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Aberrant DNA methylation distorts developmental trajectories in atypical teratoid/rhabdoid tumors

GSE197569 Homo sapiens (human) DNA methylation 31 samples Submitted 2024/03/04 Platform GPL24676Platform GPL11154
At a glance

DNA methylation · human · 31 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Homo sapiens (human)
Samples
31 samples: 24 distinct titles, 3 of them repeatedGroups 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
Aberrant DNA methylation distorts developmental trajectories in atypical teratoid/rhabdoid tumorsLife science alliance · 2024
Summary (written by the submitters)
Atypical teratoid/rhabdoid tumors (AT/RTs) are pediatric brain tumors known for their aggressiveness, exceptionally low mutation rate, and aberrant but still unresolved epigenetic regulation. To evaluate methylation associated regulation in AT/RTs, we compared them to medulloblastomas and choroid plexus tumors by integrating DNA methylation (507 samples), gene expression (120 samples), and public transcription factor (TF) binding data.
Read the full summary ↓
We showed that elevated DNA methylation masks the binding sites of TFs driving neural development and is associated with reduced transcription for specific neural regulators in AT/RTs. Hypermethylated sites largely behaved similarly in AT/RTs and pluripotent stem cells, revealing DNA methylation -driven halted cell differentiation. AT/RT-unique DNA hypermethylation was associated with polycomb repressive complex 2 members, like EZH2, and linked to suppressed genes with a role in neural development and tumorigenesis. The obtained results highlight and characterize these DNA methylation programs as drivers of AT/RT malignancy.
Published in
Aberrant DNA methylation distorts developmental trajectories in atypical teratoid/rhabdoid tumors
Pekkarinen M, Nordfors K, Uusi-Mäkelä J et al. · Life science alliance 2024 · PMID 38499326 · doi:10.26508/lsa.202302088
This dataset
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.

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 GSE197569_RAW.tar (it can run to tens of gigabytes).

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.

What the files usually look like: Look for beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA810995. Searching any of these in the dataset finder brings you back here.

Study design
24 distinct titles, 3 of them repeated
P ×5 M ×3 A ×2

How we read this: Read from 31 sample titles: 24 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
Datasets on a similar topic

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