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SPEN loss drives extra-follicular diffuse large B cell lymphoma with female-specific lethality and TLR pathway therapeutic vulnerabilities

GSE296145 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2026/04/10 Platform GPL34585Platform GPL34290
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 36 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
Mus musculus (mouse)
Samples
36 samples: 14 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)
In this study, we explore the interplay between SPEN and NOTCH2 truncating mutations, identifying an alternative, extra-follicular, trajectory of diffuse large B cell lymphomas (DLBCL) transformation. Our findings challenge the traditional germinal centre-centric model of lymphomagenesis, showing that marginal zone B cells (MZB) can give rise to aggressive lymphomas with autoimmune/aged B cells (AiBC)-like features, under the influence of these compound mutations.
Read the full summary ↓
At a mechanistic level, we found that SPEN loss re-routes NOTCH2-driven transcriptional programs, promoting a ZEB2-driven cell fate that blocks plasmacytic differentiation and skews B cell identity toward a MZB/AiBC mixed phenotype. We further show that SPENTRUNC/NOTCH2TRUNC-mutant lymphomas are associated with reduced overall survival of female DLBCL patients, due to X-chromosomal transcriptional perturbations. By characterizing their unique molecular dependencies, we identify actionable features in this aggressive DLBCL subset, paving the way for new precision medicine strategies that address the disease’s heterogeneity.
This dataset
Open GSE296145 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 GSE296145_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 PRJNA1257885 and SRA study SRP582670. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
14 conditions, mostly in duplicate
female_SN2_RNAseq ×5 WT ×4 N2 ×4 MZB_RNAseq ×3 male_SN2_RNAseq ×2 Multiome_control_GEX ×2 Multiome_control_ATAC ×2 Multiome_Spen+/-_GEX ×2 +6 more

Supports a between-group comparison across 36 samples.

How we read this: 14 replicated groups read from 36 sample titles; they account for 36 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
Datasets on a similar topic

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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.