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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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The novel triterpenoid CDDO induces apoptosis and differentiation of human osteosarcoma cells by a caspase-8 dependent mechanism.

TL;DR: It is demonstrated that treatment of osteosarcoma cells with CDDO induces differentiation, as assessed by alkaline phosphatase activity and osteocalcin production, and that this response is abrogated in cells that overexpress CrmA.
Journal Article

The novel triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid induces apoptosis of human myeloid leukemia cells by a caspase-8-dependent mechanism.

TL;DR: It is demonstrated that CDDO induces apoptosis of myeloid leukemia cells and that this novel agent activates an apoptotic signaling cascade distinct from that induced by the cytotoxic agent ara-C.
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Retinyl acetate inhibits mammary carcinogenesis induced by N-methyl-N-nitrosourea.

TL;DR: A study of the effect of a retinyl acetate on mammary carcinogenesis induced by NMU, using a modification of the procedure reported by Gullino et al.5.
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The recombinant proregion of transforming growth factor beta1 (latency-associated peptide) inhibits active transforming growth factor beta1 in transgenic mice

TL;DR: Recombinant LAP should be a useful tool for novel approaches to study and therapeutically modulate pathophysiological processes mediated by TGF-beta3, both in vitro and in vivo, after intraperitoneal administration.
Journal Article

Inhibition of 7,12-Dimethylbenz(a)anthracene-induced Mammary Carcinogenesis by Retinyl Acetate

TL;DR: Data indicate that relatively large doses of retinyl acetate significantly inhibit the development of DMBA-induced mammary adenocarcinomas and benign tumors, and may be related to the effect of retinoids on epithelial cell differentiation and/or reversal of carcinogen-induced anaplasia.