← BioTransfer GEO Dataset Finder
GEO series

Effects of crizotinib on gene expression profiles of cultured hematopoietic stem and progenitor cells (HSPCs) derived from MDS mice

GSE267954 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/08/15 Platform GPL24247
Summary
Myelodysplastic syndromes are characterized by bone marrow (BM) failure due to ineffective hematopoiesis. However, the underlying mechanisms of ineffective hematopoiesis, in which clonal expansion coexists with accelerated cell death, remain to be elucidated. Recently, we established the CBLΔE8/9/RUNX1S291fs mice (MDS mice), which develope a variety of MDS phenotypes including defects in megakaryocyte (MK) maturation. We identified crizotinib as a potent inducer of MK maturation. RNA-Seq of cultured HSPCs derived from the mice revealed that crizotinib increased the expression levels of MK and platelet-related genes.
Published in
Unraveling the impact of crizotinib to promote megakaryopoiesis for alleviating thrombocytopenia in myelodysplastic neoplasms
Kobayashi H, Komizo Y, Watanabe N et al. · Leukemia 2025 · PMID 40813622 · doi:10.1038/s41375-025-02729-w
This dataset
Download

Direct links to NCBI, no account and no request form: the whole study as GSE267954_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1113698 and SRA study SRP508826. Searching any of these in the dataset finder brings you back here.

Samples in this study

The sample list for this study is not cached yet. Press Sort into groups and it will be fetched from NCBI.

+ 4 more — browse all 4 samples with per-sample file links →

Similar datasets

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.