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MYST acetyltransferases are a targetable therapeutic vulnerability in SETBP1-mutant leukemia [CUT&Run]

GSE303627 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 46 samples Submitted 2026/04/01 Platform GPL24676Platform GPL30172Platform GPL18573Platform GPL24247Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 46 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
46 samples: 16 conditions, mostly in triplicateGroups 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
MYST Acetyltransferases Interact with SETBP1 and Are a Targetable Therapeutic Vulnerability in SETBP1-Mutant LeukemiaBlood cancer discovery · 2026
Summary (written by the submitters)
Mutations in SET binding protein 1 (SETBP1) are associated with an adverse prognosis in myeloid malignancies. These mutations stabilize SETBP1 protein, driving increased expression of a progenitor-associated gene expression program through incompletely described mechanisms. A proteomic screen revealed interactions between SETBP1 and members of the MYST acetyltransferase complexes, including the catalytic subunits—KAT6A and KAT7.
Read the full summary ↓
Mutant SETBP1 increases the localization of MYST complexes at known SETBP1 target genes, including the Hoxa cluster, where they drive increased histone acetylation and gene expression. Treatment of SETBP1D868N-expressing myeloid progenitors with MYST inhibitors reduced target gene expression. To establish the efficacy of MYST inhibition in vivo, we treated mice harboring a syngeneic SETBP1-mutant leukemia with the clinical-grade MYST inhibitor—PF-9363. This resulted in complete hematologic control and increased survival. MYST inhibition was also highly effective against a SETBP1-mutant PDX model. These studies identify MYST acetyltransferases as promising therapeutic targets in SETBP1-mutant malignancies.
Published in
MYST Acetyltransferases Interact with SETBP1 and Are a Targetable Therapeutic Vulnerability in SETBP1-Mutant Leukemia
Carlson HL, Nguyen TT, Tauchmann S et al. · Blood cancer discovery 2026 · PMID 42001499 · doi:10.1158/2643-3230.BCD-25-0446
This dataset
Open GSE303627 in finder → Find more 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 GSE303627_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 PRJNA1295944 and SRA study SRP603289. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42001499) ↗
Study design
16 conditions, mostly in triplicate
K562 cells, doxycycline-induced, KAT7 antibod… ×3 K562 cells, doxycycline-induced, KMT2A antibo… ×3 K562 cells, doxycycline-induced, SETBP1 antib… ×3 K562 cells, no doxycycline induction, KAT7 an… ×3 K562 cells, no doxycycline induction, KMT2A a… ×3 K562 cells, no doxycycline induction, SETBP1 … ×3 Lin- cells, Luciferase control, KAT7 antibody, ×3 Lin- cells, Luciferase control, KMT2A antibod… ×3 +8 more

Supports a case/control comparison: 21 samples read as cases, 14 as controls.

How we read this: 16 replicated groups read from 46 sample titles; they account for 46 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

+ 6 more — browse all 46 samples with per-sample file links →

Datasets on a similar topic

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