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Pan-Cancer Analysis Reveals Mutation-Driven TE Dysregulation as a Contributor to Immune Suppression [RNA-seq]

GSE320255 Homo sapiens (human) RNA-seq (gene expression) 14 samples Submitted 2026/04/01 Platform GPL34284
At a glance

RNA-seq (gene expression) · human · 14 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
14 samples: 6 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)
Somatic mutations and transposable element (TE) dysregulation are hallmarks of cancer, yet how specific genetic alterations influence TE activity across tumor types remains unclear. Here, we mapped mutation–TE regulatory networks across 9,622 tumors representing 33 TCGA cancer types by integrating RNA-seq, whole-exome, and DNA methylation data.
Read the full summary ↓
Comparative analysis of tumors with and without mutations identified 275 significant cancer–gene pairs associated with altered TE expression, many of which are transcription factors such as TP53, NSD1 and ARID1A. The changes in TE expression were also inversely correlated with DNA methylation changes in many cases. Unexpectedly, we observed that immune pathway activity is down-regulated when TE expression is induced, and up-regulated when TE is repressed. Functional validation in isogenic ARID1A- and CTNNB1-perturbed models recapitulated the changes in TE activity and immune responses observed in TCGA datasets. Together, these findings reveal mutation-driven TE activity reprogramming as a widespread feature and a potential source for immune modulation in human cancers.
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 GSE320255_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 PRJNA1427209 and SRA study SRP678816. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
NUGC4,WT, ×4 NUGC4,ARID1AKO, ×2 NUGC4,ARID1A,CRISPRi,vector, ×2 NUGC4,ARID1A,CRISPRi,sgRNA1, ×2 HepG2,CTNNB1,vec, ×2 HepG2,CTNNB1,OE, ×2

Supports a between-group comparison across 14 samples.

How we read this: 6 replicated groups read from 14 sample titles; they account for 14 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.