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Interlocking core regulatory circuits enable viral hijacking in Merkel cell carcinoma

GSE261681 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 43 samples Submitted 2025/05/24 Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 43 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
Merkel cell carcinomaThis series is part of our curated briefing on it.
Samples
43 samples: 37 distinct titles, 6 of them repeatedGroups 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
Interlocking host and viral cis-regulatory networks drive Merkel cell carcinomaThe Journal of clinical investigation · 2025
Summary (written by the submitters)
Merkel Cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer. The conditions and cell type(s) of MCC are unknown. Virus positive MCC (VP-MCC) is driven by T antigens expressed from integrated Merkel cell polyomavirus (MCPyV). We found that VP-MCC required lineage-specific neuroendocrine transcription factors (TFs), including ATOH1, INSM1, ISL1, LHX3, POU4F3, and SOX2 that were central to core regulatory (CR) transcriptional circuitry.
Read the full summary ↓
MCPyV small T antigen and host CR TFs co-bound VP-MCC super enhancers while T antigen expression was directly regulated by LHX3 and ISL1, establishing an interlocking network between host CR circuitry and the oncovirus. Moreover, MCPyV integration sites were enriched near VP- MCC super enhancers, further suggesting a functional relationship between viral oncogenesis and core neuroendocrine circuitry.
Published in
Interlocking host and viral cis-regulatory networks drive Merkel cell carcinoma
Miao L, Milewski D, Coxon A et al. · The Journal of clinical investigation 2025 · PMID 41392987 · doi:10.1172/JCI188924
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 GSE261681_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 PRJNA1088415 and SRA study SRP495419. Searching any of these in the dataset finder brings you back here.

Study design
37 distinct titles, 6 of them repeated
Sample_MCC26 DNase ×2 Sample_MKL1 DNase ×2 Sample_MKL2 DNase ×2 Sample_MS1 DNase ×2 Sample_UISO DNase ×2 Sample_Waga DNase ×2

How we read this: Read from 43 sample titles: 37 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

+ 3 more — browse all 43 samples with per-sample file links →

More Merkel cell carcinoma datasets

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

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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.