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Series GSE88839 Query DataSets for GSE88839
Status Public on Oct 01, 2019
Title Large-scale gene expression profiling of hepatocellular adenomas
Organism Homo sapiens
Experiment type Expression profiling by array
Summary Hepatocellular adenomas (HCA) are rare benign tumors mainly developed in women after 2 years of oral contraceptive use (Rooks et al., 1979). HCA are also related to other risk factors (obesity, vascular diseases, androgen and alcohol intake) or to different genetic diseases (Mac Cune Albright syndrome, glycogen storage diseases type 1a and MODY3 diabetes caused by HNF1A germline mutation) (Calderaro et al., 2013; Nault et al., 2013a). Bleeding and malignant transformation to hepatocellular carcinoma (HCC) can occur as severe complications observed respectively in 30-50% and 5% of the cases. In the past 10 years, we identified 4 major molecular subgroups of HCA defined by (1) mutations inactivating HNF1A (H-HCA, 35% of the HCA) (Bacq et al., 2003; Bluteau et al., 2002; Jeannot et al., 2010), (2) activation of ß-catenin by mutations in exon 3 (bHCA, 15%) (Chen et al., 2002), (3) inflammatory phenotype with STAT3 activation (IHCA, 50%) (Bioulac-Sage et al., 2009; Zucman-Rossi et al., 2006), (4) a tumor subgroup of HCA with Sonic Hedgehog pathway activation due to recurrent focal deletions (shHCA) (Nault et al. ,in preparation) and (5) the remaining unclassified tumors (UHCA, 10%) (Bioulac-Sage et al., 2009). Among bHCA, half displayed both inflammatory and ß-catenin activated phenotypes (bIHCA). Inflammatory adenomas (IHCA) are caused by IL6ST somatic mutation activating gp130 in 60% of the cases (Rebouissou et al., 2009) whereas other IHCA are mutated for STAT3 itself (Pilati et al., 2011) or GNAS (Nault et al., 2012) but in the remaining 30% cases no mutation (NM) were identified yet. This molecular classification is currently accepted in clinical practice using either immunohistochemical markers (Bioulac-Sage et al., 2009; Bioulac-Sage et al., 2007) or in radiology at MRI (Laumonier et al., 2008) and it has dramatically improved the diagnosis and prognostic assessment of HCA. HCC derived from HCA malignant transformation (HCC on HCA, 5%)
 
Overall design HCA liver tumors corresponding to 35 patients. In all cases, tumor samples were frozen (-80°C) after hepatic resection at diagnosis. Normal liver samples were used as reference samples. Comparative gene expression analysis was done using Affymetrix U133plus v2 array (GPL570)
 
Contributor(s) Zucman-Rossi J, Calderaro J, Caruso S, Couchy G, Imbeaud S, Letouzé E, Nault J, Pilati C, Rebuissou S
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Submission date Oct 17, 2016
Last update date Oct 02, 2019
Contact name Sandrine Imbeaud
E-mail(s) sandrine.imbeaud@inserm.fr
Phone +33 (0)1 53 72 51 98
Organization name INSERM, UMR U-1162, Université Paris Descartes
Department Génomique Fonctionnelle des tumeurs solides
Street address 27 rue Juliette Dodu
City Paris
ZIP/Postal code 75010
Country France
 
Platforms (1)
GPL570 [HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array
Samples (38)
GSM2349974 CHC469N (normal liver)
GSM2349975 CHC562N (normal liver)
GSM2349976 CHC934N (normal liver)
Relations
BioProject PRJNA348757

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE88839_RAW.tar 166.3 Mb (http)(custom) TAR (of CEL)
Raw data provided as supplementary file
Processed data included within Sample table

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