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Spatially-Resolved Multiomic Atlas of Leiomyosarcoma Identifies Two Clinically Relevant Epigenetically-Driven Cell States [scMultiomic]

GSE324206 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 32 samples Submitted 2026/04/01 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 32 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
Homo sapiens (human)
Topic
Soft tissue sarcomaThis series is part of our curated briefing on it.
Samples
32 samples: 32 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)
Leiomyosarcoma (LMS) is a malignant smooth muscle tumor characterized by substantial clinical and molecular heterogeneity. To investigate the cellular and regulatory landscape of LMS at single-cell resolution, we performed single-nucleus multiome sequencing to jointly profile gene expression (snRNA-seq) and chromatin accessibility (snATAC-seq) in 16 untreated primary leiomyosarcoma tumors arising from retroperitoneal, extremity, and uterine sites.
Read the full summary ↓
After quality control, 94,439 nuclei were analyzed, revealing diverse tumor and microenvironmental cell populations including macrophages, T cells, and endothelial cells. Malignant cells segregated predominantly into two major transcriptional and epigenetic states: a dedifferentiated mesenchymal-like subtype (MES) and a differentiated smooth muscle cell–like subtype (SMC). Integration of transcriptomic and chromatin accessibility profiles identified distinct regulatory programs underlying these states, including enrichment of NFI transcription factor motifs in MES cells and AP-1 family motifs in SMC cells. These data provide a comprehensive multiomic resource for understanding tumor heterogeneity and regulatory mechanisms in leiomyosarcoma.
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 GSE324206_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 PRJNA1372071. Searching any of these in the dataset finder brings you back here.

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

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 32 sample titles: 32 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
More Soft tissue sarcoma datasets

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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.