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RNA-seq in murine LSKs after Cux1 and/or Ezh2 loss, in the presence or absence of the DNA damaging agent N-ethyl-N-nitrosourea

GSE266586 Mus musculus (mouse) RNA-seq (gene expression) 39 samples Submitted 2025/01/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 39 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
39 samples
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
Multiplex gene editing models of del(7q) reveal combined CUX1 and EZH2 loss drives clonal expansion and drug resistanceBlood neoplasia · 2025
Summary (written by the submitters)
Loss of all or part of chromosome 7 [-7/del(7q)] is recurrent in myeloid neoplasms and associated with a poor response to chemotherapy. Chromosome 7-encoded genes that drive drug resistance and the consequences of combinatorial 7q tumor suppressor gene loss have remained unclear, the latter question being largely due to the challenges of modeling aneuploidy.
Read the full summary ↓
Here, we use in silico datamining to uncover 7q genes involved in chemotherapy resistance. We establish murine models of del(7q) clonal hematopoiesis and drug resistance with multiplex CRISPR-Cas9-mediated inactivation of four genes, Cux1, Ezh2, Kmt2c, and Kmt2e. Post-genotoxic exposure, combined deficiency of Cux1 and Ezh2 preferentially promotes clonal myeloid expansion in vivo, with compounding defects in DNA damage response and repair. Transcriptome analysis reveals combined Cux1 and Ezh2 loss recapitulates -7 patient gene signatures and defective DNA damage response pathways, to a greater extent than single gene loss. This work reveals a genetic interaction between CUX1 and EZH2, and sheds light on how -7/del(7q) contributes to leukemogenesis and drug resistance characteristic of these adverse-risk neoplasms. These data support the concept of 7q as a contiguous gene syndrome region, in which combined loss of multiple gene drives pathogenesis.
Published in
Multiplex gene editing models of del(7q) reveal combined CUX1 and EZH2 loss drives clonal expansion and drug resistance
Jotte MRM, Stoddart A, Martinez TC et al. · Blood neoplasia 2025 · PMID 40453147 · doi:10.1016/j.bneo.2025.100083
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 GSE266586_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: 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 PRJNA1107637 and SRA study SRP505664. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 39 more — browse all 39 samples with per-sample file links →

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