ABSTRACT Pediatric low‐grade gliomas (pLGG) are the predominant childhood central nervous system tumors. While BRAF alterations are known to drive the majority of pLGGs, a subgroup contains activating mutations or fusions involving FGFR1/2/3 . FGFR is a receptor tyrosine kinase that plays a crucial role in cell growth, differentiation, and survival through interactions with fibroblast growth factors. Furthermore, FGFR has been shown to interact with the RAS/MAPK, PI3K/AKT, and JAK/STAT pathways. The current understanding of the biological behavior, clinical trajectory, and effectiveness of targeted inhibition in FGFR ‐altered gliomas is notably limited. We sought to define the epidemiologic characteristics, molecular features, radiographic and histologic characteristics, and clinical course of patients with FGFR ‐altered pLGGs. We also explored the therapeutic implications of these abnormalities in pediatric cases and highlight both current and emerging treatment strategies for pediatric patients with FGFR ‐altered cancers.
Posorske et al. (Wed,) studied this question.
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