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Links from GEO DataSets

Items: 20

1.

Effect of EZH2 and BET bromodomain inhibition, alone and combined, on NUT carcinoma gene expression

(Submitter supplied) To determine mechanisms of synergy between EZH2 and BRD4-NUT, we treated NUT carcinoma cell lines with EZH2 inhibitor, tazemetostat, and/or BET bromodomain inhibitors (ABBV075 pan-BET inhibitor or ABBV744 BD2-selective inhibitor). We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different NUT carcinoma cell lines at two time points, 6h and 96h.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
24 Samples
Download data: TDF, XLSX
Series
Accession:
GSE208774
ID:
200208774
2.

Effect of EZH2 inhibition on NUT carcinoma gene expression over time

(Submitter supplied) To determine roughly the time point at which most transcriptional changes occur in response to tazemetostat (taz, aka EPZ-6438 (EPZ)) treatment of NUT carcinoma cells, we performed RNAseq over a time course.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
20 Samples
Download data: TDF
Series
Accession:
GSE232838
ID:
200232838
3.

CUT&RUN profiling of histone H3K27ac and H3K27me3 localization after pharmacological inhibition of EZH2 and BET proteins

(Submitter supplied) NUT carcinoma (NC), an aggressive carcinoma, is driven by the BRD4-NUT fusion oncoprotein. BRD4, a BET protein, binds to chromatin through its two bromodomains, and when fused to NUT forms very large super-enhancers, termed megadomains. Targeting BRD4-NUT with BET bromodomain inhibitors (BETi) are a promising treatment, but limited as monotherapy. To identify additional dependencies in NC, we performed a genetic rescue screen in NC cells depleted of BRD4-NUT and identified EZH2 as a top correlated hit. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30173
36 Samples
Download data: BED, BW
Series
Accession:
GSE228533
ID:
200228533
4.

Combined targeting of the BRD4-NUT-p300 axis in NUT midline carcinoma by dual selective bromodomain inhibitor, NEO2734

(Submitter supplied) NUT midline carcinoma (NMC) is a rare, aggressive subtype of squamous carcinoma that is driven by the BRD4-NUT fusion oncoprotein. BRD4, a BET protein, binds to chromatin through its two bromodomains, and NUT recruits the p300 histone acetyltransferse (HAT) to activate transcription of oncogenic target genes. BET selective bromodomain inhibitors have demonstrated on-target activity in NMC patients, but with limited efficacy. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
20 Samples
Download data: TDF, TXT
5.

A genetically engineered mouse model of NUT carcinoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24247 GPL24676
76 Samples
Download data
Series
Accession:
GSE241477
ID:
200241477
6.

A genetically engineered mouse model of NUT carcinoma (CUT&RUN)

(Submitter supplied) We created a genetically engineered mouse model (GEMM) of NC that forms a Brd4-NUTM1 fusion gene upon tamoxifen-induction of Sox2-driven Cre. Two GEMM-derived cell lines were developed whose transcriptomic and epigenetic landscapes, characterized by RNAseq and CUT&RUN, show striking overlap with those of primary GEMM tumors. GEMM primary tumor and cell lines form very large H3K27ac-enriched super-enhancers that are unique to hNC, termed megadomains, that are invariably associated with key hNC-defining transcriptional oncogenic targets, Myc and Trp63.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL24247
55 Samples
Download data: TDF
Series
Accession:
GSE241476
ID:
200241476
7.

A genetically engineered mouse model (GEMM) of NUT carcinoma (RNA-Seq)

(Submitter supplied) NUT carcinoma (NC) is a highly aggressive subtype of squamous carcinoma driven by the BRD4-NUT fusion oncoprotein. Closely resembling human NC (hNC), GEMM tumors (mNC) are poorly differentiated squamous carcinomas that express high levels of MYC and metastasize to organs (liver, lung) and regional lymph nodes. Two GEMM-derived cell lines were developed whose transcriptomic and epigenetic landscapes, characterized by RNAseq and CUT&RUN, show striking overlap with those of primary GEMM tumors. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24247 GPL24676
21 Samples
Download data: TDF
Series
Accession:
GSE241474
ID:
200241474
8.

NUT Carcinoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL24676
32 Samples
Download data: NARROWPEAK
Series
Accession:
GSE179694
ID:
200179694
9.

RNA-seq on NUT Carcinoma (NC) cell lines treated with DMSO, Panobinostat or IRBM6

(Submitter supplied) HDAC inhibitor induce transcriptional program driving cellular differentiation and growth arrest in NUT Carcinoma (NC) cell lines TC-797 and 10-15.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL18573
16 Samples
Download data: XLS
10.

