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ARID1A Mutations Promote Immune Evasion of Follicular Lymphoma Through Reduced FAS-Mediated Apoptosis by Hindering RUNX3-ETS1 Cooperativity.

GSE230036 Homo sapiens (human) RNA-seq (gene expression) 30 samples Submitted 2025/02/10 Platform GPL18460
At a glance

RNA-seq (gene expression) · human · 30 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)
Topic
Follicular lymphomaThis series is part of our curated briefing on it.
Samples
30 samples: 15 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.
Paper
ARID1A mutations protect follicular lymphoma from FAS-dependent immune surveillance by reducing RUNX3/ETS1-driven FAS-expressionCell death and differentiation · 2025
Summary (written by the submitters)
The cell death receptor FAS and its ligand (FASLG) play a crucial role in the negative selection of B cells during the germinal center (GC) reaction. Failure to eliminate potentially harmful B cells can lead to the development B cell malignancies. Follicular lymphoma (FL) is a prototypic GC-derived B cell malignancy. Translocation and overexpression of antiapoptotic BCL2 is a hallmark of FL.
Read the full summary ↓
Additional alterations have been shown to be clinically relevant, including mutations in ARID1A. ARID1A is part of the SWI/SNF nucleosome remodeling complex that regulates DNA accessibility (“openness”). However, the contribution of ARID1A mutations to the development and the biology of FL remains unclear. Based on a functional screen, we investigated the link between ARID1A mutations and FAS/FASLG-induced apoptosis in FL. We analyzed 151 diagnostic FL biopsies and found that ARID1A mutations were recurrent and mainly disruptive, with an overall frequency of 18%. Additionally, we observed that ARID1A mutant FL showed significantly lower FAS expression in the FL tumor cell population. Functional experiments in t(14;18)+ B lymphoma cells demonstrated that ARID1A is directly involved in the regulation of FAS, and ARID1A loss leads to decreased FAS protein and gene expression. However, ARID1A loss did not affect FAS promoter openness. Instead, we identified and experimentally validated a previously unknown co-transcriptional complex consisting of RUNX3 and ETS1 that regulates FAS expression, and ARID1A loss leads to reduced RUNX3 promotor openness and gene expression. The reduced FAS levels induced by ARID1A loss rendered lymphoma cells resistant to both soluble and T cell membrane-anchored FASLG-induced apoptosis. Furthermore, we observed an additional accumulation of ARID1A mutations in relapsed/refractory FL biopsies, indicating that we have identified a functionally and clinically relevant mechanism how FL cells can escape T cell mediated killing, which may also profoundly impact the efficacy of subsequent therapies, including CAR T cells.
Published in
ARID1A mutations protect follicular lymphoma from FAS-dependent immune surveillance by reducing RUNX3/ETS1-driven FAS-expression
Antoniolli M, Solovey M, Hildebrand JA et al. · Cell death and differentiation 2025 · PMID 39843653 · doi:10.1038/s41418-025-01445-3
This dataset
Open GSE230036 in finder → Find more human RNA-seq datasets → Follicular lymphoma landscape →
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 GSE230036_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 PRJNA957256 and SRA study SRP433340. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39843653) ↗
Study design
15 conditions, mostly in duplicate
Ly1_cas9_1 ×2 Ly1_cas9_7 ×2 Ly1_cas9_9 ×2 Ly1_het_F10 ×2 Ly1_het_F9 ×2 Ly1_KO_E8 ×2 Ly1_KO_G1 ×2 Ly1_KO_H3 ×2 +7 more

Supports a between-group comparison across 30 samples.

How we read this: 15 replicated groups read from 30 sample titles; they account for 30 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
More Follicular lymphoma datasets

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