GEO series

Therapy-resistance in AT/RT is driven by epithelial-mesenchymal transition, extracellular matrix changes, and enrichment of CD1A+ CD207+ dendritic cells [RNA-seq_FFPE]

GSE298140 Homo sapiens (human) Single-nucleus RNA-seq 12 samples Submitted 2026/07/08 Platform GPL34284

At a glance

Single-nucleus RNA-seq · human · 12 samples

What it is: Single-nucleus RNA-seqGene activity measured in individual nuclei (used when whole cells are hard to isolate, for example from frozen tissue). Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism: Homo sapiens (human)
Samples: 12 samples: 12 × ATRT-MYC primary tumor #Groups 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: Molecular changes during AT/RT progression associated with epithelial-mesenchymal transition and extracellular matrix changesActa neuropathologica · 2026

Summary (written by the submitters)

Atypical teratoid/rhabdoid tumors (AT/RT) are the most common malignant brain tumors during infancy and associated with a dismal prognosis. 50% of the patients suffer from progressions or recurrences, but the underlying mechanisms remain largely unknown. To identify mechanisms of progression and recurrence, we performed single-nucleus RNA sequencing of eight primary-recurrence pairs.

Read the full summary ↓

Tumor cells and cells of the tumor microenvironment (TME) were analysed separately. Therapy-resistant tumor cells were identified through the comparison of global gene expression profiles between primary and recurrent tumor cell populations using CIBERSORT. Histology, in vitro experiments, bulk RNA sequencing, and survival analyses were performed to validate our findings. Paired primary and recurrent AT/RT tumor samples showed significant differences in their gene expression profiles. The TME of AT/RT recurrences was characterized by enrichment of CD1A+ CD207+ dendritic cells (DCs), which were per se associated with inferior survival in relapsed patients. Differentially expressed genes of AT/RT-MYC primary tumor cells that potentially persist after therapy, were involved in the organization of the extracellular matrix (ECM), developmental processes, and diverse immune signalling pathways. In addition, recurrences demonstrated a significantly higher proportion of cells undergoing partial epithelial-mesenchymal transition (pEMT) compared to primary tumors, a feature that we confirmed following treating AT/RT-MYC tumor cells in vitro. Finally, patients with primary tumors strongly expressing respective genes displayed a significantly worse survival. We identified pEMT, ECM remodeling, and enrichment of CD1A+ CD207+ DCs as potential mechanisms of therapy resistance in AT/RT which could be employed to improve therapy in the future.

Published in

Molecular changes during AT/RT progression associated with epithelial-mesenchymal transition and extracellular matrix changes

Altendorf L, Althammer A, Roy R et al. · Acta neuropathologica 2026 · PMID 42384079 · doi:10.1007/s00401-026-03050-1

This dataset

Open GSE298140 in finder → Find more human 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 GSE298140_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1268416 and SRA study SRP588107. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42384079) ↗

Study design

12 × ATRT-MYC primary tumor #

Supports a between-group comparison across 12 samples.

How we read this: 1 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

GSM9009024 ATRT-MYC primary tumor #1 ATRT-MYC primary tumor #
GSM9009025 ATRT-MYC primary tumor #2 ATRT-MYC primary tumor #
GSM9009026 ATRT-MYC primary tumor #3 ATRT-MYC primary tumor #
GSM9009027 ATRT-MYC primary tumor #4 ATRT-MYC primary tumor #
GSM9009028 ATRT-MYC primary tumor #5 ATRT-MYC primary tumor #
GSM9009029 ATRT-MYC primary tumor #6 ATRT-MYC primary tumor #
GSM9009030 ATRT-MYC primary tumor #7 ATRT-MYC primary tumor #
GSM9009031 ATRT-MYC primary tumor #8 ATRT-MYC primary tumor #
GSM9009032 ATRT-MYC primary tumor #9 ATRT-MYC primary tumor #
GSM9009033 ATRT-MYC primary tumor #10 ATRT-MYC primary tumor #
GSM9009034 ATRT-MYC primary tumor #11 ATRT-MYC primary tumor #
GSM9009035 ATRT-MYC primary tumor #12 ATRT-MYC primary tumor #

Datasets on a similar topic

GSE298139 Therapy-resistance in AT/RT is driven by epithelial-mesenchymal transition, extracellular matrix changes, and enrichment of CD1A+ CD207+ dendritic cells [snRNA-seq] 16 samples shares cd207, cd1a, epithelial-mesenchymal, therapy-resistance, extracellular, transition, enrichment
GSE298141 Therapy-resistance in AT/RT is driven by epithelial-mesenchymal transition, extracellular matrix changes, and enrichment of CD1A+ CD207+ dendritic cells [RNA-seq_cell_lines] 4 samples shares cd207, cd1a, epithelial-mesenchymal, therapy-resistance, extracellular, transition, enrichment
GSE303526 Human gastric extracellular matrix hydrogels maintain organoid growth and reduce gene expression associated with epithelial-mesenchymal transition and inflammation 8 samples shares epithelial-mesenchymal, extracellular, transition
GSE122476 Circulating CD1c+ myeloid dendritic cells are precursors to Langerhans cell histiocytosis (LCH) lesion CD1a+CD207+cells 57 samples shares cd207, cd1a
GSE122674 Circulating CD1c+ myeloid dendritic cells are precursors to Langerhans cell histiocytosis (LCH) lesion CD1a+CD207+cells 12 samples shares cd207, cd1a
GSE256412 Epigenetic changes regulating the epithelial-mesenchymal transition in human trophoblast differentiation 22 samples shares epithelial-mesenchymal, transition
GSE290615 miRNA/mRNA analysis of Chlamydia trachomatis-infected endometrial biopsies indicate increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation 15 samples shares epithelial-mesenchymal, transition
GSE266169 Cellular crosstalk mediated by TGF-β drives epithelial-mesenchymal transition in patient-derived multilineage biliary organoids 14 samples shares epithelial-mesenchymal, transition

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