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IGF2BP1 in 17q-gain cooperates with MYCN to regulate purine biosynthesis and immunotherapy efficacy in neuroblastoma

GSE333427 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/05/31 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 9 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
9 samples: 3 × DMSO vs 3 × CHIR-124 vs 3 × PrexasertibGroups 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)
Concurrent chromosomal 17q-gain and MYCN amplification define a subset of neuroblastoma associated with particularly adverse clinical outcomes. However, how these genetic alterations synergize to promote tumor progression and whether their cooperation confers therapeutic vulnerabilities remain elusive. We herein performed a CRISPR-based functional screen targeting 17q-gain genes and identified the RNA m6A reader IGF2BP1 as a critical MYCN collaborator to promote aggressive neuroblastomas via activation of PAICS, a key enzyme involved in de novo purine biosynthesis.
Read the full summary ↓
Rewiring of PAICS-mediated nucleotide metabolism enabled tumor cells to sustain necessary purine pools for productive transcription of replicative stress-responsive genes, including CHK1, to cope with the exacerbated replication stress. Pharmacological inhibition of CHK1 elicited a robust immune reprogramming, leading to activation of cGAS-STING signaling, upregulation of MHC-I expression and synergistic tumor suppression with immune checkpoint blockade. Altogether, we identify an IGF2BP1/MYCN-PAICS-CHK1 axis that drives aggressive neuroblastoma phenotypes and constitutes an actionable vulnerability for therapeutic intervention.
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 GSE333427_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 PRJNA1471068 and SRA study SRP704075. Searching any of these in the dataset finder brings you back here.

Study design
3 × DMSO vs 3 × CHIR-124 vs 3 × Prexasertib

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 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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