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Integrative Hi-C maps of pancreatic cancer

GSE149103 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 66 samples Submitted 2021/08/11 Platform GPL20795
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 66 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
Homo sapiens (human)
Topic
Pancreatic cancerThis series is part of our curated briefing on it.
Samples
66 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.
Paper
High-resolution Hi-C maps highlight multiscale 3D epigenome reprogramming during pancreatic cancer metastasisJournal of hematology & oncology · 2021
Summary (written by the submitters)
Pancreatic cancer's poor prognosis is caused by distal metastasis, which is associated with epigenomic changes. However, the roles of 3D epigenome in pancreatic cancer biology, especially its metastasis, remain unclear. Here we compare the 3D epigenomic and transcriptomic features among cells derived from pancreatic epithelial, primary and metastatic pancreatic cancer by integrated analysis of in situ Hi-C, ChIP-seq, ATAC-seq, and RNA-seq data.
Read the full summary ↓
We found A/B compartments, topologically associated domains (TADs), chromatin loops changed significantly in metastatic pancreatic cancer cells, which is associated with epigenetic state alterations. Moreover, we identified upregulated genes, which are located in switched compartments, common TADs with epigenetic state changing, specific TAD boundaries, and metastasis-specific enhancer-promoter loops, are related to cancer metastasis. We also find that the transcription factors mediated specific enhancer-promoter loops formation are also associated with metastasis. Taken together, these results provide a 3D epigenomic map of pancreatic cancer metastasis, which expands our knowledge of the epigenetic mechanism of pancreatic cancer metastasis and enables a better understanding of pancreatic cancer pathobiology.
Published in
High-resolution Hi-C maps highlight multiscale 3D epigenome reprogramming during pancreatic cancer metastasis
Ren B, Yang J, Wang C et al. · Journal of hematology & oncology 2021 · PMID 34348759 · doi:10.1186/s13045-021-01131-0
This dataset
Open GSE149103 in finder → Find more human RNA-seq datasets → Pancreatic cancer landscape →
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 GSE149103_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 PRJNA626067 and SRA study SRP257058. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 34348759) ↗
Samples in this study

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