Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer

By S. Minucci, Pier Giuseppe Pelicci. Nature Reviews. Cancer, 2006

2,200 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/490ac41cd1fbdf4d57fdbd6a58f4179ad413a5be

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Citations in the corpus

Cancer epigenetics: from mechanism to therapy. (2012, background): “Indeed, some of the approved drugs (against HDACs) have little enzyme specificity, and their mechanism of action remains contentious (Minucci and Pelicci, 2006).”
Transcriptional control of human p53-regulated genes (2008, background): “The strongest evidence to support the idea that post-translational modifications of p53 are relevant to the p53 regulatory mechanism is the fact that HDAC inhibitors have been shown to simultaneously increase levels of acetylated p53 and induce apoptosis and senescence in cancerous and normal cell”
HATs and HDACs: from structure, function and regulation to novel strategies for therapy and prevention (2007, background): “Many pharmaceutical companies have active programs on related inhibitors that target the classical family of HDACs (for recent reviews, see Minucci and Pelicci, 2006; Marchion and Munster, 2007; Rasheed et al., 2007).”
Covalent histone modifications: miswritten, misinterpreted, and miserased in human cancers (2010, result): “In support, the clinical success of HDAC inhibitors in cutaneous T cell lymphoma and DNA demethylating agents in myelodysplastic syndrome offers a compelling argumen”
Histone Deacetylase Inhibitors: Overview and Perspectives (2007, background): “HDACi: Mechanisms of Action The mechanisms of HDACi-induced transformed cell growth arrest and cell death are complex and not completely elucidated (1, 4-8).”
Targeting polyamine metabolism and function in cancer and other hyperproliferative diseases (2007, background): “Among the most interesting agents are the various class I/II histone deacetylase inhibitors (HDACIs”
Discovery and development of SAHA as an anticancer agent (2007, background): “…and (C) the expression of proteins (e.g. Trx), which modulate the accumulation of reactive oxygen species (ROS) facilitated cell death (Johnstone and Licht, 2003; Rosato et al., 2003a; Shao et al., 2004; Bhalla, 2005; Dokmanovic and Marks, 2005; Minucci and Pelicci, 2006; Yoo and Jones, 2006).”
The epigenomics of cancer. (2007, background): “The demonstration that histone deacetylase inhibitors have antitumor potential (Marks et al., 2001; Minucci and Pelicci, 2006) has led to the development of a series of inhibitors.”