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Leukemia aggressiveness is driven by chromatin remodeling and expression changes of core regulators [ChIP-seq]

GSE280195 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 25 samples Submitted 2026/04/08 Platform GPL17021
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 25 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
Mus musculus (mouse)
Samples
25 samples: 20 distinct titles, 5 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
Multiomic analysis of clonal development reveals new regulators of leukemic cell growthGenes & development · 2026
Summary (written by the submitters)
Molecular mechanisms driving clonal aggressiveness in leukemia are not fully understood. We tracked and analyzed MLL-rearranged leukemic clones independently evolving towards higher aggressiveness. More aggressive subclones lost their growth differential ex vivo but restored it upon secondary transplantation, suggesting molecular memory of aggressiveness.
Read the full summary ↓
Development of aggressiveness was associated with clone-specific gradual modulation of chromatin states and expression levels across the genome, with a surprising preferential trend of reversing the earlier changes between normal and leukemic progenitors. To focus on the core aggressiveness program, we identified genes with consistent changes of expression and chromatin marks that were maintained in vivo and ex vivo in both clones. Overexpressing selected core genes (Smad1 as aggressiveness driver, Irx5 and Plag1 as suppressors) affected leukemic progenitor growth in the predicted way and had convergent downstream effects on central transcription factors and repressive epigenetic modifiers, suggesting a broader regulatory network of leukemic aggressiveness.
Published in
Multiomic analysis of clonal development reveals new regulators of leukemic cell growth
Bonilla G, Morris A, Kundu S et al. · Genes & development 2026 · PMID 41638911 · doi:10.1101/gad.353186.125
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 GSE280195_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 PRJNA1177102 and SRA study SRP540494. Searching any of these in the dataset finder brings you back here.

Study design
20 distinct titles, 5 of them repeated
Aggressive, clone 1, H3K4me ×2 Aggressive, clone 2, H3K4me ×2 Early, clone 1, H3K4me ×2 Early, clone 2, H3K4me ×2 Normal, H3K4me ×2

How we read this: Read from 25 sample titles: 20 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
Datasets on a similar topic

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