GEO series

Tp53 and Tet2 mutations cooperatively transform GMP (RNA-Seq)

GSE285355 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/05/12 Platform GPL21103

At a glance

RNA-seq (gene expression) · mouse · 12 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 12 samples: 3 × GMP.WT vs 3 × GMP.TP53 vs 3 × GMP.Tet2 vs 3 × GMP.dKOGroups 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: TP53 mutations and TET2 deficiency cooperate to drive leukemogenesis and establish an immunosuppressive environmentThe Journal of clinical investigation · 2025

Summary (written by the submitters)

Mutations and deletions in TP53 are associated with adverse outcome in patients with myeloid malignancies and developing improved therapies for TP53-mutant leukemias is of urgent need. Here we identify mutations in TET2 as the most commonly co-existing mutation in TP53 mutant acute myeloid leukemia (AML) patients. Combined hematopoietic-specific deletion of TET2 and TP53 in mice enhanced self-renewal compared to deletion of either gene alone.

Read the full summary ↓

Tet2/Tp53 double knockout mice developed serially transplantable AML. Both mice as well as patients with AML and combined TET2/TP53 alterations upregulated innate immune signaling in malignant cells. Mice with TET2/TP53 loss had expansion of monocytic myeloid-derived suppressor cells which impaired T cell proliferation. Moreover, patients and mice with TP53/TET2 double mutant AML upregulated TIGIT ligands CD155 on malignant cells. TIGIT blocking antibodies augmented the ability of NK cells to kill Tet2/Tp53 double mutant AML cells, reduced leukemic burden, and extended the survival of TET2/TP53 double knockout mice. These data thereby identify a previously unexplored link between TET2 and TP53 mutations and highlight therapeutic means to overcome the immunosuppressive bone marrow environment in this adverse subtype of AML.

Published in

TP53 mutations and TET2 deficiency cooperate to drive leukemogenesis and establish an immunosuppressive environment

Zhang P, Whipp EC, Skuli SJ et al. · The Journal of clinical investigation 2025 · PMID 40111422 · doi:10.1172/JCI184021

This dataset

Open GSE285355 in finder → Find more mouse RNA-seq 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 GSE285355_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1203221 and SRA study SRP553955. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40111422) ↗

Study design

3 × GMP.WT vs 3 × GMP.TP53 vs 3 × GMP.Tet2 vs 3 × GMP.dKO

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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

GSM8701284 GMP.WT.1 GMP.WT
GSM8701285 GMP.WT.2 GMP.WT
GSM8701286 GMP.WT.3 GMP.WT
GSM8701287 GMP.TP53.1 GMP.TP53
GSM8701288 GMP.TP53.2 GMP.TP53
GSM8701289 GMP.TP53.3 GMP.TP53
GSM8701290 GMP.Tet2.1 GMP.Tet2
GSM8701291 GMP.Tet2.2 GMP.Tet2
GSM8701292 GMP.Tet2.3 GMP.Tet2
GSM8701293 GMP.dKO.1 GMP.dKO
GSM8701294 GMP.dKO.2 GMP.dKO
GSM8701295 GMP.dKO.3 GMP.dKO

Datasets on a similar topic

GSE279386 Tp53 and Tet2 mutations cooperatively transform progenitors (RNA-Seq) 24 samples shares tp53, tet2, cooperatively, mutations, transform, rna-seq
GSE171815 Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (RNA-seq - mus musculus) 27 samples shares tp53, transform, rna-seq
GSE266948 Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (scRNA-seq - mus musculus) 10 samples shares tp53, transform, rna-seq
GSE190903 RNA-Seq of genetically engineered mouse models (GEMMs) of PDA with or without KRAS and/or TP53 mutations 6 samples shares tp53, mutations, rna-seq
GSE314281 bulkRNA-seq LSKs CMPs MEPs GMPs from bone marrow and spleen 32 samples shares gmp, rna-seq
GSE190226 Concomitant loss of TET2 and TET3 results in T cell expansion and genomic instability [BGI-RNA-Seq] 21 samples shares tet2, rna-seq
GSE327454 TET2-mutant clonal hematopoiesis prevents T-cell exhaustion and suppresses cancer metastasis [RNA-seq] 19 samples shares tet2, rna-seq
GSE264595 The XPO7-NPAT axis represents key vulnerabilities in TP53-mutated acute myeloid leukemia (RNA-Seq) 18 samples shares tp53, rna-seq

Search all mouse RNA-seq datasets in GEO →

Share this dataset

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.