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Your search keyword '"Libbrecht, Louis"' showing total 13 results
Start Over Author "Libbrecht, Louis" Journal journal of hepatology
13 results on '"Libbrecht, Louis"'

5. The placental growth factor as a target against hepatocellular carcinoma in a diethylnitrosamine-induced mouse model

Author

Heindryckx, Femke, primary, Coulon, Stephanie, additional, Terrie, Ellen, additional, Casteleyn, Christophe, additional, Stassen, Jean-Marie, additional, Geerts, Anja, additional, Libbrecht, Louis, additional, Allemeersch, Joke, additional, Carmeliet, Peter, additional, Colle, Isabelle, additional, and Van Vlierberghe, Hans, additional

Published
2013
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6. Molecular characterization of hepatocellular adenomas developed in patients with glycogen storage disease type I

Author

Calderaro, Julien, primary, Labrune, Philippe, additional, Morcrette, Guillaume, additional, Rebouissou, Sandra, additional, Franco, Dominique, additional, Prévot, Sophie, additional, Quaglia, Alberto, additional, Bedossa, Pierre, additional, Libbrecht, Louis, additional, Terracciano, Luigi, additional, Smit, G. Peter A., additional, Bioulac-Sage, Paulette, additional, and Zucman-Rossi, Jessica, additional

Published
2013
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13. The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules.

Author

Rebouissou S, Couchy G, Libbrecht L, Balabaud C, Imbeaud S, Auffray C, Roskams T, Bioulac-Sage P, and Zucman-Rossi J

Subjects
Adult, Aged, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular pathology, Carcinoma, Hepatocellular physiopathology, Down-Regulation genetics, Extracellular Matrix genetics, Extracellular Matrix metabolism, Female, Focal Nodular Hyperplasia pathology, Humans, Liver Cirrhosis metabolism, Liver Cirrhosis pathology, Liver Cirrhosis physiopathology, Liver Neoplasms metabolism, Liver Neoplasms pathology, Liver Neoplasms physiopathology, Male, Middle Aged, RNA, Messenger metabolism, Reverse Transcriptase Polymerase Chain Reaction, Up-Regulation genetics, Focal Nodular Hyperplasia metabolism, Focal Nodular Hyperplasia physiopathology, Gene Expression Profiling, beta Catenin genetics, beta Catenin metabolism
Abstract

Background/aims: Focal nodular hyperplasias (FNHs) are benign liver lesions considered to be a hyperplastic response to increased blood flow in normal liver. In contrast, FNH-like lesions/nodules occur in cirrhotic liver but share similar histopathological features. We conducted a transcriptome analysis to identify biological pathways deregulated in FNH., Methods: Gene expression profiles obtained in FNH and normal livers were compared. Differentially-expressed genes were validated using quantitative-RT-PCR in 70 benign liver tumors including FNH-like lesions., Results: Among the deregulated genes in FNHs, 19 displayed physiological restricted distribution in the normal liver. All six perivenous genes were up-regulated in FNH, whereas 13 periportal genes were down-regulated. Almost all these genes are known to be regulated by beta-catenin. Glutamine synthetase was markedly overexpressed in anastomosed areas usually centered on visible veins. Moreover, activated hypophosphorylated beta-catenin protein accumulated in FNH in the absence of activating mutations. These results suggest the zonated activation of the beta-catenin pathway in FNH, whereas the other benign hepatocellular tumors, including FNH-like lesions, demonstrated an entirely different pattern of beta-catenin expression., Conclusions: In FNH, increased activation of the beta-catenin pathway was found restricted to enlarged perivenous areas. FNH-like nodules may have a different pathogenetic origin.

Published
2008
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