GEO series

Transcriptional and chromatin accessibility landscapes of hematopoiesis in a mouse model of breast cancer

GSE274040 Mus musculus (mouse) Other 16 samples Submitted 2025/02/05 Platform GPL24247

At a glance

mouse · 16 samples

Organism: Mus musculus (mouse)
Samples: 16 samples: 16 samples, each with a distinct title — no replicated groupsGroups 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.
Paper: Transcriptional and chromatin accessibility landscapes of hematopoiesis in a mouse model of breast cancerJournal of immunology (Baltimore, Md. : 1950) · 2025

Summary (written by the submitters)

Hematopoietic abnormalities, including myeloid-skewing, anemia, and extramedullary hematopoiesis, are often observed in cancer patients, with evidence suggesting that they promote the development of myeloid-derived suppressor cells. However, our understanding of the mechanisms underlying these hematopoietic phenotypes remains incomplete.

Read the full summary ↓

Here, using the MMTV-PyMT mouse model of breast cancer, we characterize the transcriptional and chromatin accessibility landscapes of bone marrow and spleen hematopoietic progenitors using single-cell ATAC+RNA sequencing. We show that for the uncommitted hematopoietic stem and progenitor cells (HSPCs) in the BM, tumor growth induces a moderate upregulation of the myeloid-bias transcriptional signature and no significant chromatin accessibility changes. Compared to BM HSPCs, spleen HSPCs do not show a further upregulation of the myeloid-bias signature, and instead show the signature of Notch signaling, which has been associated with erythroid commitment. In addition, we also identify a cluster of spleen HSPCs in tumor-bearing animals with a transcriptional signature of mobilization, while our paired chromatin data suggest that AP-1 factors play a key role in HSPC mobilization. Furthermore, in contrast to the subtle tumor-induced changes in BM HSPCs, prominent transcriptional and chromatin changes are observed in dendritic cell (DC) progenitors, consistent with known cancer-associated DC defects. Our chromatin data also confirms, in an unbiased manner, that Stat3 and CEBP are both key contributors to DC defects. Overall, we provide a comprehensive dataset for understanding the hematopoietic consequences of cancer.

Published in

Transcriptional and chromatin accessibility landscapes of hematopoiesis in a mouse model of breast cancer

Fan C, Wu J, Barisas DAG et al. · Journal of immunology (Baltimore, Md. : 1950) 2025 · PMID 40152115 · doi:10.1093/jimmun/vkaf026

This dataset

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Download · which file do I need?

Direct links to NCBI, 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.

All supplementary files ↗

3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE274040_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Whole study · RAW.tar ↓

Also filed as BioProject PRJNA1144502. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40152115) ↗

Study design

16 samples, each with a distinct title — no replicated groups

Supports a case/control comparison: 12 samples read as cases, 4 as controls.

How we read this: Read from 16 sample titles: 16 distinct titles with little repetition. 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

GSM8442329 BM_ctrl_rep1_GEX
GSM8442330 BM_ctrl_rep1_ATAC
GSM8442331 BM_ctrl_rep2_GEX
GSM8442332 BM_ctrl_rep2_ATAC
GSM8442333 BM_tumor_rep1_GEX
GSM8442334 BM_tumor_rep1_ATAC
GSM8442335 BM_tumor_rep2_GEX
GSM8442336 BM_tumor_rep2_ATAC
GSM8442337 SP_tumor_rep1_GEX
GSM8442338 SP_tumor_rep1_ATAC
GSM8442339 SP_tumor_rep2_GEX
GSM8442340 SP_tumor_rep2_ATAC
GSM8442341 SP_tumor_rep3_GEX
GSM8442342 SP_tumor_rep3_ATAC
GSM8442343 SP_tumor_rep4_GEX
GSM8442344 SP_tumor_rep4_ATAC

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