Anticancer activities of histone deacetylase inhibitors

By Jessica E. Bolden, M. Peart, Ricky W. Johnstone. Nature reviews. Drug discovery, 2006

2,938 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ba099c9c7fa4c40d0322dd0c0098f5dc68a828fc

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Manel Esteller
2. S. Baylin
3. Peter A. Jones
4. E. Olson
5. Ricky W. Johnstone
6. PA Marks
7. E. Seto
8. W-S Xu

Citations in the corpus

• Histone Deacetylase Inhibitors as Anticancer Drugs (2017, background): “HATs catalyze the transfer of an acetyl group from acetyl-CoA to the ε-NH2 group of lysine residues in proteins, while HDACs remove it [12].”
• Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications (2016, background): “pressed in colorectal, cervical and gastric cancer [77, 78].”
• Histone Deacetylase Inhibitors: Potential in Cancer Therapy (2009, background): “TSA and vorinostat inhibit VEGF-induced expression of VEGF receptors and induce semaphorin III expression in endothelial cells.”
• New and emerging HDAC inhibitors for cancer treatment. (2014, neutral): “While HDACis were historically identified on the basis of their ability to induce tumor cell differentiation (38, 39), induction of tumor cell apoptosis is the biological outcome most often reported (40).”
• Chemoproteomics profiling of HDAC inhibitors reveals selective targeting of HDAC complexes (2011, background): “This increases the risk of toxic liabilities and also limits the use of these compounds as research tool”
• EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition. (2013, background): “Vorinostat has been shown to induce the expression of several genes other than BIM (13).”
• HDAC family: What are the cancer relevant targets? (2009, background): “The activity of HDAC inhibitors on cancer cells have been extensively reviewed elsewhere and it is now generally accepted that these compounds have a broad spectrum of anti-tumoral activity against a variety of cancer cells in cell culture and animal models [82,83].”
• Combination Epigenetic Therapy Has Efficacy in Patients with Refractory Advanced Non Small Cell Lung Cancer (2011, background): “Other classes of HDACs shuttle between the nucleus and cytoplasm, or are predominantly cytoplasmic, and target a much broader array of protein targets (17, 18).”
• The TRAIL apoptotic pathway in cancer onset, progression and therapy (2008, background): “Histone deacetylase inhibitors (HDACi) are promising new anticancer agents that can induce tumour cell apoptosis, inhibit cell proliferation by blocking progression through the G1 or G2/M phases of the cell cycle, induce cellular differentiation, suppress angiogenesis and modulate anti-tumour immuni”
• Histone Deacetylase Inhibitors: Overview and Perspectives (2007, background): “HDAC2 and HDAC3 proteins are increased in colon cancer samples (1, 2, 5, 27).”