Histone-deacetylase inhibitors: novel drugs for the treatment of cancer

By Ricky W. Johnstone. Nature reviews. Drug discovery, 2002

1,513 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/11cf85e29fe2e5b819700454409741531219fa0c

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Citations in the corpus

Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer (2006, background): “A relatively wide range of structures have been identified that are able to inhibit the activity of class 1, class 2 and class 4 HDAC”
Anticancer activities of histone deacetylase inhibitors (2006, background): “A large number of studies have demonstrated that various TNF receptor super family members and their ligands are transcriptionally activated following HDACi treatment (see Ref”
Deacetylase inhibition promotes the generation and function of regulatory T cells (2007, background): “HATs generally increase accessibility and promote gene transcription, whereas HDACs typically dampen histone-DNA and histone–nonhistone protein interaction”
Molecular evolution of the histone deacetylase family: functional implications of phylogenetic analysis. (2004, background): “Consistent with this prediction, HDAC1 and HDAC2 exist in similar complexes including Sin3, NuRD/ NRD/Mi2, and CoREST.(2,32,33) They are also both widely expressed.”
Phase 2 trial of oral vorinostat (suberoylanilide hydroxamic acid, SAHA) for refractory cutaneous T-cell lymphoma (CTCL). (2007, neutral): “All patients 4/13 (31) 9.1, 61.4 1/11 (9) 0.2, 41.3 3/9 (33) 7.5, 70.1 8/33 (24) 11.1, 42.3 Stage less than IIB* 0/2 (0) 0.0, 84.2 0/1 (0) 0.0, 97.5 1/2 (50) 1.3, 98.7 1/5 (20) 0.5, 71.6 Stage at least IIB† 4/11 (36) 10.9, 69.2 1/10 ( 10 ) 0.3, 44.5 2/7 (29) 3.7, 71.0 7/28 (25) 10.7, 44.9 Sezary syn”
Cancer epigenetics. (2005, background): “It is now realized that CpG island hypermethylation is just one facet of an integrated change in chromatin structure and in histone modifications (10,11), including histone H3 and H4 deacetylation (12), histone H3 lysine 9 methylation (13), histone H4 sumoylation (14) and reduced histone H3 lysine 4”
Drug discovery from medicinal plants. (2005, methodology): “…at UIC, as well as panels of diverse mechanistic and cell-based assays at RTI and BMS. Examples of mechanism-based assays include a proteasome inhibition assay (Almond and Cohen, 2002; Adams, 2004) and a histone deacetylase (HDAC) inhibition assay (Johnstone, 2002; Villar-Garea and Esteller, 2004).”
From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites. (2016, neutral): “, Johnstone, A.M., Lobley, G.E., Wallace, R.J., et al. (2011). High-protein, reduced-carbohydrate weight-loss diets promote metabolite profiles likely to be detrimental to colonic health.”
The role of histone deacetylases (HDACs) in human cancer (2007, background): “…of acetylated lysine in histone tails is associated with a more relaxed chromatin state and gene-transcription activation, while the deacetylation of lysine residues is associated with a more condensed chromatin state and transcriptional gene silencing ( Johnstone, 2002; Iizuka and Smith, 2003).”
Histone Deacetylase Inhibitors in Clinical Studies as Templates for New Anticancer Agents (2015, background): “Although not fully understood, the clinical activities of these compounds are thought to be mediated in part by the induction of histone acetylation where the chromatin configuration adopts a permissive or more open form for potential reactivation of aberrantly suppressed genes, leading to inhibitio”