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BRAF/MEK Inhibition Induces Cell State Transitions Boosting Immune Checkpoint Sensitivity in BRAFV600E-mutant Glioma

GSE287972 Mus musculus (mouse) RNA-seq (gene expression) 15 samples Submitted 2025/04/25 Platform GPL24676Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 15 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
15 samples: 6 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
BRAF/MEK inhibition induces cell state transitions boosting immune checkpoint sensitivity in BRAF(V600E)-mutant gliomaCell reports. Medicine · 2025
Summary (written by the submitters)
Resistance to BRAF plus MEK inhibition (BRAFi+MEKi) in BRAFV600E-mutant gliomas drives rebound, progression, and high mortality, yet it remains poorly understood. This study addresses the urgent need to develop treatments for BRAFi+MEKi-resistant glioma in generated mouse models and patient-derived materials. BRAFi+MEKi reveals glioma plasticity by heightening cell state transitions along glial differentiation trajectories, giving rise to astrocyte- and immunomodulatory oligodendrocyte (OL)-like states.
Read the full summary ↓
PD-L1 upregulation in OL-like cells links cell state transitions to tumor evasion, possibly orchestrated by Galectin-3. BRAFi+MEKi induces interferon response signatures, tumor infiltration, and suppression of T cells. Combining BRAFi+MEKi with immune checkpoint inhibition enhances survival in a T cell-dependent manner, reinvigorates T cells, and outperforms individual or sequential therapies in mice. Elevated PD-L1 expression in BRAF-mutant versus BRAF-wildtype glioblastoma supports the rationale for PD-1 inhibition in patients. These findings underscore the potential of targeting glioma plasticity and highlight combination strategies to overcome therapy resistance in BRAFV600E-mutant HGG.
Published in
BRAF/MEK inhibition induces cell state transitions boosting immune checkpoint sensitivity in BRAF(V600E)-mutant glioma
Xing YL, Panovska D, Park JW et al. · Cell reports. Medicine 2025 · PMID 40505659 · doi:10.1016/j.xcrm.2025.102183
This dataset
Open GSE287972 in finder → Find more RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE287972_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1215388 and SRA study SRP559710. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40505659) ↗
Study design
6 conditions, mostly in duplicate
2341, DMSO, 72hrs, biol ×2 2341, BRAFi+MEKI, 72hrs, biol ×2 STN49, DMSO, 24 hrs, biol ×2 STN49, BRAFi+MEKi, 24 hrs, biol ×2 STN49, DMSO, 48 hrs, biol ×2 STN49, BRAFi+MEKi, 48 hrs, biol ×2 aGBM5, DMSO, 48hr; BRAFi+MEKi, 24hr, 48hr ×1 Patient 12, pre-BRAFi+MEKi treatment ×1 +1 more

Supports a case/control comparison: 2 samples read as cases, 7 as controls.

How we read this: 6 replicated groups read from 15 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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