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Updated: Jan 21, 2026
Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures
Published on: January 9, 2019
Response of metastatic glioma to vemurafenib
Katie Emily Leaver1, Niushen Zhang1, Jennifer L Ziskin1
1Neuro Oncology, Stanford, California (L.R., R.P.T.); Neurology, Stanford, California (K.E.L., N.Z.); Neuropathology, Stanford University Medical Center, Palo Alto, California (J.L.Z., H.V.).
Abstract:
Extraneural metastatic disease of glioma is rare and poses unique therapeutic challenges. Increasingly, the ability to sequence genetic alterations in tumors has allowed for the identification of common oncogenic signatures such as the activating BRAF mutation and may be useful in therapeutic decision making. We report two patients with widespread aggressive gliomas whose tumors were found to express the BRAF mutation and then responded robustly albeit transiently when exposed to vemurafenib. Although both patients succumbed to their disease, our results suggest that targeting BRAF might be appropriate for patients with aggressive gliomas that express this mutation.
Insights
Aggressive gliomas with BRAF mutations may respond to targeted therapy. This study shows BRAF inhibition can be effective, though transiently, in patients with extraneural metastatic glioma.
Area of Science:
- Neuro-oncology
- Molecular oncology
- Genetics
Background:
- Extraneural metastatic disease in glioma is uncommon and presents significant therapeutic difficulties.
- Identifying common oncogenic alterations, like the BRAF mutation, through tumor genetic sequencing is becoming crucial for guiding treatment decisions.
Purpose of the Study:
- To report on two cases of aggressive gliomas with extraneural metastases.
- To investigate the efficacy of targeting the BRAF mutation in these patients.
Main Methods:
- Genetic sequencing of tumor samples to identify the BRAF mutation.
- Treatment of patients with vemurafenib, a BRAF inhibitor.
Main Results:
- Both patients' tumors harbored the activating BRAF mutation.
- Both patients demonstrated a robust, though temporary, response to vemurafenib treatment.
- Despite treatment, both patients ultimately succumbed to their aggressive glioma.
Conclusions:
- Targeting BRAF with inhibitors like vemurafenib may be a viable therapeutic strategy for patients with aggressive gliomas harboring this specific mutation.
- Further research is warranted to optimize BRAF-targeted therapies for glioma, potentially improving long-term outcomes.
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