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Integrated ChIP-seq and Transcriptomic Profiling of Histone Modifications Across Breast Cancer Progression in MCF10A-Derived Cell Lines

GSE271705 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/07/01 Platform GPL16791
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 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
Breast cancerThis series is part of our curated briefing on it.
Samples
12 samples: 3 × MCF10A vs 3 × MCF10AT1 vs 3 × MCF10CA1a vs 3 × MCF10DCISGroups 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)
Cancer arises from complex epigenetic mechanisms that drive tumorigenesis. Gene regulatory elements play a pivotal role in reprogramming gene expression patterns, facilitating tumor initiation, progression, and metastasis. However, a comprehensive characterization of epigenetic alterations across cancer development remains incomplete, particularly for the spectrum of post-translational histone modifications in the evolution of breast tumors.
Read the full summary ↓
In this study, we explored the dynamic landscape of epigenetic changes using a breast cancer progression model based on the MCF10A cell line. We integrated ChIP-seq and transcriptomic profiling to investigate the epigenetic heterogeneity across four MCF10A-derived cancer cell lines: normal (MCF10A), HRAS G12V transformed, ductal carcinoma in situ (DCIS), and metastatic (CA1a). Our analysis revealed significant changes in chromatin patterns at regulatory elements, including stage-specific variability in H3K27me3 and H3K9me3-marked heterochromatin domains. These profiles underly the epigenomic changes in each of these cell states to provide insights into human breast cancer progression.
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 GSE271705_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 PRJNA1132961 and SRA study SRP518505. Searching any of these in the dataset finder brings you back here.

Study design
3 × MCF10A vs 3 × MCF10AT1 vs 3 × MCF10CA1a vs 3 × MCF10DCIS

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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 Breast cancer datasets

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