2014
DOI: 10.18632/oncotarget.2289
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Abstract: Epigenetic modifications, like histone acetylation, are essential for regulating gene expression within cells. Cancer cells acquire pathological epigenetic modifications resulting in gene expression patterns that facilitate and sustain tumorigenesis. Epigenetic manipulation therefore is emerging as a novel targeted therapy for cancer. Histone Acetylases (HATs) and Histone Deacetylases (HDACs) regulate histone acetylation and hence gene expression. Histone deacetylase (HDAC) inhibitors are well known to affect … Show more

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Cited by 145 publications
(132 citation statements)
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“…HDAC inhibitors upregulate MHCI antigen presentation of natural killer (NK) ligands on tumor cells but may have repressive effects on other immune subsets (64). Polycomb repression of chromatin, linked to neoplastic processes in Ewing, synovial, and rhabdomyosarcomas is also critical for stable lineage commitments and T-cell tolerance, with loss of function contributing to depletion of regulatory T cells and activation of effector T cells (65,66).…”
Section: The Cutting Edge: Interface Between Immuno-oncology and Precmentioning
confidence: 99%
“…HDAC inhibitors upregulate MHCI antigen presentation of natural killer (NK) ligands on tumor cells but may have repressive effects on other immune subsets (64). Polycomb repression of chromatin, linked to neoplastic processes in Ewing, synovial, and rhabdomyosarcomas is also critical for stable lineage commitments and T-cell tolerance, with loss of function contributing to depletion of regulatory T cells and activation of effector T cells (65,66).…”
Section: The Cutting Edge: Interface Between Immuno-oncology and Precmentioning
confidence: 99%
“…Such side effects have, to some extent, discouraged pursuit of HDACi as therapies for chronic inflammatory diseases (Gupta et al, 2012), where safe, longterm therapeutic regimenes are required. HDACi immunomodulatory properties are complex (Bode and Dalpke, 2011;Kroesen et al, 2014) and not simply anti-inflammatory (Leoni et al, 2002;Grabiec et al, 2008;Halili et al, 2009;Fairlie and Sweet, 2012). Treatment of mouse macrophages with Trichostatin downregulates many inflammatory genes, thus compromising host defense (Roger et al, 2011), whereas they can also upregulate proinflammatory genes and promote cytokine secretion (Wang et al, 2011;Kroesen et al, 2014).…”
Section: Introductionmentioning
confidence: 99%
“…HDACi immunomodulatory properties are complex (Bode and Dalpke, 2011;Kroesen et al, 2014) and not simply anti-inflammatory (Leoni et al, 2002;Grabiec et al, 2008;Halili et al, 2009;Fairlie and Sweet, 2012). Treatment of mouse macrophages with Trichostatin downregulates many inflammatory genes, thus compromising host defense (Roger et al, 2011), whereas they can also upregulate proinflammatory genes and promote cytokine secretion (Wang et al, 2011;Kroesen et al, 2014). Indeed, we previously showed that Trichostatin differentially regulates many inflammatory and proarthritic genes in human and mouse macrophages in response to toll-like receptor 4 stimulation Schroder et al, 2012), suggesting therapeutic effects of HDACi in arthritis, but also potentially adverse reactions.…”
Section: Introductionmentioning
confidence: 99%
“…More recently, HDACi have been studied for their ability to enhance the efficacy of cancer immunotherapies. Somewhat counter-intuitively, HDACi were initially reported to exert anti-inflammatory effects [52]; however, there is emerging evidence supporting the immune stimulating effects of HDACi and their potential utility when applied in combination with existing immunotherapy platforms (reviewed in [53]). HDACi can directly affect tumor cell recognition by T cells by increasing tumor cell expression of MHC (I and II) and costimulatory molecules, as well as by enhancing the function of the antigen processing/presentation machinery in tumor cells [53].…”
Section: Hdac Inhibitorsmentioning
confidence: 99%
“…Somewhat counter-intuitively, HDACi were initially reported to exert anti-inflammatory effects [52]; however, there is emerging evidence supporting the immune stimulating effects of HDACi and their potential utility when applied in combination with existing immunotherapy platforms (reviewed in [53]). HDACi can directly affect tumor cell recognition by T cells by increasing tumor cell expression of MHC (I and II) and costimulatory molecules, as well as by enhancing the function of the antigen processing/presentation machinery in tumor cells [53]. Selective HDAC6 inhibition results in hyper-acetylation of HSP90 and to an inhibition in its chaperone activity [54,55], suggesting HDAC6i may mimic HSP90i in enhancing the antitumor efficacy of DC-based vaccines future science group Review Fecek & Storkus (see above).…”
Section: Hdac Inhibitorsmentioning
confidence: 99%