← BioTransfer GEO Dataset Finder
GEO series

Targeting the oncohistone-ASCL1 axis disrupts plasticity and suppresses pediatric gliomas [RNA-seq]

GSE269557 Homo sapiens (human) RNA-seq (gene expression) 44 samples Submitted 2026/07/10 Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 44 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
Homo sapiens (human)
Samples
44 samples: 18 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.
Summary (written by the submitters)
Phenotypic plasticity, a hallmark of cancer facilitated by epigenomic reprogramming, represents a significant challenge but also therapeutic opportunity for cancer treatment. How plasticity is regulated in diffuse midline gliomas (DMGs), incurable pediatric brain tumors characterized by oncogenic H3K27M histone mutations, is not understood.
Read the full summary ↓
Here we demonstrate that H3K27M-driven plasticity requires the lineage-specific, pioneer transcription factor (TF) ASCL1. Prolonged differentiation reveals clinically relevant plasticity in DMGs, which segregate into ASCL1-high, neural progenitor cell (NPC)-like gliomaspheres and ASCL1-low, mesenchymal (MES)-like adherent subpopulations. Direct transcriptional activation by ASCL1 enables super enhancers to sustain NPC programs de-repressed by H3K27M. H3K27M loss induces an irreversible MES-like state, suppresses plasticity by abolishing the ASCL1-high state, and is largely phenocopied by loss of ASCL1. Knocking out ASCL1 in DMG lines robustly inhibited tumor growth and significantly extended survival of recipient mice. Our results suggest targeting epigenetic plasticity to suppress master TF-driven progenitor states as a general therapeutic opportunity in cancer.
This dataset
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.

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 GSE269557_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1122517 and SRA study SRP513143. Searching any of these in the dataset finder brings you back here.

Study design
18 conditions, mostly in duplicate
ASCL1KO_TSM ×3 Control_TSM ×3 DKO_TSM ×3 K27MKO_TSM ×3 BT869_ASCL1KO_Day0 ×3 BT869_ASCL1KO_Day3 ×3 BT869_Control_Day0 ×3 BT869_Control_Day3 ×3 +10 more

Supports a between-group comparison across 44 samples.

How we read this: 18 replicated groups read from 44 sample titles; they account for 44 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

+ 4 more — browse all 44 samples with per-sample file links →

Datasets on a similar topic

Search all human RNA-seq datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.