Publication date: April 2017
Source:Human Pathology, Volume 62
Author(s): Christine Sempoux, Bettina Bisig, Gabrielle Couchy, Charles Balabaud, Jessica Zucman-Rossi, Paulette Bioulac-Sage
In 1984, a 24-year-old woman underwent a right hepatectomy after a 17-cm nodule, diagnosed as a hepatocellular adenoma with some atypia. The resection was incomplete. Follow-up was interrupted. In 1996, a computed tomographic scan revealed a large multifocal hepatocellular carcinoma confirmed on biopsies. The patient died the same year. We reviewed these nodules using immunohistochemistry and gene sequencing. C-reactive protein was overexpressed in the tumor resected in 1984. Glutamine synthetase was heterogeneous in the tumor, with a few tumor nuclei expressing β-catenin. Glypican and heat shock protein 70 were negative. In this β-catenin–activated inflammatory hepatocellular adenoma, S45 β-catenin–activating mutation was detected on fixed tissue, embedded in paraffin without TERT promoter mutation. An identical CTNNB1 mutation was identified in the 1996 liver tumor together with a TERT promoter mutation showing that this hepatocellular carcinoma results from the malignant transformation of the initial β-catenin inflammatory adenoma.
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Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00302841026182,00306932607174,alsfakia@gmail.com,
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Πέμπτη 16 Μαρτίου 2017
Malignant transformation of a β-catenin inflammatory adenoma due to an S45 β-catenin–activating mutation present 12 years before
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