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A High-Throughput Screen on Primary Glioblastoma-Associated Macrophages Identifies HDAC Inhibitors as Enhancers of Phagocytosis and Potent Partners for Immunotherapy [CUT&Tag]

GSE330003 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2026/07/07 Platform GPL34290
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 14 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
14 samples: 4 × GBM TAM, Pracinostat, H3K27Ac CUT&Tag, vs 4 × GBM TAM, Pracinostat, IgG control CUT&Tag, vs 3 × GBM TAM, DMSO vehicle, H3K27Ac CUT&Tag, vs 3 × GBM TAM, DMSO vehicle, IgG control CUT&Tag,Groups 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)
This study presents the first high-throughput chemical screen on primary tumor-associated macrophages (TAMs) freshly isolated from surgical glioblastoma (GBM) patient samples, testing 1,365 compounds to identify drugs that enhance TAM phagocytosis. HDAC inhibitors, particularly Pracinostat and Resminostat, emerged as potent enhancers of phagocytosis, demonstrating synergy with CD47 blockade across multiple primary human TAM-GBM combinations.
Read the full summary ↓
In a xenograft GBM model, Pracinostat suppressed tumor growth and extended survival with additive benefit when combined with CD47 antibodies. RNA-seq and H3K27Ac CUT&Tag profiling of Pracinostat-treated TAMs in vivo revealed a two-tier mechanism: transcriptional reprogramming toward a pro-inflammatory state via NF-kB activation, and epigenetic priming of FcgR-mediated phagocytic machinery, providing a mechanistic basis for the observed synergy with CD47 blockade.
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 GSE330003_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1462363 and SRA study SRP697738. Searching any of these in the dataset finder brings you back here.

Study design
4 × GBM TAM, Pracinostat, H3K27Ac CUT&Tag, vs 4 × GBM TAM, Pracinostat, IgG control CUT&Tag, vs 3 × GBM TAM, DMSO vehicle, H3K27Ac CUT&Tag, vs 3 × GBM TAM, DMSO vehicle, IgG control CUT&Tag,

Supports a between-group comparison across 14 samples.

How we read this: 4 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.