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Eradication of tumors with pre-existing antigenic heterogeneity by vaccine-mediated co-engagement of CAR T and endogenous T cells

GSE211938 Mus musculus (mouse) RNA-seq (gene expression) 23 samples Submitted 2025/08/07 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 23 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
23 samples: 23 samples, each with a distinct title — no replicated groupsGroups 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)
Chimeric Antigen Receptor (CAR) T-cell therapy can be effective in treating human cancer but, loss/downregulation of the antigen recognized by the CAR poses a major obstacle to tumor eradication. Here, we report an approach for vaccine boosting CAR T-cells, which triggers engagement of the endogenous immune system to stop antigen-negative tumor escape.
Read the full summary ↓
Vaccine boosting enhanced CAR T-cell polyfunctionality, increased tumor antigen uptake by dendritic cells, and elicited priming of endogenous anti-tumor T cells (antigen spreading). This process required vaccine-induced enhancements in CAR T IFN-γ production and a metabolic shift in CAR T-cells toward oxidative phosphorylation. Antigen spreading induced by vaccine-boosted CAR-T therapy enabled control of solid tumors with substantial pre-existing heterogeneity, which was further enhanced by genetically amplifying CAR T IFN-γ expression. Thus, CAR T cell-derived IFN-γ plays a critical role in promoting endogenous anti-tumor immunity, and vaccine boosting provides a clinically-translatable strategy to drive such responses against solid tumors.
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 GSE211938_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 PRJNA872942 and SRA study SRP394040. Searching any of these in the dataset finder brings you back here.

Study design
23 samples, each with a distinct title — no replicated groups

Supports a case/control comparison: 5 samples read as cases, 5 as controls.

How we read this: Read from 23 sample titles: 23 distinct titles with little repetition. 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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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.