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Dabrafenib and trametinib in BRAFV600E mutated glioma
Nicholas F Brown1,2, Thomas Carter1,2, Neil Kitchen3
1Department of Oncology, University College London Hospitals, 250 Euston Road, London, NW1 2PG, UK.
Abstract:
BRAFV600E mutations have been identified in a number of glioma subtypes, most frequently in pleomorphic xanthoastrocytoma, ganglioglioma, pilocytic astrocytoma, and epithelioid glioblastoma. Although the development of BRAF inhibitors has dramatically improved the clinical outcome for patients with BRAFV600E mutant tumors, resistance develops in a majority of patients due to reactivation of the MAPK pathway. Addition of MEK inhibition to BRAF inhibition improves survival. Here we report successful treatment of two patients with BRAFV600E mutant pleomorphic xanthoastrocytoma using the BRAF inhibitor dabrafenib in combination with the MEK inhibitor trametinib.
Insights
BRAFV600E-mutant pleomorphic xanthoastrocytoma can be effectively treated with combined BRAF and MEK inhibitors. This combination therapy, using dabrafenib and trametinib, offers a promising approach for patients with this rare glioma subtype.
Area of Science:
- Neuro-oncology
- Molecular oncology
- Genetics
Background:
- BRAFV600E mutations are prevalent in specific glioma subtypes, including pleomorphic xanthoastrocytoma.
- BRAF inhibitors improve outcomes for BRAFV600E-mutant tumors, but resistance frequently emerges via MAPK pathway reactivation.
- Combined BRAF and MEK inhibition enhances survival in BRAFV600E-mutant cancers.
Observation:
- Two patients with BRAFV600E-mutant pleomorphic xanthoastrocytoma were treated.
- Treatment involved the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib.
Findings:
- Successful treatment outcomes were achieved in both patients.
- The combination therapy demonstrated efficacy in managing BRAFV600E-mutant pleomorphic xanthoastrocytoma.
Implications:
- Combined BRAF and MEK inhibition is a viable therapeutic strategy for BRAFV600E-mutant pleomorphic xanthoastrocytoma.
- This approach may overcome resistance mechanisms associated with single-agent BRAF inhibition.
- Further investigation into this combination therapy for rare gliomas is warranted.
