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Neuropathology. 2016 Oct;36(5):448-455. doi: 10.1111/neup.12293. Epub 2016 Mar 2.

Gliosarcomas lack BRAFV600E mutation, but a subset exhibit β-catenin nuclear localization.

Author information

1
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA.
2
Department of Pathology, University of California-San Francisco, San Francisco, CA, USA.
3
Department of Neurosurgery, Washington University School of Medicine, St. Louis, MO, USA.
4
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA.

Abstract

Gliosarcoma (GS) is a rare subtype of glioblastoma (GBM) characterized by both glial and mesenchymal components. Unlike GBM, there are no specific prognostic markers, and optimized treatments for patients with GS do not exist. Recent reports describe BRAFV600E mutation in malignant peripheral nerve sheath tumors, and aberrant Wnt signaling and CTNNB1 (β-catenin gene) mutations have been described in GBM. We sought to determine whether GS tumors harbor BRAFV600E mutations or aberrant Wnt signaling, as indicated by nuclear localization of β-catenin, by immunohistochemical detection. Forty-eight (48) cases of primary and secondary adult GS (including recurrent ones) were evaluated by immunohistochemical techniques for the presence of nuclear β-catenin and the BRAFV600E mutation. A small subset (6/46, 13%) showed nuclear localization of β-catenin. None of the cases harbored BRAFV600E mutations (0/48). These results are the first to describe the presence of Wnt signaling pathway abnormalities, manifested by nuclear β-catenin, in a subset, as well as the lack of BRAFV600E mutation in GS. We propose a potential role for Wnt pathway alterations in the pathogenesis of a subset of GS.

KEYWORDS:

BRAF-V600E; WNT pathway; beta-catenin; glioblastoma; gliosarcoma

PMID:
26932501
DOI:
10.1111/neup.12293
[Indexed for MEDLINE]

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