ChIP-seq analysis of BRD4-NUT and H3K27ac distribution in NUT Carcinoma cell line TC-797 treated with DMSO or Panobinostat

(Submitter supplied) BRD4-NUT and H3K27ac are depleted from megadomains in NUT Carcinoma (NC) cell line TC-797 after treatment with Panobinostat.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
16 Samples
Download data: NARROWPEAK
Series
Accession:
GSE179692
ID:
200179692
11.

Chromatin-associated protein interactions drive megadomain formation in NUT midline carcinoma

(Submitter supplied) To investigate the mechanism that drives dramatic mistargeting of active chromatin in NUT-midline carcinoma, we have identified protein interactions unique to the BRD4-NUT fusion oncoprotein compared to wild type BRD4. Using crosslinking, affinity purification, and mass spectrometry, we identify the p300 acetyltransferase as ectopically associated with BRD4 through the NUT fusion in both NMC and non-NMC cell types. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
20 Samples
Download data: TDF
12.

Epigenetic reprogramming in hepatic carcinogenesis

(Submitter supplied) Genomic sequencing of hepatocellular carcinoma (HCC) uncovers a paucity of actionable mutations, underscoring the necessity to exploit epigenetic vulnerabilities for therapeutics. In HCC, EZH2-mediated H3K27me3 represents a major oncogenic chromatin modification, but how it modulates the therapeutic vulnerability of signaling pathways remains unknown. Here, we identified that EZH2 maintains H3K27 methylome through epigenetic silencing of specific gene sets. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18480
10 Samples
Download data: BW
Series
Accession:
GSE113326
ID:
200113326
13.

Cell state-dependent chromatin targeting in NUT carcinoma

(Submitter supplied) ChIP-seq profiles of BRD4-NUT in HUES64 & HUES64 derived mesoderm (dME). ChIP-seq profiles of BRD4-NUT in Ntera-2 (NT2) cells & Ntera-2 (NT2) differentiated cells after 4 hr and 16 hr retinoic acid treatment..
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
20 Samples
Download data: BED, BW
Series
Accession:
GSE229558
ID:
200229558
14.

Epigenetic pattern after EZH1,2 inhibition in lymohoma cells

(Submitter supplied) Although global H3K27me3 reprogramming is a hallmark of cancer, no effective therapeutic strategy for H3K27me3-high malignancies harboring EZH2WT/WT has yet been established. We explored epigenome and transcriptome in EZH2WT/WT aggressive lymphomas, and found that mutual interference and compensatory function of co-expressed EZH1 and EZH2 rearrange their own genome-wide distribution, thereby establishing restricted chromatin and gene expression signatures. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL19784
117 Samples
Download data: TXT, XLSX
Series
Accession:
GSE138342
ID:
200138342
15.

Expression analysis after EZH1,2 inhibition in lymohoma cells

(Submitter supplied) To define gene expression alteration by EZH1/2 ihibition, we performed gene expression profiling in lymphoma cells after treatment of inhibitors or shRNAs
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL13497 GPL21185
42 Samples
Download data: TXT
Series
Accession:
GSE138282
ID:
200138282
16.

ChIP-seq and RNA-seq from human lymphoma cell lines

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL16791
14 Samples
Download data: TXT
Series
Accession:
GSE114270
ID:
200114270
17.

RNA-seq data from human lymphoma cell lines

(Submitter supplied) RNA-seq experiments were performed on OCI-Ly19 EZH2-wild type cell line (LY19WT) and a syngenic OCI-Ly19 cell line expressing the mutated protein EZH2-Y646F (LY19Y646F). We investigated the transcriptome changes between the two conditions.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
Series
Accession:
GSE114265
ID:
200114265
18.

ChIP-seq data for H3K27me3 from human lymphoma cell lines

(Submitter supplied) ChIP-seq experiments for H3K27me3 histone mark were performed on OCI-Ly19 EZH2-wild type cell line (LY19WT) and a syngenic OCI-Ly19 cell line expressing the mutated protein EZH2-Y646F (LY19Y646F). We investigated the genome-wide changes in H3K27me3 levels between the two conditions.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE114264
ID:
200114264
19.

Genes altered by miR-766-5p in two cancer cell lines

(Submitter supplied) To identify genes affected by miR-766-5p overexpression, we transfected with 10nmol of miR-766-5p or miR-negative control (NC) in HCT116-/-, or MIAPaCa2 cells. After 2 days, RNA was extracted, and then expression analysis was performed using agilent microarray.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17077
8 Samples
Download data: TXT
Series
Accession:
GSE180688
ID:
200180688
20.

Combined inhibition of EZH2 and degradation of Ikaros has synergistic effects in germinal center B-cell diffuse large B-cell lymphoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL21697
40 Samples
Download data: BEDGRAPH, TXT, XLS
Series
Accession:
GSE152069
ID:
200152069
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