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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.

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
6.

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
7.

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
8.

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
9.

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
10.

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
11.

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
12.

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
13.

Recovery and analysis of nascent RNA

(Submitter supplied) Nascent transcription profiles are shown for scaled megadomains and 100kb flanking regions before BRD4-NUT induction (0h) and at different time points (2h, 3h, 7h) following induction in 293T cells. Increase of the transcription from 0h to 7h after induction. Average level of transcriptional activity is reduced within the megadomains and their flanking regions following JQ1 treatment of TC-797 cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
14 Samples
Download data: TDF, TXT
14.

Chip-seq mapping of active chromatin marks in BRD4-NUT and different NMC cells

(Submitter supplied) BRD4-NUT megadomains is an order of magnitude larger than super-enhancer regions and displays a more continuously enriched profile rather than appearing as a cluster of individual peaks.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
53 Samples
Download data: TDF
Series
Accession:
GSE70870
ID:
200070870
15.

Chip-seq BRD4NUT-BioTAP mapping in 293Trex and 797 cells

(Submitter supplied) BRD4-NUT megadomains is an order of magnitude larger than super-enhancer regions and displays a more continuously enriched profile rather than appearing as a cluster of individual peaks.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: TDF
Series
Accession:
GSE70869
ID:
200070869
16.

The oncogenic BRD4-NUT chromatin regulator drives aberrant transcription within large topological domains

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL16791
75 Samples
Download data: TDF
Series
Accession:
GSE70868
ID:
200070868
17.

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
18.

Brd4::Nutm1 fusion gene initiates NUT carcinoma in vivo [RNA-seq]

(Submitter supplied) NUT carcinoma (NC) is an aggressive cancer with no effective treatment. About 70% of NUT carcinoma is associated with chromosome translocation events that lead to the formation of a BRD4::NUTM1 fusion gene. Because the BRD4::NUTM1 gene is unequivocally cytotoxic when ectopically expressed in cell lines, questions remain on whether the fusion gene can initiate NC. Here, we report the first genetically engineered mouse model (GEMM) for NUT carcinoma that recapitulates the t(15;19) chromosome translocation in mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TXT
Series
Accession:
GSE263558
ID:
200263558
19.

Differentiation of NUT midline carcinoma by epigenomic reprogramming

(Submitter supplied) Knockdown of the oncogene, BRD4-NUT, in a rare cancer, termed NUTmidline carcinoma (NMC), results in morphologic features consistent with squamous differentiation. Treatment with the HDAC-inhibitor, TSA, appears to cause the same phenotype. Here, we use gene expression profiling to compare the changes in gene expression following BRD4-NUT knockdown and TSA treatment.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
20 Samples
Download data: CEL
Series
Accession:
GSE18668
ID:
200018668
20.

HDAC inhibitors result in widespread alteration of the histone acetylation landscape and BRD4 targeting to gene bodies 

(Submitter supplied) Histone acetylation is associated with active transcription and serves as a binding site for reader proteins that function in transcriptional initiation and elongation. Histone acetylation levels are regulated through the actions of histone acetyltransferases (HATs) and histone deacetylases (HDACs) that antagonistically control the overall balance of this posttranslational modification. HDAC inhibitors (HDACi) are potent agents that disrupt this balance and are used clinically to treat a range of human diseases including cancer. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
30 Samples
Download data: BW, TXT
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