentiation, while CDDO-Me is an antagonist in this assay.
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Prevention of Breast Cancer in the Rat with 9-cis-Retinoic Acid as a Single Agent and in Combination with Tamoxifen

TL;DR: For suppression of carcinogenesis in vivo, 9cRA was much more potent than all-trans-retinoic acid, both as a single agent or in combination with TAM, although both retinoids had equivalent inhibitory effects on DNA synthesis in cultured human breast cancer cell lines.
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Novel triterpenoid CDDO-Me is a potent inducer of apoptosis and differentiation in acute myelogenous leukemia

TL;DR: CDDO-Me is an MDR-1- and a p53-independent compound that exerts strong antiproliferative, apoptotic, and differentiating effects in myeloid leukemic cell lines and in primary AML samples when given in submicromolar concentrations.