The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules.
(2008) Journal of Hepatology — Vol. 49, n° 1, p. 61-71 (2008)
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- 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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Rebouissou, S., Couchy, G., Libbrecht, L., Balabaud, C., Imbeaud, S., Auffray, C., Roskams, T., Bioulac-Sage, P., & Zucman-Rossi, J. (2008). The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules. Journal of Hepatology, 49(1), 61-71. https://doi.org/10.1016/j.jhep.2008.03.013 (Original work published 2008)