Gene Set: MARKS_HDAC_TARGETS_UP

Standard name MARKS_HDAC_TARGETS_UP
Systematic name M8023
Brief description Genes whose transcription is up-regulated by histone deacetylase inhibitors.
Full description or abstract The path to the discovery of suberoylanilide hydroxamic acid (SAHA, vorinostat) began over three decades ago with our studies designed to understand why dimethylsulfoxide causes terminal differentiation of the virus-transformed cells, murine erythroleukemia cells. SAHA can cause growth arrest and death of a broad variety of transformed cells both in vitro and in vivo at concentrations that have little or no toxic effects on normal cells. It was discovered that SAHA inhibits the activity of histone deacetylases (HDACs), including all 11 known human class I and class II HDACs. HDACs have many protein targets whose structure and function are altered by acetylation including histones and non-histone proteins component of transcription factors controlling gene expression and proteins that regulate cell proliferation, migration and death. SAHA is in clinical trials and has significant anticancer activity against both hematologic and solid tumors at doses well tolerated by patients. A new drug application has been approved for SAHA (vorinostat) treatment of cutaneous T-cell lymphoma.
Collection C2: curated gene sets
      CGP: chemical and genetic perturbations
Source publication Pubmed 17322921   Authors: Marks PA
Exact source Table 2: Induced
Related gene sets (show 2 additional gene sets from the source publication)

(show 2 gene sets from the same authors)
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Organism Homo sapiens
Contributed by Arthur Liberzon (MSigDB Team)
Source platform HUMAN_GENE_SYMBOL
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Version history 3.0: First introduced

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