Multiome analysis of PDxOs (HCI-003, HCI-005, HCI-011) treated with a CDK4/6 inhibitor for 3 weeks
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 36 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
- 36 samples: 36 samples, each with a distinct title — no replicated groupsGroups 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.
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 GSE338025_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 PRJNA1492128 and SRA study SRP716426. Searching any of these in the dataset finder brings you back here.
Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.
How we read this: Read from 36 sample titles: 36 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.
- GSM9864763 HCI-003, CDKi, MN87, mRNA
- GSM9864764 HCI-003, CDKi, MN87, ATAC
- GSM9864765 HCI-003, CDKi, MN87, RREMS
- GSM9864766 HCI-003, DMSO, MN87, mRNA
- GSM9864767 HCI-003, DMSO, MN87, ATAC
- GSM9864768 HCI-003, DMSO, MN87, RREMS
- GSM9864769 HCI-003, CDKi, MN93, mRNA
- GSM9864770 HCI-003, CDKi, MN93, ATAC
- GSM9864771 HCI-003, CDKi, MN93, RREMS
- GSM9864772 HCI-003, DMSO, MN93, mRNA
- GSM9864773 HCI-003, DMSO, MN93, ATAC
- GSM9864774 HCI-003, DMSO, MN93, RREMS
- GSM9864775 HCI-005, CDKi, MN93, mRNA
- GSM9864776 HCI-005, CDKi, MN93, ATAC
- GSM9864777 HCI-005, CDKi, MN93, RREMS
- GSM9864778 HCI-005, DMSO, MN93, mRNA
- GSM9864779 HCI-005, DMSO, MN93, ATAC
- GSM9864780 HCI-005, DMSO, MN93, RREMS
- GSM9864781 HCI-005, CDKi, MN94, mRNA
- GSM9864782 HCI-005, CDKi, MN94, ATAC
- GSM9864783 HCI-005, CDKi, MN94, RREMS
- GSM9864784 HCI-005, DMSO, MN94, mRNA
- GSM9864785 HCI-005, DMSO, MN94, ATAC
- GSM9864786 HCI-005, DMSO, MN94, RREMS
- GSM9864787 HCI-011, CDKi, MN87, mRNA
- GSM9864788 HCI-011, CDKi, MN87, ATAC
- GSM9864789 HCI-011, CDKi, MN87, RREMS
- GSM9864790 HCI-011, DMSO, MN87, mRNA
- GSM9864791 HCI-011, DMSO, MN87, ATAC
- GSM9864792 HCI-011, DMSO, MN87, RREMS
- GSM9864793 HCI-011, CDKi, MN93, mRNA
- GSM9864794 HCI-011, CDKi, MN93, ATAC
- GSM9864795 HCI-011, CDKi, MN93, RREMS
- GSM9864796 HCI-011, DMSO, MN93, mRNA
- GSM9864797 HCI-011, DMSO, MN93, ATAC
- GSM9864798 HCI-011, DMSO, MN93, RREMS
- GSE304272 Transcriptomic profiling of irradiated senescent IMR90 cells treated with CDK4/6 or JAK inhibitors 12 samples shares cdk4, inhibitor, treated
- GSE285861 Using prognostic signatures and machine learning to identify core features associated with response to CDK4/6 inhibitor-based therapy in metastatic breast cancer 168 samples shares cdk4, inhibitor
- GSE308451 CDK4/6 and SHP2 mediate BRAF/MEK inhibitor resistance in Class 2 and 3 BRAF mutant cancers 90 samples shares cdk4, inhibitor
- GSE282705 BLU-222, a Potent CDK2 Inhibitor, Synergizes with CDK4/6 Inhibitors to Overcome Drug Resistance in HR–Positive and Triple-Negative Breast Cancer by Inducing p21 and p27 90 samples shares cdk4, inhibitor
- GSE300130 Exploiting Androgen Receptor Cell Cycle Effects to Enhance CDK4/6 Inhibitor Efficacy in Estrogen Receptor Positive Metastatic Breast Cancer 61 samples shares cdk4, inhibitor
- GSE325486 ESR1 mutations shape the clonal dynamics, genetic diversity and cellular states of acquired resistance to CDK4/6 inhibitors 57 samples shares cdk4, inhibitor
- GSE296805 An immunological mechanism of resistance to CDK4/6 inhibitors in breast cancer 50 samples shares cdk4, inhibitor
- GSE303026 CDK8/19 inhibition suppresses adaptive resistance to CDK4/6 inhibitors in vitro and in vivo 44 samples shares cdk4, inhibitor
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.