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MYCN sustains a progenitor-stage differentiation block in human neuroepithelial stem cells to drive ETMR-like tumourigenesis [RNA-seq]

GSE339373 Homo sapiens (human) RNA-seq (gene expression) 11 samples Submitted 2026/07/23 Platform GPL28038
At a glance

RNA-seq (gene expression) · human · 11 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
11 samples: 5 × NES tumours derived from inducing MYCN(T58A) in vivo, vs 3 × NES cells, MYCN(T58A) induced (dox), vs 3 × NES cells, MYCN(T58A) uninduced (dox),Groups 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)
Embryonal tumours with multilayered rosettes (ETMRs) are aggressive paediatric brain tumours driven in most cases by amplification of the chromosome 19 microRNA cluster (C19MC), which upregulates the oncogene MYCN. Whether MYCN dysregulation alone is sufficient to produce ETMR-like tumours, independent of the broader C19MC machinery, has not been tested.
Read the full summary ↓
Here, we show that sustained MYCN expression in human neuroepithelial stem (NES) cells, i.e. primitive neural progenitors resembling the proposed cell of origin of ETMR, is sufficient to generate ETMR-like brain tumours in vivo. These tumours share methylation and transcriptional signatures with ETMR and reproduce its primitive, stem-like cellular hierarchy. MYCN-expressing tumour cells are arrested at an early neural progenitor stage, and MYCN withdrawal arrests growth and engages neuronal differentiation. Our findings identify sustained MYCN as sufficient to drive an ETMR-like developmental arrest in primitive human neural cells.
This dataset
Open GSE339373 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 GSE339373_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 PRJNA1498541 and SRA study SRP719955. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
5 × NES tumours derived from inducing MYCN(T58A) in vivo, vs 3 × NES cells, MYCN(T58A) induced (dox), vs 3 × NES cells, MYCN(T58A) uninduced (dox),

Supports a between-group comparison across 11 samples.

How we read this: 3 replicated groups read from 11 sample titles; they account for 11 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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