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Rps15 mutation drives B cell malignancy through translational rewiring, oxidative stress and genomic instability

GSE293841 Mus musculus (mouse) RNA-seq (gene expression) 51 samples Submitted 2025/06/01 Platform GPL19057Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 51 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
51 samples: 10 conditions, mostly in triplicateGroups 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
Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instabilityNature communications · 2026
Summary (written by the submitters)
Ribosomal protein mutations are increasingly associated with cancer risk and thought to perturb ribosome function. At the same time, they reportedly activate p53, a critical anti-cancer barrier. To determine how these mutations overcome this protective block to enable tumorigenesis, we generated an in vivo model of the hotspot Rps15-S138F mutation identified as a putative driver of chronic lymphocytic leukemia.
Read the full summary ↓
Under pre-leukemic conditions, this mutation induced protein instability, ribosome biogenesis defects and altered translation resulting in oxidative stress, DNA damage and induction of a p53-dependent response that promote initial cellular hypo-proliferation. However, aged mice with mutated Rps15 eventually developed B-cell leukemia (37% penetrance), which exhibited increased Myc activity with strong pro-survival and proliferation signatures. Mutant Rps15 thus induces both hypo- and hyper-proliferative signals, initially weighted towards cell cycle arrest; and that through translational rewiring, oxidative stress, DNA damage response defects and genomic instability set the stage for the acquisition of additional driving mutations, such as TP53 deletion, that can overcome this cell cycle block to trigger tumorigenesis.
Published in
Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability
Gutierrez C, Kwok M, Ruthen N et al. · Nature communications 2026 · PMID 41912510 · doi:10.1038/s41467-026-70655-1
This dataset
Open GSE293841 in finder → Find more mouse 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 GSE293841_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 PRJNA1246569 and SRA study SRP576523. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41912510) ↗
Study design
10 conditions, mostly in triplicate
B-cells from old, Rps15-S138F heterozygous mu… ×3 B-cells from old, Rps15 wildtype mouse, ×3 B-cells from leukemic, Rps15-S138F heterozygo… ×3 B-cells from leukemic, Rps15-S138F/+, Trp53 +… ×3 B-cells from leukemic, Rps15-S138F, Trp53 +/-… ×3 B-cells from young, Rps15-S138F heterozygous … ×3 B-cells from young, Rps15-S138F homozygous mu… ×3 B-cells from young, Rps15 wildtype mouse, ×3 +25 more

Supports a case/control comparison: 30 samples read as cases, 15 as controls.

How we read this: 10 replicated groups read from 51 sample titles; they account for 28 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

+ 11 more — browse all 51 samples with per-sample file links →

Datasets on a similar topic

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