Biomarker-guided treatment strategies for patients with gliomas in clinical practice

Clicks: 13
ID: 332853
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #274 of 287 articles by views in journal of neuro-oncology

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 287 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Targeted therapy has made important contributions to improving outcomes for patients with many solid tumors, but has had only limited activity so far in patients with gliomas, notably glioblastoma. Failure of targeted therapy in glioblastoma is likely due to redundance of oncogenic pathway activation and so far the inability to identify suitable targets and apply biomarker-based enrichment strategies in clinical trial designs. In contrast, in non-glioblastoma tumors, there are promising developments which have already changed clinical practice: inhibition of mutant isocitrate dehydrogenase (IDH) exemplified by vorasidenib, the first approved drug specifically for IDH-mutant gliomas, has changed the landscape for targeted therapy of WHO grade 2 gliomas. Furthermore, dordaviprone, an antagonist of dopamine receptor D2/3 (DRD2/3) and an allosteric agonist of the mitochondrial protease caseinolytic mitochondrial matrix peptidase proteolytic subunit (ClpP), emerges as a potentially active agent in patients with recurrent K27M-mutant diffuse midline gliomas. Finally, BRAF mutations, neurotrophic tyrosine receptor kinase ( r fibroblast growth factor receptor (FGFR) gene fusions continue to raise interest as therapeutic targets at least for subsets of patients with gliomas. Almost no targeted therapy approaches for ependymomas have emerged. Improved clinical trial designs including shared control arms early on and using pharmacodynamic endpoints ideally in enriched patient populations are the path forward towards the identification of further active treatments for patients with gliomas.
Reference Key
openalex_W7222918487 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Émilie Le Rhun, Ingo K. Mellinghoff, Tobias Weiß, Marian Christoph Neidert, Wolfgang Wick, Michael Weller
Are you one of these authors? Claim your profile
Journal journal of neuro-oncology
Year 2026
DOI
10.1093/neuonc/noag238
URL
https://doi.org/10.1093/neuonc/noag238
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.