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Dominant Malignant Clones Leverage Lineage Restricted Epigenomic Programs to Drive Ependymoma Development [snMultiome]

GSE314911 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 21 samples Submitted 2026/03/25 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 21 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Samples
21 samples: 10 × 10xMultiome, PF-EPN brain tumor, PF vs 6 × 10xMultiome, ZFTA-RELA fusion EPN brain tumor, Z vs 5 × 10xMultiome, PLAG/L fusion brain tumor, PLAG/LGroups 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
Dominant clones leverage developmental epigenomic states to drive ependymomaNature · 2026
Summary (written by the submitters)
ZFTA-RELA (ZR) is the most recurrent genetic alteration seen in pediatric supratentorial ependymoma (EPN) and is sufficient to initiate tumors in mice. Despite the oncogenic potential of ZR, it is observed nearly exclusively in childhood EPN, with tumors located distinctly in the supratentorial region of the central nervous system (CNS).
Read the full summary ↓
We hypothesized that specific chromatin modules accessible during brain development would render distinct cell lineage programs at direct risk of transformation by ZR. To this end, we performed combined single nucleus ATAC and RNA (snMultiome) sequencing of the developing mouse forebrain, as compared to ZR-driven mouse and human EPN. We demonstrate that specific developmental lineage programs present in transient progenitor cells and regulated by PLAG/L family transcription factors (TF) are at risk of neoplastic transformation. Binding of this chromatin network by ZR or other PLAG/L family motif targeting fusion oncoproteins lead to persistent chromatin accessibility at oncogenic loci and oncogene expression. Cross-species analysis of mouse and human ZR EPN reveals significant cell type heterogeneity mirroring incomplete neurogenic and gliogenic differentiation, with a small percentage of cycling progenitor-like or radial glial-like cells that establish a putative tumor cell hierarchy. In vivo lineage tracing studies reveal neoplastic clones that aggressively dominate tumor growth and establish the entire EPN cellular hierarchy. These findings unravel developmental epigenomic states critical for fusion oncoprotein-driven transformation and elucidate how these states continue to shape tumor progression.
Published in
Dominant clones leverage developmental epigenomic states to drive ependymoma
Kardian AS, Sun H, Ippagunta S et al. · Nature 2026 · PMID 41882368 · doi:10.1038/s41586-026-10270-8
This dataset
Open GSE314911 in finder → Find more human 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 GSE314911_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1393117. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41882368) ↗
Study design
10 × 10xMultiome, PF-EPN brain tumor, PF vs 6 × 10xMultiome, ZFTA-RELA fusion EPN brain tumor, Z vs 5 × 10xMultiome, PLAG/L fusion brain tumor, PLAG/L

Supports a between-group comparison across 21 samples.

How we read this: 3 replicated groups read from 21 sample titles; they account for 21 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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