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07.05.2018 | Brief Report

β-catenin (CTNNB1) mutation and LEF1 expression in sinonasal glomangiopericytoma (sinonasal-type hemangiopericytoma)

verfasst von: Yuka Suzuki, Shu Ichihara, Tomonori Kawasaki, Hiroyuki Yanai, Satoshi Kitagawa, Yoshie Shimoyama, Shigeo Nakamura, Masato Nakaguro

Erschienen in: Virchows Archiv | Ausgabe 2/2018

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Abstract

Sinonasal glomangiopericytoma (SN-GPC) is an uncommon mesenchymal tumor with myoid differentiation. Recently, mutations in exon 3 of the gene coding for β-catenin (CTNNB1) and its nuclear expression were discovered in SN-GPC. β-catenin protein is a key regulatory molecule of the canonical Wnt signaling pathway. The expression of β-catenin target proteins is not well characterized in SN-GPC. We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.
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Metadaten
Titel
β-catenin (CTNNB1) mutation and LEF1 expression in sinonasal glomangiopericytoma (sinonasal-type hemangiopericytoma)
verfasst von
Yuka Suzuki
Shu Ichihara
Tomonori Kawasaki
Hiroyuki Yanai
Satoshi Kitagawa
Yoshie Shimoyama
Shigeo Nakamura
Masato Nakaguro
Publikationsdatum
07.05.2018
Verlag
Springer Berlin Heidelberg
Erschienen in
Virchows Archiv / Ausgabe 2/2018
Print ISSN: 0945-6317
Elektronische ISSN: 1432-2307
DOI
https://doi.org/10.1007/s00428-018-2370-9

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