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FANCM is Required for the PAX3::FOXO1-Driven Oncogenic Program in Rhabdomyosarcoma [ChIP-Seq]

GSE292876 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2026/08/04 Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 18 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
18 samples: 6 conditions, mostly in triplicateGroups 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)
Alveolar rhabdomyosarcoma (ARMS) is a highly aggressive pediatric soft tissue sarcoma driven by the PAX3::FOXO1 fusion protein. Despite multipronged treatment approaches, survival rates for patients with fusion-positive (FP) ARMS remain poor, underscoring the need for novel therapeutic strategies. Here, we employ sequential multimodal CRISPR/Cas9 genetic screens to identify essential genes in FP ARMS, revealing FANCM, a key component of the Fanconi Anemia pathway, as a critical dependency.
Read the full summary ↓
FANCM loss selectively impairs FP ARMS cell growth in vitro and in vivo, reduces PAX3::FOXO1 levels, and induces myogenic differentiation. Mechanistically, FANCM depletion exacerbates replication stress, particularly at PAX3::FOXO1 target gene loci, which leads to ATR/ATM-mediated DNA damage signaling and selective downregulation of the fusion-driven oncogenic program. CRISPR exon-tiling screens highlighted FANCM's helicase and DNA-binding domains as essential for its FP-specific dependency, linking FANCM-mediated replication fork binding and downstream ATR signaling to FP ARMS survival. This study positions FANCM as a promising therapeutic target in FP ARMS and introduces a novel paradigm for exploiting replication stress vulnerabilities in oncofusion-driven malignancies.
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 GSE292876_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 PRJNA1241794 and SRA study SRP572994. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
Rh4 Native Cells, H3K27Ac (ChIP), ×3 Rh4 Native Cells, H3K27Ac (WCE), ×3 Rh4 Native Cells, ishFANCM_SMC, pRPA32 (ChIP), ×3 Rh4 Native Cells, ishFANCM_SMC, pRPA32 (WCE), ×3 Rh4 Native Cells, ishFANCM, pRPA32 (ChIP), ×3 Rh4 Native Cells, ishFANCM, pRPA32 (WCE), ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 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
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.