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

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

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)235-239
Number of pages5
JournalVirchows Archiv
Volume473
Issue number2
DOIs
Publication statusPublished - Aug 1 2018

Keywords

  • CTNNB1
  • LEF1
  • Sinonasal glomangiopericytoma
  • β-catenin

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

Fingerprint

Dive into the research topics of 'β-catenin (CTNNB1) mutation and LEF1 expression in sinonasal glomangiopericytoma (sinonasal-type hemangiopericytoma)'. Together they form a unique fingerprint.

Cite this