GEO series

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

GSE324064 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 21 samples Submitted 2026/06/22 Platform GPL18573

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 21 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: 21 samples: 21 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 is a smooth muscle–derived malignancy marked by significant clinical heterogeneity. The extent and nature of cellular heterogeneity and molecular underpinnings remain poorly understood. To address this at transcriptomic and epigenomic levels, we performed single-nucleus multiome sequencing on untreated primary leiomyosarcoma tissues.

Read the full summary ↓

Malignant cells segregated almost exclusively into two previously unrecognized and epigenetically distinct states: a dedifferentiated, mesenchymal-like subtype (MES) and a differentiated smooth muscle–enriched subtype (SMC). Chromatin accessibility profiling revealed strong enrichment of nuclear factor I (NFI) transcription factor motifs in MES cells, whereas AP-1 family motifs—most prominently FOSL2—were selectively accessible in SMC cells. Established leiomyosarcoma cell lines faithfully recapitulated these subtypes, and targeted depletion of NFI or AP-1 factors suppressed proliferation, invasion, and in vivo tumor growth, demonstrating functional dependency on these transcriptional programs. Spatial transcriptomics across 328 tissue cores from 128 leiomyosarcomas showed that immunosuppressive macrophages preferentially cluster around MES regions, revealing a subtype-specific tumor–immune niche. Clinically, MES-dominant tumors were associated with significantly worse patient outcomes. Through an epigenetic inhibitor screen, we identify and validate SMARCA4/2 inhibition as a promising therapeutic vulnerability for MES leiomyosarcomas. Together, this work defines two epigenetically driven, transcription factor–regulated, and clinically relevant states of leiomyosarcoma, revealing mechanistic underpinnings of tumor heterogeneity and uncovering actionable therapeutic strategies.

This dataset

Open GSE324064 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Soft tissue sarcoma landscape →

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.

Series matrix ↓

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 GSE324064_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

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 PRJNA1433372 and SRA study SRP681646. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

21 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 21 sample titles: 21 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

GSM9567668 Leio012 ChIP-seq for NFIA
GSM9567669 Leio012 ChIP-seq for NFIB
GSM9567670 Leio012 ChIP-seq for NFIC
GSM9567671 Leio012 ChIP-seq for NFIX
GSM9567672 Leio012 ChIP-seq for BACH2
GSM9567673 Leio012 ChIP-seq for FOSL2
GSM9567674 Leio012 ChIP-seq Input
GSM9567675 SKLMS01 ChIP-seq for NFIA
GSM9567676 SKLMS01 ChIP-seq for NFIB
GSM9567677 SKLMS01 ChIP-seq for NFIC
GSM9567678 SKLMS01 ChIP-seq for NFIX
GSM9567679 SKLMS01 ChIP-seq for BACH2
GSM9567680 SKLMS01 ChIP-seq for FOSL2
GSM9567681 SKLMS01 ChIP-seq Input
GSM9567682 HUtSMC ChIP-seq for NFIA
GSM9567683 HUtSMC ChIP-seq for NFIB
GSM9567684 HUtSMC ChIP-seq for NFIC
GSM9567685 HUtSMC ChIP-seq for NFIX
GSM9567686 HUtSMC ChIP-seq for BACH2
GSM9567687 HUtSMC ChIP-seq for FOSL2
GSM9567688 HUtSMC ChIP-seq Input

More Soft tissue sarcoma datasets

GSE287694 Integration of whole genome sequencing analysis with unique patient-derived models reveals clinically relevant drug targets in TFCP2 fusion-defined intraosseous rhabdomyosarcoma 2 samples same disease briefing · shares clinically, relevant
GSE303151 CDK8 Inhibition Releases the Muscle Differentiation Blockade in Fusion-driven Alveolar Rhabdomyosarcoma [CUT&RUN] 50 samples same disease briefing
GSE292876 FANCM is Required for the PAX3::FOXO1-Driven Oncogenic Program in Rhabdomyosarcoma [ChIP-Seq] 18 samples same disease briefing
GSE275736 A multitargeting approach rewires cell identity in fusion-negative rhabdomyosarcoma [bulk_ATACseq] 8 samples same disease briefing
GSE329566 CDK8 Inhibition Releases the Muscle Differentiation Blockade in Fusion-driven Alveolar Rhabdomyosarcoma [ChIP-Seq] 8 samples same disease briefing
GSE224170 Chromatin status of rhabdomyosarcoma (RMS) cell line RH30 in repsonse to MyoD CRISPR/Cas9 deletion [RMS ATAC-seq] 6 samples same disease briefing
GSE303149 CDK8 Inhibition Releases the Muscle Differentiation Blockade in Fusion-driven Alveolar Rhabdomyosarcoma [ATAC-seq] 6 samples same disease briefing
GSE312030 Combined inhibition of HRAS and MEK induces tumor regression and restores myogenic differentiation in HRAS-mutant rhabdomyosarcoma 159 samples same disease briefing

Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

Share this dataset

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.