Letter to the editor BRAF-V600E mutation in pediatric and adult glioblastoma

With the recent identification of the BRAF rearrangement/ duplication in pediatric pilocytic astrocytomas (PA),1–3 there has been renewed interest in the contribution of the BRAF gene to brain tumorigenesis. While the signature KIAA1549:BRAF fusion represents a common alteration in PA, activating mutations in the BRAF kinase gene (V600E) are more commonly observed in other glioma histological subtypes and malignancy grades. In this regard, we and others have previously found relatively few BRAF-V600E mutations in PA (,10 % cases),1–4 whereas BRAF-V600E mutations are frequently identified in pleomorphic xanthoastrocytomas (WHO grades II and III; 50%–65% cases),5–8 gangliogliomas (20%–75 % cases),6–10 and to a lesser frequency in diffuse gliomas,6,11 dysembryoplastic neuroepithelial tumors,10 desmoplastic infantile astrocytoma/ganglioglioma,10 and atypical teratoid/rhabdoid tumors arising in a background of either gangliogliomaor pleomorphic xanthoastrocytoma.7 In con-trast, approximately 5 % of adult high-grade gliomas, as well as a distinctive subset of adult diffuse low-grade gliomas, harbor BRAF-V600E mutations.6,11,12 Since most BRAF-V600E-positive glial neoplasmsareencountered inyoungpersons,we investigated the frequency of this mutation in pediatric high-grade gliomas. Immunohistochemical analyses were conducted using a BRAF-V600E-specific antibody on tissue microarrays containing pediatric gliomas from2different institutions (WashingtonUniver