Clinical development of histone deacetylase inhibitors as anticancer agents.

By D. Drummond, C. Noble, D. Kirpotin, Zexiong Guo, G. Scott, C. Benz. Annual Review of Pharmacology and Toxicology, 2005

649 citations recorded by the source corpus.

Subfields: Molecular Biology, Organic Chemistry

View Paper: https://www.semanticscholar.org/paper/994c4de0bb9d322d86a1c023cc8ceed4e7b0181a

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Citations in the corpus

Discovery and preclinical validation of drug indications using compendia of public gene expression data (2011, background): “HDAC inhibitors are anticancer agents that act by inhibiting cancer cell proliferation and inducing apoptosis ( 39 – 41 ).”
DNA methylation and gene silencing in cancer (2005, background): “A variety of HDAC inhibitors have been shown to inhibit histone deacetylation in human tumor cells, leading to accumulation of acetylated histone proteins”
Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer (2006, background): “HDACi in clinical development The first studies on the clinical use of HDACi have been published recentl”
Anticancer activities of histone deacetylase inhibitors (2006, background): “Circumstantial evidence for tumour-selectivity comes from the results of clinical trials and preclinical animal experiments demonstrating that HDACi can have potent anticancer activities at concentrations that are minimally toxic to the hos”
Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug (2007, background): “, α-tubulin), angiogenesis (hypoxia-inducible factor (HIF)-1α) and reactive oxygen species (ROS)-facilitated cell deat”
GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon (2009, background): “Thus, the bacterial fermentation product butyrate causes cell death in colon cancer cells by two independent but complementary mechanisms: one through SLC5A8-mediated entry of butyrate into cells with subsequent inhibition of HDACs, and the second through GPR109A independent of HDACs.”