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Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment

GSE268992 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 31 samples Submitted 2025/06/25 Platform GPL16173Platform GPL21626Platform GPL17021Platform GPL30172
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 31 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
31 samples: 13 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
Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironmentGenome medicine · 2025
Summary (written by the submitters)
Monocytes are recruited to tumors and undergo transcriptional reprogramming resulting in tumor-promoting functions. Epigenomic features, such as post-translational modification of histones and chromatin accessibility, are key determinants of transcription factor binding and thereby play an important role in determining transcriptional responses to the tissue environment.
Read the full summary ↓
It remains unknown whether systemic tumor-associated signals could alter the epigenomic landscape of peripheral monocytes before they reach the tumor, thus shaping their subsequent response to the tumor microenvironment. Here, we performed genome-wide analyses of multiple histone modifications (H3K4me1, H3K4me3, H3K27ac) and chromatin accessibility in a mouse model and found that the distal tumor caused extensive remodeling of both H3K4me3+ promoters and H3K4me1+ enhancers in peripheral monocytes. Specifically, this involved the repression of interferon-responsive regulatory elements as well as the stablishment of enhancers harboring binding motifs for transcription factor families downstream of pro-inflammatory signaling, such as C/EBP, AP-1 and STAT. Reprogrammed enhancers in peripheral monocytes could be linked to sustained gene expression changes that persisted after tumor infiltration. In addition, key pro-tumor genes upregulated in tumor-infiltrating monocytes showed epigenetic priming already in the circulation. Overall, these results indicate that the epigenomic landscape of peripheral monocytes is altered in response to a distal tumor, and this can shape the transcriptional response of monocytes to the tumor microenvironment.
Published in
Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment
Kiss M, Halasz L, Hadadi E et al. · Genome medicine 2025 · PMID 40702585 · doi:10.1186/s13073-025-01511-y
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 GSE268992_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 PRJNA1119638 and SRA study SRP511511. Searching any of these in the dataset finder brings you back here.

Study design
13 conditions, mostly in duplicate
Ly6C-hi monocyte blood healthy RNA-seq ×3 Ly6C-hi monocyte blood LLC tumor-bearing RNA-… ×3 Ly6C-hi monocyte LLC tumor RNA-seq ×3 Ly6C-hi monocyte blood healthy ATAC-seq ×3 Ly6C-hi monocyte blood LLC tumor-bearing ATAC… ×3 Ly6C-hi monocyte blood healthy H3K4me3 CUT&Run ×2 Ly6C-hi monocyte blood LLC tumor-bearing H3K4… ×2 Ly6C-hi monocyte blood healthy IgG control CU… ×2 +5 more

Supports a case/control comparison: 15 samples read as cases, 14 as controls.

How we read this: 13 replicated groups read from 31 sample titles; they account for 31 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
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