Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Cavard Agilent


ABSTRACT: Through the combined use of glutamine synthase / GLUL immunostaining, and CTNNB1 genotyping, we previously analyzed nearly 200 hepatocellular carcinomas (HCC). Little was reported on HCC with mutant B-catenin excepted their low genomic instability, their lack of association with hepatitis B virus and their well-differentiated pattern. We have demonstrated that HCC with mutant B-catenin exhibit specific features such as an homogeneous well differentiated pattern with a mixture of microtrabecular and acinar architecture, the absence of steatosis and the presence of frequent extra-cellular cholestasis. The aim of our study was to characterize the bile components in HCC with mutant B-catenin. To this end, we carried out transcriptome profiling of five typical B-catenin activated HCCs and we analysed the composition of the bile accumulated in these tumors. The transcriptional analysis of these tumors showed overexpression of genes belonging both to the synthesis (CYP7A1, CYP27A1 and CYP7B1) and transport (ABCG2/BCRP, ABCC2/MRP2, ABCB11/BSEP, OATP8/SLC01B3) of bile acids. However, the composition of bile in these tumors is not significantly modified. The large amount of bilirubin in these tumors follows the increase in biliverdin pigment reflecting the characteristic green color of these tumors and biliary acids content is not profoundly altered. Surprisingly, the main change affects the non-tumoral counterparts of HCC with mutant B-catenin which display an unexpected high content in biliary acids. These observations suggest that increased bile acids level due to an underlying pathology may play a role in the emergence of HCC with mutant B-catenin.

ORGANISM(S): Homo sapiens

SUBMITTER: florent dumont 

PROVIDER: E-MEXP-2821 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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