Histone deacetylases and cancer: causes and therapies

By PA Marks, R. Rifkind, V. Richon, R. Breslow, Thomas A. Miller, W. Kelly. Nature Reviews. Cancer, 2001

1,931 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/683f4446614b4f456790404097f7c628c0a2cb07

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Citations in the corpus

Pathogenesis of Human Papillomaviruses in Differentiating Epithelia (2004, background): “proteins are localized exclusively to the nucleus (100).”
Histone-deacetylase inhibitors: novel drugs for the treatment of cancer (2002, background): “gov/cancer_information/cancer_type/leukemia/">leukaemias and solid tumours to express differentiated characteristics and stop proliferatin”
Modulation of NF‐κB‐dependent transcription and cell survival by the SIRT1 deacetylase (2004, background): “The SIRT1 paradox: pro-survival or pro-death The maintenance of HDAC activity provides a survival and growth advantage in some types of cancers (Marks et al, 2001).”
SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells (2004, background): “In the past few years, much progress has been made towards a better understanding of the molecular mechanisms of CRC and HCC, including the role of histone modificatio”
Histone Deacetylase Inhibitors: Overview and Perspectives (2007, background): “HDAC2 and HDAC3 proteins are increased in colon cancer samples (1, 2, 5, 27).”
Epigenetic Determinants of Cancer. (2016, background): “Some of these, such as 4-phenylbutyrate or valproic acid (VPA), have been in clinical use to treat other conditions for some time (Marks et al. 2001; Richon and O’Brien 2002), whereas newer ones are now in clinical trials.”
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.”
Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy (2006, background): “Also, alterations in chromatin structure, for example, chromatin condensation because of histone deacetylation, may block transcription by preventing the access of transcription factors to the DNA (Marks et al., 2001).”
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.”