From Molecular Alterations to the Targeted Therapy: Treatment of Thalamic Glioma in Pediatric Patients

TL;DR

This paper discusses how molecular alterations in thalamic gliomas can guide targeted therapies for better outcomes in pediatric patients.

Contribution

The paper highlights specific molecular mutations and their relevance to targeted therapy in pediatric thalamic gliomas.

Findings

Thalamic gliomas are categorized into DMG and LGG with distinct molecular alterations.

EGFR mutations are common in bithalamic high-grade gliomas, making them a unique group.

Targeted therapies like tyrosine kinase inhibitors improve survival in some cases.

Abstract

Thalamic gliomas are among the most challenging pediatric brain tumors due to the delicate functions of the thalamus. Limited surgical intervention leads to the use of adjuvant therapies, including targeted therapy. Thalamic gliomas can be divided into two distinct groups: diffuse midline glioma (DMG) and low-grade glioma (LGG). The most common mutations that can be targeted for treatment are the KIAA1549-BRAF fusion; BRAF V600E mutation; EGFR, FGFR, PDGFR, NTRK, and CDK4/6 mutations; other MAP kinase pathway alterations; and PI3K/AKT/mTOR activation. The bithalamic high-grade glioma especially demonstrates EGFR mutations which makes it a distinct entity. Targeted therapy, including tyrosine kinas inhibitors has been shown to improve the overall survival compared to conventional therapy in certain situations. Demonstrating the mutation carried by the tumor is very critical in this regard. The purpose of this article is to focus on the treatment of thalamic glioma in pediatric patients in light of molecular information.

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