GEO series

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

GSE263359 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 11 samples Submitted 2025/03/30 Platform GPL21626

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 11 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: 11 samples: 3 × Ptch1GNP ATAC vs 3 × PNC ATAC vs 3 × Tumor ATAC vs 2 × Tumor Chd7_KOGroups 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.

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

Open GSE263359 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 GSE263359_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 PRJNA1096765 and SRA study SRP499988. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

3 × Ptch1GNP ATAC vs 3 × PNC ATAC vs 3 × Tumor ATAC vs 2 × Tumor Chd7_KO

Supports a between-group comparison across 11 samples.

How we read this: 4 replicated groups read from 11 sample titles; they account for 11 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

GSM8190201 Ptch1GNP ATAC_1 Ptch1GNP ATAC
GSM8190202 Ptch1GNP ATAC_2 Ptch1GNP ATAC
GSM8190203 Ptch1GNP ATAC_3 Ptch1GNP ATAC
GSM8190204 PNC ATAC_1 PNC ATAC
GSM8190205 PNC ATAC_2 PNC ATAC
GSM8190206 PNC ATAC_3 PNC ATAC
GSM8190207 Tumor ATAC_1 Tumor ATAC
GSM8190208 Tumor ATAC_2 Tumor ATAC
GSM8190209 Tumor ATAC_3 Tumor ATAC
GSM8190210 Tumor Chd7_KO rep1 Tumor Chd7_KO
GSM8190211 Tumor Chd7_KO rep2 Tumor Chd7_KO

Datasets on a similar topic

GSE263360 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [CUT&Tag] 36 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
GSE263358 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [RNA-seq] 21 samples shares kmt2c, chd7, medulloblastoma, abnormalities, modification, progression, chromatin
GSE293000 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [scRNA-seq] 1 samples shares kmt2c, chd7, medulloblastoma, abnormalities, modification, progression, 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
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
GSE240360 Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [ATAC-Seq] 21 samples shares medulloblastoma, chromatin, atac-seq
GSE267770 KMT2C Deficiency Drives Luminal Transdifferentiation into Double-Negative Prostate Cancer and Sensitizes to Fatty Acid Synthase Inhibition [ATAC-seq] 5 samples shares kmt2c, atac-seq

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