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Article

Tumor heterogeneity underlies clinical outcome and MEK inhibitor response in somatic NF1-mutant glioblastoma.

JCI insight - 23 Sept 2025

Pan Sixuan, Mirchia Kanish, Payne Emily, Liu S John, Al-Adli Nadeem, Peeran Zain, Shukla Poojan, Young Jacob S, Gupta Rohit, Wu Jasper, Pak Joanna, Ozawa Tomoko, Na Brian, Reddy Alyssa T, Braunstein Steve E, Phillips Joanna J, Chang Susan, Solomon David A, Perry Arie, Raleigh David R, Berger Mitchel S, Abate Adam R, Vasudevan Harish N

Abstract excerpt

Tumor suppressor NF1 is recurrently mutated in glioblastoma, leading to aberrant activation of Ras/rapidly accelerated fibrosarcoma (RAF)/MEK signaling. However, how tumor heterogeneity shapes the molecular landscape and efficacy of targeted therapies remains unclear. Here, we combined bulk and single-cell genomics of human somatic NF1-mutant, isocitrate dehydrogenase (IDH) wild-type glioblastomas with functional...

Read the complete abstract on PubMed

Topics

Glioblastoma
Humans
Animals
Mice
Neurofibromin 1

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Brain Neoplasms

Protein Kinase Inhibitors

Mutation

Cell Line, Tumor

Benzimidazoles

Cyclin-Dependent Kinase Inhibitor p16

Source

Open in PubMed Open full text

Identifiers

PMID: 40985888
DOI: 10.1172/jci.insight.192658
PMCID: PMC12487855

Genes

NF1
CDKN2A

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 24 Oct 2026.

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