The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules.
In: ISSN: 0168-8278, 2008
Online
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Zugriff:
International audience ; 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.
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The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules.
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Autor/in / Beteiligte Person: | Rebouissou, Sandra ; Couchy, Gabrielle ; Libbrecht, Louis ; Balabaud, Charles ; Imbeaud, Sandrine ; Auffray, Charles ; Roskams, Tania ; Bioulac-Sage, Paulette ; Zucman-Rossi, Jessica ; Génomique Fonctionnelle des Tumeurs Solides (U1162) ; Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM) ; Institut Universitaire d'Hématologie (IUH) ; Université Paris Diderot - Paris 7 (UPD7) ; Liver Research Unit of the Laboratory of Morphology and Molecular Pathology ; Catholic University of Leuven = Katholieke Universiteit Leuven (KU Leuven) ; Fibrose hépatique et cancer du foie ; Université Bordeaux Segalen - Bordeaux 2-IFR66-Institut National de la Santé et de la Recherche Médicale (INSERM) ; d'Hépato-Gastro-Entérologie, Service ; CHU Bordeaux-Hôpital Saint-André ; Génomique Fonctionnelle et Biologie Systémique pour la Santé ; Centre National de la Recherche Scientifique (CNRS) ; Centre de génétique moléculaire (CGM) ; Service de pathologie Bordeaux ; Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux-Groupe hospitalier Pellegrin ; Inserm (Réseaux de recherche clinique et réseaux de recherche en santé des populations), the comité Dordogne de la Ligue contre le Cancer, the SNFGE and the program “Carte d'identité des tumeurs” by the ligue Nationale Contre le Cancer. SR is supported by a Ligue Nationale Contre le Cancer doctoral fellowship. |
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Zeitschrift: | ISSN: 0168-8278, 2008 |
Veröffentlichung: | HAL CCSD ; Elsevier, 2008 |
Medientyp: | academicJournal |
DOI: | 10.1016/j.jhep.2008.03.013 |
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