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Dual inhibition of FACT and RRM2 suppresses the progression of pancreatic ductal adenocarcinoma driven by the oncohistone H2BG53D

GSE298580 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 64 samples Submitted 2025/10/26 Platform GPL18573Platform GPL24676Platform GPL20795Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 64 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
Pancreatic cancerThis series is part of our curated briefing on it.
Samples
64 samples: 16 conditions, mostly in duplicateGroups 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
Dual inhibition of FACT and RRM2 suppresses the progression of pancreatic ductal adenocarcinoma driven by the oncohistone H2BG53DCell reports · 2025
Summary (written by the submitters)
Pancreatic Ductal Adenocarcinoma (PDAC) is a highly lethal cancer with frequent genetic mutations. We previously reported the identification of the histone H2BG53-to-D mutation in PDAC patients and revealed that the mutation destabilizes nucleosomes and promotes cell migration. However, how H2BG53D impacts chromatin and the significance in PDAC development remain largely unknown.
Read the full summary ↓
Using the genetically engineered mouse models, we demonstrate that H2BG53D accelerates PDAC initiation and metastasis. Moreover, H2BG53D mutation elevates the interaction between nucleosomes and the Facilitates Chromatin Transcription (FACT) complex. FACT depletion reverses transcriptional changes and oncogenic effects induced by H2BG53D mutation. In search of a novel therapeutic strategy for H2BG53D-PDAC, our genome-wide CRISPR/Cas9 screen identified Ribonucleotide Reductase Regulatory Subunit M2 (RRM2) as a druggable target. Remarkably, dual inhibition of RRM2 and FACT exhibits potent cytotoxic effects on PDAC cells in vitro and significantly prolongs the survival of H2BG53D-PDAC mice. This study deciphers the roles and mechanisms of H2BG53D in PDAC progression and proposes a promising therapeutic strategy for this aggressive cancer.
Published in
Dual inhibition of FACT and RRM2 suppresses the progression of pancreatic ductal adenocarcinoma driven by the oncohistone H2BG53D
Qin T, Wan YCE, Hu S et al. · Cell reports 2025 · PMID 41284383 · doi:10.1016/j.celrep.2025.116596
This dataset
Open GSE298580 in finder → Find more RNA-seq datasets → Pancreatic cancer 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 GSE298580_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 PRJNA1269972 and SRA study SRP588989. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41284383) ↗
Study design
16 conditions, mostly in duplicate
WT7-NT ×2 WT16-NT ×2 GD3-NT ×2 GD32-NT ×2 WT7-sh49 ×2 WT16-sh49 ×2 GD3-sh49 ×2 GD32-sh49 ×2 +40 more

Supports a case/control comparison: 14 samples read as cases, 16 as controls.

How we read this: 16 replicated groups read from 64 sample titles; they account for 32 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

+ 24 more — browse all 64 samples with per-sample file links →

More Pancreatic cancer datasets

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