STANDARD_NAME	WANG_ESOPHAGUS_CANCER_VS_NORMAL_DN
SYSTEMATIC_NAME	M12212
COLLECTION	C2:CGP
MSIGDB_URL	https://www.gsea-msigdb.org/gsea/msigdb/human/geneset/WANG_ESOPHAGUS_CANCER_VS_NORMAL_DN
NAMESPACE	HUMAN_GENE_SYMBOL
DESCRIPTION_BRIEF	Down-regulated genes specific to esophageal adenocarcinoma (EAC) relative to normal tissue.
DESCRIPTION_FULL	To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.
PMID	16449976
GEOID	
AUTHORS	Wang S,Zhan M,Yin J,Abraham JM,Mori Y,Sato F,Xu Y,Olaru A,Berki AT,Li H,Schulmann K,Kan T,Hamilton JP,Paun B,Yu MM,Jin Z,Cheng Y,Ito T,Mantzur C,Greenwald BD,Meltzer SJ
CONTRIBUTOR	Arthur Liberzon
CONTRIBUTOR_ORG	MSigDB Team
EXACT_SOURCE	Table 2S: Fold change < 1
FILTERED_BY_SIMILARITY	
EXTERNAL_NAMES_FOR_SIMILAR_TERMS	
EXTERNAL_DETAILS_URL	
SOURCE_MEMBERS	ACAA1,ACOX1,ADIPOR1,ADK,ALDH1A3,ALDH3A1,ALDH4A1,AMFR,AP3S1,ARF3,ARL7,ARRD3,ASCC1,ATXN3,BENE,C10orf116,C9orf60,CAPNS1,CAST,CDK7,CNN3,CR2,CRYAB,CS,DDX3X,DKFZp566E144,DNAJB1,DUSP5,DUSP7,EPHX1,EREG,FLJ11193,FOSL2,FPGT,FUT1,GAN15,GJB2,GM2A,GOLGA2,GPC1,GPR109B,GPX3,GTF3C1,hCDCrel-1,HECTD1,IGFBP2,IMPA1,KCNK5,KIAA0830,KIF1C,KIK5,KRT5,MAL,MAPKAPK3,MGC11335,MLLT4,MOSPD3,NALP2,NCOA1,NCOA3,NRBP,NRP1,NSDHL,NUCB2,OXCT1,PCL1,PDCD4,PGAM1,PGF,PITPNA,PLXNC1,PMM1,PPP2R2C,PPP4R1,PRDX6,RAB6A,RABGGTA,RAC1,RAPA2,RFP2,RHF1,RPP30,RRO1L,RXRA,S100A11,S100A12,SEPT8,SH3GL1,SHMT1,SIAT7B,SLC16A6,SLC1A3,SLC26A2,SLC27A4,SLC9A3R1,STAT4,STIM1,STK17B,STK38,SYNGY3,TBC1D10,TEF3,TIAM1,TM4SF6,TM4SF9,TXNL5,UPP1,WWP1,YWHAQ
GENE_SYMBOLS	ACAA1,ACOX1,ADIPOR1,ADK,ALDH1A3,ALDH3A1,ALDH4A1,AMFR,AP3S1,ARF3,ARL4C,,ASCC1,ATXN3,MALL,ADIRF,ZER1,CAPNS1,CAST,CDK7,CNN3,CR2,CRYAB,CS,DDX3X,REXO2,DNAJB1,DUSP5,DUSP7,EPHX1,EREG,C5orf22,FOSL2,FPGT,FUT1,,GJB2,GM2A,GOLGA2,GPC1,HCAR3,GPX3,GTF3C1,HECTD1,IGFBP2,IMPA1,KCNK5,ENDOD1,KIF1C,,KRT5,MAL,MAPKAPK3,GFOD2,AFDN,MOSPD3,NLRP2,NCOA1,NCOA3,NRBP1,NRP1,NSDHL,NUCB2,OXCT1,PHF1,PDCD4,PGAM1,PGF,PITPNA,PLXNC1,PMM1,PPP2R2C,PPP4R1,PRDX6,RAB6A,RABGGTA,RAC1,,TRIM13,,RPP30,,RXRA,S100A11,S100A12,SEPTIN8,SH3GL1,SHMT1,ST6GALNAC2,SLC16A6,SLC1A3,SLC26A2,SLC27A4,NHERF1,STAT4,STIM1,STK17B,STK38,,TBC1D10A,TRIM37,TIAM1,TSPAN6,TSPAN5,TXNDC17,UPP1,WWP1,YWHAQ,
FOUNDER_NAMES