STANDARD_NAME	MARKS_HDAC_TARGETS_UP
SYSTEMATIC_NAME	M8023
COLLECTION	C2:CGP
MSIGDB_URL	https://www.gsea-msigdb.org/gsea/msigdb/human/geneset/MARKS_HDAC_TARGETS_UP
NAMESPACE	HUMAN_GENE_SYMBOL
DESCRIPTION_BRIEF	Genes whose transcription is up-regulated by histone deacetylase inhibitors.
DESCRIPTION_FULL	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.
PMID	17322921
GEOID	
AUTHORS	Marks PA
CONTRIBUTOR	Arthur Liberzon
CONTRIBUTOR_ORG	MSigDB Team
EXACT_SOURCE	Table 2: Induced
FILTERED_BY_SIMILARITY	
EXTERNAL_NAMES_FOR_SIMILAR_TERMS	
EXTERNAL_DETAILS_URL	
SOURCE_MEMBERS	APAF1,BAD,BAK1,BCL2L11,CASP3,CASP8,CASP9,CCNE1,CD95,DFFA,DR5,FAS,FASLG,GADD45B,GLRX,GSN,HIST3H2BB,MCM3,MT1L,RARB,TP53,TRAIL,TXN,TXNIP
GENE_SYMBOLS	APAF1,BAD,BAK1,BCL2L11,CASP3,CASP8,CASP9,CCNE1,FAS,DFFA,TNFRSF10B,FAS,FASLG,GADD45B,GLRX,GSN,H2BC26,MCM3,MT1L,RARB,TP53,TNFSF10,TXN,TXNIP
FOUNDER_NAMES