| Literature DB >> 29736797 |
Yuka Suzuki1, Shu Ichihara2, Tomonori Kawasaki2, Hiroyuki Yanai3, Satoshi Kitagawa4, Yoshie Shimoyama1, Shigeo Nakamura1, Masato Nakaguro5.
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.Entities:
Keywords: CTNNB1; LEF1; Sinonasal glomangiopericytoma; β-catenin
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Year: 2018 PMID: 29736797 DOI: 10.1007/s00428-018-2370-9
Source DB: PubMed Journal: Virchows Arch ISSN: 0945-6317 Impact factor: 4.064