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β-catenin accumulation and mutation of the CTNNB1 gene in hepatoblastoma

✍ Scribed by Hendrik Bläker; Walter J. Hofmann; Ralf J. Rieker; Roland Penzel; Matthias Graf; Herwart F. Otto

Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
275 KB
Volume
25
Category
Article
ISSN
1045-2257

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✦ Synopsis

Hepatoblastoma is a rare malignant tumor of the liver that occurs in children at an average age of 2 to 3 years. Epidemiologic studies have shown an increased frequency of this tumor type in families affected by adenomatous polyposis coli. In addition to the epidemiologic data, molecular genetic studies suggest that inactivation of the APC tumor suppressor may be involved in hepatoblastoma tumorigenesis. A major function of APC is the downregulation of ␤-catenin, a transcription-activating protein with oncogenic potential. In an ongoing immunohistochemical study of ␤-catenin expression in sporadic cases of tumor types that are associated with adenomatous polyposis coli, we observed increased ␤-catenin levels in the cytoplasm and in the nuclei of three investigated hepatoblastomas. Sequencing of exon 3 of the ␤-catenin gene (CTNNB1) revealed an activating mutation in one of the tumor samples. Our data indicate for the first time that ␤-catenin accumulation may play a role in the development of hepatoblastoma and that activating mutations of the ␤-catenin gene may substitute biallelic APC inactivation in this tumor type.

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