M
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 combination of the histone deacetylase inhibitor vorinostat and synthetic triterpenoids reduces tumorigenesis in mouse models of cancer
Kim M. Tran,Renee Risingsong,Darlene B. Royce,Charlotte R. Williams,Michael B. Sporn,Patricia A. Pioli,Lalji K. Gediya,Vincent C. O. Njar,Karen T. Liby +8 more
TL;DR: SAHA enhanced the ability of synthetic triterpenoids to delay formation of estrogen receptor-negative mammary tumors in MMTV-polyoma middle T mice and suppress secreted levels of the pro-angiogenic factor matrix metalloproteinase-9.
Journal Article
Studies on chromatin. II. Effects of carcinogens and hormones on rat liver chromatin.
TL;DR: Intense stimulation of the liver by pituitary hormones increased the RNA and total protein (but not the histone protein) content of liver chromatin, while in the resultant tumors the RNA content of chromatin was greatly increased.
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Human neuroblastoma cells rapidly enter cell cycle arrest and apoptosis following exposure to C-28 derivatives of the synthetic triterpenoid CDDO.
Jennifer L. Alabran,Adam Cheuk,Karen T. Liby,Michael B. Sporn,Javed Khan,John J. Letterio,Konstantin Leskov +6 more
TL;DR: After treatment of human neuroblastoma cells with CDDO-Me, cell cycle studies show depletion of the S-phase, while apoptosis studies show conformational activation and mitochondrial translocation of Bax protein, as well as activation of caspases -3 and -8.
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CDDO-Imidazolide induces DNA damage, G2/M arrest and apoptosis in BRCA1-mutated breast cancer cells
TL;DR: Results show that CDDO-Im induces ROS and subsequent DNA damage, thereby facilitating the activation of the DNA damage checkpoint, G2/M arrest, and finally apoptosis in BRCA1-mutated cancer cells.