Divergently evolved FOXA1 mutations drive prostate tumorigenesis or therapy-resistant intra-luminal plasticity
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 113 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
- 113 samples: 85 distinct titles, 24 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
- Divergent FOXA1 mutations drive prostate tumorigenesis and therapy-resistant cellular plasticityScience (New York, N.Y.) · 2025
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 GSE282406_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 PRJNA1188505 and SRA study SRP542557. Searching any of these in the dataset finder brings you back here.
How we read this: Read from 113 sample titles: 85 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.
- GSM8606350 Ms1706_Control_AR
- GSM8606351 Ms1706_CRE_AR
- GSM8606352 Ms2114_Control_KLF5
- GSM8606353 Ms2114_Control_TSF
- GSM8606354 Ms2114_CRE_CST
- GSM8606355 Ms2114_CRE_KLF5
- GSM8606356 Ms1947_Control_TFS
- GSM8606357 Ms1947_CRE_CST
- GSM8606358 Ms1218_CRE_sgNC_No_EGF_DHT_Rep1
- GSM8606359 Ms1218_CRE_sgNC_No_EGF_DHT_Rep2
- GSM8606360 Ms1218_sgNC_24h_10nM_DHT_Rep1
- GSM8606361 Ms1218_sgNC_24h_10nM_DHT_Rep2
- GSM8606362 Ms1218_sgNC_No_EGF_DHT_Rep1
- GSM8606363 Ms1218_sgNC_No_EGF_DHT_Rep2
- GSM8606364 Ms1218_sgNC_Rep1
- GSM8606365 Ms1218_sgNC_Rep2
- GSM8606366 Ms1218_sgTrp53_Rep1
- GSM8606367 Ms1218_sgTrp53_Rep2
- GSM8606368 Ms1706_R261G_control_NoED_Rep1
- GSM8606369 Ms1706_R261G_control_NoED_Rep2
- GSM8606370 Ms1706_R261G_CRE_NoED__Rep2
- GSM8606371 Ms1706_R261G_CRE_NoED_Rep1
- GSM8606372 Ms1936_Class_3_control_NoED_Rep1
- GSM8606373 Ms1936_Class_3_control_NoED_Rep2
- GSM8606374 Ms1936_Class_3_CRE_NoED_Rep1
- GSM8606375 Ms1936_Class_3_CRE_NoED_Rep2
- GSM8606376 Ms1947_P358fs_C_control_NoED_Rep1
- GSM8606377 Ms1947_P358fs_C_control_NoED_Rep2
- GSM8606378 Ms1947_P358fs_C_CRE_NoED_Rep1
- GSM8606379 Ms1947_P358fs_C_CRE_NoED_Rep2
- GSM8606380 Ms2114_P358fs_A_control_NoED_Rep1
- GSM8606381 Ms2114_P358fs_A_control_NoED_Rep2
- GSM8606382 Ms2114_P358fs_A_CRE_NoED_Rep1
- GSM8606383 Ms2114_P358fs_A_CRE_NoED_Rep2
- GSM8606384 Ms3888_5ul_CRE_36h_NoED_Rep1
- GSM8606385 Ms3888_5ul_CRE_36h_NoED_Rep2
- GSM8606386 Ms3888_5ul_Ctrl_36h_NoED_Rep1
- GSM8606387 Ms3888_5ul_Ctrl_36h_NoED_Rep2
- GSM8606388 Ms#3651_3646_R265-71del+/+; Trp53f/f PbCre-_AD_Ctrl
- GSM8606389 Ms#3652_R265-71del+/+; Trp53f/f PbCre+_AD_Case
+ 73 more — browse all 113 samples with per-sample file links →
- GSE280876 Divergently evolved FOXA1 mutations drive prostate tumorigenesis or therapy-resistant intra-luminal plasticity [Single-cell Multiome] 54 samples shares foxa1, therapy-resistant, tumorigenesis, intra-luminal, divergently, plasticity, mutations, prostate
- GSE280834 Divergently evolved FOXA1 mutations drive prostate tumorigenesis or therapy-resistant intra-luminal plasticity [ChIP-seq] 17 samples shares foxa1, therapy-resistant, tumorigenesis, intra-luminal, divergently, plasticity, mutations, prostate
- GSE280835 Divergent FOXA1 mutations drive prostate tumorigenesis or therapy-resistant intra-luminal plasticity [RNA-Seq] 38 samples shares foxa1, therapy-resistant, tumorigenesis, intra-luminal, plasticity, mutations, prostate
- GSE285574 Foxa1 mutations co-opt nascent transcription factor networks in partnership with androgen receptor to enhance prostate tumorigenicity 38 samples shares foxa1, mutations, prostate
- GSE313915 FOXA1 loss drives basal/squamous de-differentiation of prostate cancer and induces an immunosuppressive tumor microenvironment 12 samples shares foxa1, prostate
- GSE300614 Cooperativity between Ras pathway mutations in colonic tumorigenesis 27 samples shares tumorigenesis, mutations
- GSE224831 Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis [Prox1 OE iHep Timecourse RNA-seq] 16 samples shares tumorigenesis, plasticity
- GSE224830 Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis [Prox1 OE iHep Timecourse scRNA-seq] 13 samples shares tumorigenesis, plasticity
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.