GEO series

Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [scRNA-seq]

GSE293000 Mus musculus (mouse) Single-cell RNA-seq 1 samples Submitted 2025/03/30 Platform GPL21626

At a glance

Single-cell RNA-seq · mouse · 1 samples

What it is: Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart.
Organism: Mus musculus (mouse)
Samples: 1 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.

Summary (written by the submitters)

Medulloblastoma, a common malignant pediatric brain tumor that typically originating from the cerebellum, is characterized by mutations in chromatin modifiers, highlighting the significance of epigenomic abnormalities in their progression. To prove this significance, the development and use of animal models that closely recapitulate the disease have been highly effective.

Read the full summary ↓

However, due to substantial time and cost limitations of developing genetically engineered mouse models, a complete understanding of the oncogenic potential of chromatin modifiers’ mutations found in human medulloblastomas is still elusive. In this study, we address this by CRISPR-mediated gene editing platform to knock out chromatin modifiers mutated human in SHH-subgroup medulloblastoma as well as the Ptch1 gene in cerebellar granule neuron progenitors. We functionally screened molecules involved tumor formation, identifying CHD7 and KMT2C as tumor suppressor genes. Multi-layered omics analysis revealed that these molecules epigenetically regulate the expression of Neurod1 that encodes a transcription factor crucial for neuronal differentiation, through histone H3 modification. Mutations impairing these factors suppress Neurod1, accelerating tumor growth. Conversely, forced expression of Neurod1 inhibits proliferation and promotes differentiation, underscoring its role as a key regulator in medulloblastoma aggressiveness. These findings not only demonstrate converging epigenomic abnormalities in SHH-subgroup medulloblastoma but also hold significant potential for evaluating epigenetic drugs targeting medulloblastoma, advancing the development of novel treatments.

This dataset

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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 GSE293000_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 PRJNA1242324 and SRA study SRP573322. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 1 more — browse all 1 samples with per-sample file links →

Datasets on a similar topic

GSE263358 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [RNA-seq] 21 samples shares kmt2c, chd7, medulloblastoma, abnormalities, modification, progression, chromatin
GSE263362 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression 71 samples shares kmt2c, chd7, medulloblastoma, abnormalities, modification, progression, chromatin
GSE263360 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [CUT&Tag] 36 samples shares kmt2c, chd7, medulloblastoma, abnormalities, modification, progression, chromatin
GSE263359 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [ATAC-seq] 11 samples shares kmt2c, chd7, medulloblastoma, abnormalities, modification, progression, chromatin
GSE255570 Chromatin remodeler CHD7 regulates neurogenic gene expression via controlling chromatin accessibility and modifications of histone marks H3K27me3 and H3K4me3 [Mouse RNA-seq] 4 samples shares chd7, modification, chromatin
GSE255571 Chromatin remodeler CHD7 regulates neurogenic gene expression via controlling chromatin accessibility and modifications of histone marks H3K27me3 and H3K4me3 [Mouse CUT&Tag] 10 samples shares chd7, modification, chromatin
GSE237289 Loss of Kmt2c or Kmt2d drives brain metastasis via KDM6A-dependent upregulation of MMP3 [scRNA-seq] 9 samples shares kmt2c, scrna-seq
GSE267773 KMT2C Deficiency Drives Luminal Transdifferentiation into Double-Negative Prostate Cancer and Sensitizes to Fatty Acid Synthase Inhibition [scRNA-Seq] 8 samples shares kmt2c, scrna-seq

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