The Lysine Demethylase Kdm4C is an Oncogenic Driver and Regulates ERK Activity in KRAS Mutant Pancreatic Ductal Adenocarcinoma
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 26 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)
- Samples
- 26 samples: 8 conditions, mostly in triplicateGroups 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
- The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal AdenocarcinomaCancer research communications · 2026
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.
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.
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE300200_RAW.tar (it can run to tens of gigabytes).
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 peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.
Also filed as BioProject PRJNA1279220 and SRA study SRP592839. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 24 samples.
How we read this: 8 replicated groups read from 26 sample titles; they account for 24 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.
- GSM9053558 AsPC1, KDM4C WT, rep1 AsPC1, KDM4C WT,
- GSM9053559 AsPC1, KDM4C WT, rep2 AsPC1, KDM4C WT,
- GSM9053560 AsPC1, KDM4C WT, rep3 AsPC1, KDM4C WT,
- GSM9053561 AsPC1, KDM4C KO1, rep1 AsPC1, KDM4C KO1,
- GSM9053562 AsPC1, KDM4C KO1, rep2 AsPC1, KDM4C KO1,
- GSM9053563 AsPC1, KDM4C KO1, rep3 AsPC1, KDM4C KO1,
- GSM9053564 AsPC1, shNT, Day 90, rep1 AsPC1, shNT, Day 90,
- GSM9053565 AsPC1, shNT, Day 90, rep2 AsPC1, shNT, Day 90,
- GSM9053566 AsPC1, shNT, Day 90, rep3 AsPC1, shNT, Day 90,
- GSM9053567 AsPC1, shKDM4C-1, Day 90, rep1 AsPC1, shKDM4C-1, Day 9…
- GSM9053568 AsPC1, shKDM4C-1, Day 90, rep2 AsPC1, shKDM4C-1, Day 9…
- GSM9053569 AsPC1, shKDM4C-1, Day 90, rep3 AsPC1, shKDM4C-1, Day 9…
- GSM9055556 AsPC1, KDM4C WT
- GSM9055557 AsPC1, KDM4C WT, H3K27Ac, rep1 AsPC1, KDM4C WT, H3K27A…
- GSM9055558 AsPC1, KDM4C WT, H3K36me3, rep1 AsPC1, KDM4C WT, H3K36m…
- GSM9055559 AsPC1, KDM4C WT, H3K27Ac, rep2 AsPC1, KDM4C WT, H3K27A…
- GSM9055560 AsPC1, KDM4C WT, H3K36me3, rep2 AsPC1, KDM4C WT, H3K36m…
- GSM9055561 AsPC1, KDM4C WT, H3K27Ac, rep3 AsPC1, KDM4C WT, H3K27A…
- GSM9055562 AsPC1, KDM4C WT, H3K36me3, rep3 AsPC1, KDM4C WT, H3K36m…
- GSM9055563 AsPC1, KDM4C KO1
- GSM9055564 AsPC1, KDM4C KO1, H3K27Ac, rep1 AsPC1, KDM4C KO1, H3K27…
- GSM9055565 AsPC1, KDM4C KO1, H3K36me3, rep1 AsPC1, KDM4C KO1, H3K36…
- GSM9055566 AsPC1, KDM4C KO1, H3K27Ac, rep2 AsPC1, KDM4C KO1, H3K27…
- GSM9055567 AsPC1, KDM4C KO1, H3K36me3, rep2 AsPC1, KDM4C KO1, H3K36…
- GSM9055568 AsPC1, KDM4C KO1, H3K27Ac, rep3 AsPC1, KDM4C KO1, H3K27…
- GSM9055569 AsPC1, KDM4C KO1, H3K36me3, rep3 AsPC1, KDM4C KO1, H3K36…
- GSE273073 A hPSC-Derived Progressive Pancreatic Ductal Adenocarcinoma Model Reveals Dual Pathways in ERK-Driven Cellular Plasticity 93 samples shares erk, adenocarcinoma, pancreatic
- GSE272460 Transcriptome analysis of pancreatic progenitor organoids (POs) carrying PDAC related mutations, treated with ERK inhibitors and depleted of AP-1 factors 40 samples shares erk, pancreatic
- GSE265906 Epigenetic and oncogenic inhibitors cooperatively drive differentiation and kill KRAS-mutant colorectal cancers [LOVO_BCat] 24 samples shares kras, oncogenic
- GSE310675 CRISPR-Cas9 Screening Identifies Resistance Mechanisms to KRAS Inhibition in Pancreatic Cancer 12 samples shares kras, pancreatic
- GSE300595 Multiomic sequencing identifies myeloid cell associations with neoadjuvant chemotherapy treatment response in pancreatic adenocarcinoma (PDAC) 24 samples shares adenocarcinoma, pancreatic
- GSE290274 KLF5 modulates epigenetic modifications driving human pancreatic ductal adenocarcinoma metastasis [Multiome] 16 samples shares adenocarcinoma, pancreatic
- GSE71729 Virtual Microdissection of Pancreatic Ductal Adenocarcinoma Reveals Tumor and Stroma Subtypes. 357 samples shares adenocarcinoma, pancreatic
- GSE205154 Bulk RNA-Seq gene expression data for 289 primary and metastatic pancreatic ductal adenocarcinoma (PDAC) tumor samples from FFPE blocks. 289 samples shares adenocarcinoma, pancreatic
Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.