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ΔNp73 isoform defines a TP53mutant-like poor risk subgroup of acute myeloid leukemia

GSE310074 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 11 samples Submitted 2026/02/01 Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 11 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
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
11 samples: 2 × MOLM13 empty vecto vs 2 × MOLM13 DNp73-OE vs 2 × MOLM13 KOGroups 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
ΔNp73 isoform defines a TP53-mutant-like poor-risk subgroup of acute myeloid leukemiaCell reports. Medicine · 2026
Summary (written by the submitters)
Among acute myeloid leukemia (AML) patients, a subgroup remains notoriously refractory to current treatment options, with underlying mechanisms poorly understood. Here, using a multi-omics approach, we reveal that this resistant patient subgroup is characterized by high expression of the oncogenic TP73 isoform ΔNp73, exhibiting similarly poor outcomes as TP53-mutant AML.
Read the full summary ↓
ΔNp73, which lacks a transcriptional activation domain but retains chromatin binding properties, competes with TP53 for specific gene targets, thereby downregulating TP53 signaling. We demonstrate that the transcription factor CEBPA controls ΔNp73 expression in AML cells by binding to an intragenic enhancer region. Genetic or pharmacological inhibition of the transcriptional activity of CEBPA with guanfacine reduces ΔNp73 levels and restores drug sensitivity involving ferroptosis-mediated cell death, acting synergistically with venetoclax. Our study sheds light on a previously undercharacterized poor risk subgroup of AML, which may support patient stratification and inform treatment considerations.
Published in
ΔNp73 isoform defines a TP53-mutant-like poor-risk subgroup of acute myeloid leukemia
Pereira-Martins DA, Ortiz C, Weinhäuser I et al. · Cell reports. Medicine 2026 · PMID 41512877 · doi:10.1016/j.xcrm.2025.102540
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 GSE310074_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 PRJNA1365095 and SRA study SRP645240. Searching any of these in the dataset finder brings you back here.

Study design
2 × MOLM13 empty vecto vs 2 × MOLM13 DNp73-OE vs 2 × MOLM13 KO

Supports a between-group comparison across 6 samples.

How we read this: 3 replicated groups read from 11 sample titles; they account for 6 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 Acute myeloid leukemia datasets

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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.