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Chimeric Antigen Receptor-Macrophage Extracellular Vesicles Reprogram Immune Microenvironment for Cancer Therapy.

GSE306326 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2026/05/21 Platform GPL16791Platform GPL17021
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples
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)
Immunotherapy has become a new milestone in cancer treatment, with chimeric antigen receptor (CAR)-T cell therapy proven to be an effective method for treating hematologic malignancies. However, its efficacy in solid tumors remains limited. Macrophages, the most infiltrative innate immune cells in the tumor microenvironment, are being genetically engineered to express CARs, rapidly emerging as a promising new therapy for non-hematologic malignancies.
Read the full summary ↓
Yet, CAR- Macrophages therapy is associated with unique acute toxicities and is susceptible to immunosuppressive mechanisms. Here, we propose using CAR macrophages-derived extracellular vesicles (CAR-MEVs) as an optimization of CAR-Ms therapy. Compared to CAR-Ms cells, CAR-MEVs exhibit lower toxicity and enhanced drug delivery capabilities. In an in vivo liver cancer model, CAR-MEVs administration proved safer than CAR-Ms therapy, reducing tumor burden and prolonging overall survival. In a humanized mouse model, CAR-MEVs further demonstrated the ability to induce a pro-inflammatory tumor microenvironment and enhance anti-tumor T cell activity. Mechanistically, CAR-MEVs target tumor cells, inducing immunogenic cell death (ICD) and subsequently leading to neutrophil infiltration in tumor tissues. We demonstrated that the anti-tumor effects of CAR-MEVs depend on neutrophils and are partially reliant on inducible nitric oxide synthase (iNOS). This study supports the potential of macrophage extracellular vesicles as a novel therapeutic approach for 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 GSE306326_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 PRJNA1310462 and SRA study SRP612514. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 12 more — browse all 12 samples with per-sample file links →

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