GEO series

Disruption of basal cell identity by Rank signaling drives mammary tumorigenesis

GSE272968 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 15 samples Submitted 2026/01/16 Platform GPL34328

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 15 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: Mus musculus (mouse)
Samples: 15 samples: 5 conditions, mostly in triplicateGroups 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: Rank signaling drives basal cell-lineage infidelity leading to mammary tumorigenesisNature communications · 2026

Summary (written by the submitters)

Rank signaling regulates mammary gland development and epithelial cell differentiation. Rank receptor is expressed by mammary basal and luminal populations, but, unlike luminal Rank, the contribution of basal Rank signaling to MG homeostasis remains poorly studied. We have combined timely regulated basal specific Rank expression with lineage tracing models and unveiled that basal Rank signaling controls basal cell identity in postnatal mammary glands.

Read the full summary ↓

Ectopic basal Rank disrupts basal but also luminal cell identity, resulting in aberrant luminal-like differentiation of basal cells and impaired lactogenesis. Mechanistically, overactivation of basal Rank signaling leads to basal cell lineage infidelity, illustrated by the appearance of premalignant lesions composed by a basal-derived hybrid population with alveolar features which ultimately generates basal and luminal breast adenocarcinomas. Proteomic, transcriptomic and chromatin analyses support that the loss of tumor suppressive epigenetic regulators driven by basal Rank contributes to epithelial cell dedifferentiation and tumorigenesis. The basal Rank signature generated associates to poor prognosis particularly in human adenocarcinomas of the luminal subtype stressing the clinical relevance of our findings. Interestingly, our results reinforce the idea that luminal breast tumors might originate from basal cells that have suffered a luminal-like aberrant dedifferentiation triggered by Rank signaling

Published in

Rank signaling drives basal cell-lineage infidelity leading to mammary tumorigenesis

Redondo-Pedraza J, Santamaría PG, Sanchez-Juan A et al. · Nature communications 2026 · PMID 41760656 · doi:10.1038/s41467-026-70020-2

This dataset

Open GSE272968 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE272968_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1139725 and SRA study SRP521922. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41760656) ↗

Study design

5 conditions, mostly in triplicate

K14-Ctrl, LC, ×3 K14-Ctrl, BC, ×3 K14-Rank, LC, ×3 K14-Rank, BC, ×3 K14-Rank, B/L hybrid, ×3

Supports a between-group comparison across 15 samples.

How we read this: 5 replicated groups read from 15 sample titles; they account for 15 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

GSM8415693 K14-Ctrl, LC, replicate 1 K14-Ctrl, LC,
GSM8415694 K14-Ctrl, BC, replicate 1 K14-Ctrl, BC,
GSM8415695 K14-Rank, LC, replicate 1 K14-Rank, LC,
GSM8415696 K14-Rank, BC, replicate 1 K14-Rank, BC,
GSM8415697 K14-Rank, B/L hybrid, replicate 1 K14-Rank, B/L hybrid,
GSM8415698 K14-Ctrl, LC, replicate 2 K14-Ctrl, LC,
GSM8415699 K14-Ctrl, BC, replicate 2 K14-Ctrl, BC,
GSM8415700 K14-Rank, LC, replicate 2 K14-Rank, LC,
GSM8415701 K14-Rank, BC, replicate 2 K14-Rank, BC,
GSM8415702 K14-Rank, B/L hybrid, replicate 2 K14-Rank, B/L hybrid,
GSM8415703 K14-Ctrl, LC, replicate 3 K14-Ctrl, LC,
GSM8415704 K14-Ctrl, BC, replicate 3 K14-Ctrl, BC,
GSM8415705 K14-Rank, LC, replicate 3 K14-Rank, LC,
GSM8415706 K14-Rank, BC, replicate 3 K14-Rank, BC,
GSM8415707 K14-Rank, B/L hybrid, replicate 3 K14-Rank, B/L hybrid,

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