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This research aims to identify the pathways driving resistance in BRAFV600E pediatric gliomas and to highlight actionable therapeutics.

November 1, 2025Neuro-OncologyOpen Access

DDDR-83. Dynamic kinome reprogramming drives resistance to treatments in BRAFV600E pediatric gliomas, revealing actionable therapeutic vulnerabilities

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Functional kinome mapping reveals treatment efficacy and druggability in gliomas, indicating potential therapeutic vulnerabilities.

This research aims to identify the pathways driving resistance in BRAFV600E pediatric gliomas and to highlight actionable therapeutics.
Characterized phospho-signaling circuits in pediatric tumors, mouse models, and cell models before and after treatment
Compared kinase activity signatures post dabrafenib and trametinib treatment
Utilized single-cell RNA sequencing for tissue profiling
Assessed druggability of candidate pathways in combination strategies
Identified feedback activation of RTKs like EGFR after BRAF+MEK inhibition
Found potential drugs that synergize with dabrafenib and trametinib
Demonstrated pathways that enforce tumor survival and proliferation
Proposed novel treatment combinations to improve outcomes in BRAFV600E gliomas

Panovska et al. (2025) studied this question.

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