GEO series

The impact of Fulvestrant on Estrogen Receptor-Driven Chromatin Dynamics in breast cancer cells points to a disconnect between chromatin opening and histone acetylation [ATAC-seq]

GSE301554 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 9 samples Submitted 2026/05/25 Platform GPL21697

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 9 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)
Samples: 9 samples
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)

Background: Epigenetic dysregulations are linked to various diseases, including cancer. Among them, breast cancer is the second leading cause of cancer-related deaths in women with 50% of mortalities attributable to estrogen receptor-positive (ER+) tumors. Endocrine therapies targeting the Estrogen Receptor (ER) such as Tamoxifen, Fulvestrant and Aromatase inhibitors, are widely used in the clinic.

Read the full summary ↓

Among these therapeutic agents, Fulvestrant has been shown to fully antagonize ER activity, primarily through the rapid degradation and elimination of ER from target tissues. However, recent findings indicate that ER, when engaged with Fulvestrant, retains the ability to translocate to the nucleus and bind DNA whereas appearing transcriptionally inert. Results: In this study we aimed to further investigate the effects of Fulvestrant and Estradiol, an ER natural ligand, on ER cistrome, chromatin accessibility, and H3K27ac genome-wide patterns in an ER+ breast cancer cell line. Using the innovative CUT&Tag technology, we first confirmed that both Fulvestrant and Estradiol promote ER binding to DNA. Our findings revealed that Estradiol not only enhances chromatin accessibility but also increases H3K27ac levels at ER binding sites. In contrast, while Fulvestrant does not significantly alter chromatin accessibility, it can induce increases in H3K27ac levels at a subset of ER binding sites. Our observations suggest that Fulvestrant may modulate breast cancer transcriptional landscape by impacting H3K27ac dynamics, even in the absence of changes in chromatin accessibility. Conclusions: This study provides new insights on the mechanistic impact of Fulvestrant on Estrogen Receptor activity and their potential implications on target gene expression, particularly highlighting a novel putative role of H3K27ac dynamics in these processes.

This dataset

Open GSE301554 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →

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 GSE301554_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 PRJNA1285437 and SRA study SRP597725. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 9 more — browse all 9 samples with per-sample file links →

Datasets on a similar topic

GSE301553 The impact of Fulvestrant on Estrogen Receptor-Driven Chromatin Dynamics in breast cancer cells points to a disconnect between chromatin opening and histone acetylation [CUT&Tag] 18 samples shares receptor-driven, fulvestrant, acetylation, disconnect, chromatin, estrogen, dynamics
GSE310291 The impact of Fulvestrant on Estrogen Receptor-Driven Chromatin Dynamics in Breast Cancer Cells [RNA-seq] 48 samples shares receptor-driven, fulvestrant, chromatin, estrogen, dynamics
GSE264726 Combined inhibition of KAT6A/B and Menin reverses estrogen receptor-driven gene expression programs in breast cancer (ChIP-Seq) 69 samples shares receptor-driven, estrogen
GSE243834 Investigation of melanoma cell chromatin acetylation states with high and low levels of ALDH1A3 20 samples shares acetylation, chromatin
GSE288071 Sequential histone H1 N76/77 deamidation and K75 acetylation facilitate chromatin relaxation and genome stability by DNA repair 16 samples shares acetylation, chromatin
GSE282758 Disruption of histone acetylation homeostasis reveals multilayered chromatin regulation for transcriptional resiliency 12 samples shares acetylation, chromatin
GSE238104 High-dimensional analysis reveals increased chromatin heterogeneity and reduced histone acetylation driven by mutant-IDH1 [Cut&Run] 10 samples shares acetylation, chromatin
GSE220868 METTL3 Promotes Histone H3K9 Acetylation through Recruitment of Histone Acetyltransferase 1 to Chromatin (ChIP-Seq) 10 samples shares acetylation, chromatin

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.