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Links from GEO DataSets

Items: 20

1.

Pbrm1 regulates interferon signaling in mouse AML [RNA-seq Mouse]

(Submitter supplied) CRISPR/Cas9 screening approaches are powerful tools to identify in vivo cancer dependencies. Hematopoietic malignancies are genetically complex disorders in which sequential acquisition of somatic mutations generates clonal diversity. With time, additional cooperating mutations may drive disease progression. Using an in vivo pooled gene editing screen of epigenetic factors in primary murine hematopoietic stem and progenitor cells (HSPCs), we sought to uncover unrecognized genes that contribute to leukemia progression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
9 Samples
Download data: TXT
Series
Accession:
GSE211261
ID:
200211261
2.

Pbrm1 regulates interferon signaling in mouse AML

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24247 GPL24676
26 Samples
Download data: BW, NARROWPEAK, TXT
Series
Accession:
GSE211263
ID:
200211263
3.

Pbrm1 regulates interferon signaling in mouse AML [RNA-seq HAP1]

(Submitter supplied) CRISPR/Cas9 screening approaches are powerful tools to identify in vivo cancer dependencies. Hematopoietic malignancies are genetically complex disorders in which sequential acquisition of somatic mutations generates clonal diversity. With time, additional cooperating mutations may drive disease progression. Using an in vivo pooled gene editing screen of epigenetic factors in primary murine hematopoietic stem and progenitor cells (HSPCs), we sought to uncover unrecognized genes that contribute to leukemia progression. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TXT
Series
Accession:
GSE211262
ID:
200211262
4.

Pbrm1 regulates interferon signaling in mouse AML [ChIP-seq HAP1]

(Submitter supplied) CRISPR/Cas9 screening approaches are powerful tools to identify in vivo cancer dependencies. Hematopoietic malignancies are genetically complex disorders in which sequential acquisition of somatic mutations generates clonal diversity. With time, additional cooperating mutations may drive disease progression. Using an in vivo pooled genetic mutagenesis screen of epigenetic factors in primary murine HSPCs, we sought to uncover unrecognized genes that contribute to leukemia progression. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
5 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE211260
ID:
200211260
5.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER [tet-MUC1 shRNA]

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: CSV
Series
Accession:
GSE212587
ID:
200212587
6.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
18 Samples
Download data
Series
Accession:
GSE212170
ID:
200212170
7.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER [BT549_shPBRM1]

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: CSV
Series
Accession:
GSE212169
ID:
200212169
8.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER [BT549_shIRF1]

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: CSV
Series
Accession:
GSE212168
ID:
200212168
9.

Muc1-C Induces Pbrm1-Mediated Chromatin Remodeling in Driving Chronic Inflammation and DNA Damage Resistance in Triple-Negative Breast Cancer

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
18 Samples
Download data: CSV
Series
Accession:
GSE206212
ID:
200206212
10.

The effects of PBRM1 loss on the ccRCC transcriptome

(Submitter supplied) Subunits of SWI/SNF chromatin remodeling complexes are frequently mutated in human malignancies. The PBAF complex is composed of multiple subunits, including the tumor suppressor protein PBRM1 (BAF180), as well as ARID2 (BAF200), that are unique to this SWI/SNF complex. PBRM1 is mutated in various cancers, with a high mutation frequency in clear cell renal cell carcinoma (ccRCC). In this study, we integrate RNA-seq, histone modification ChIP-seq, and ATAC-seq data to show that loss of PBRM1 results in de novo gains in H3K4me3 peaks throughout the epigenome including activation of a retinoic acid biosynthesis and signaling gene signature. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: SF
Series
Accession:
GSE196129
ID:
200196129
11.

Transcriptome profiling of Caki2 cells re-expressing Polybromo-1 (PBRM1)

(Submitter supplied) PBRM1 is a component of the PBAF chromatin remodelling complex and has been observed to be deregulated in a significant proportion of patients with clear-cell Renal Cell Carcinoma (ccRCC). This study employs RNA-Seq to identify differentially expressed genes in cellular models of ccRCC by expressing PBRM1 in PBRM1-deficient Caki2 cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
12.

Gene expression profiling of murine tumors derived from Renca control knockout vs Pbrm1 knockout tumor clones

(Submitter supplied) We investigated the influence of Pbrm1 on the tumor microenvironment in murine tumors. We employed a Renca-BALB/c murine immune competent model for our study. We compared Renca control knockout tumors to two Pbrm1 KO tumor clones (n=5 for each of two clones).
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
15 Samples
Download data: CSV
Series
Accession:
GSE145919
ID:
200145919
13.

Transcription control by the ENL YEATS domain in acute leukemia

(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
Platform:
GPL18573
38 Samples
Download data: WIG
Series
Accession:
GSE82118
ID:
200082118
14.

Transcription control by the ENL YEATS domain in acute leukemia [RNA-seq]

(Submitter supplied) Recurrent chromosomal translocations involving the mixed lineage leukemia gene (MLL) give rise to highly aggressive acute leukemia associated with poor clinical outcomes. The preferential involvement of chromatin-associated factors in MLL rearrangements belies a dependency on transcriptional control. To identify new targets for therapeutic development in MLL, we performed a genome-scale CRISPR-Cas9 knockout screen in MLL-AF4 leukemia. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: TXT
15.

Transcription control by the ENL YEATS domain in acute leukemia [ChIP-seq]

(Submitter supplied) Recurrent chromosomal translocations involving the mixed lineage leukemia gene (MLL) give rise to highly aggressive acute leukemia associated with poor clinical outcomes. The preferential involvement of chromatin-associated factors in MLL rearrangements belies a dependency on transcriptional control. To identify new targets for therapeutic development in MLL, we performed a genome-scale CRISPR-Cas9 knockout screen in MLL-AF4 leukemia. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
20 Samples
Download data: WIG
Series
Accession:
GSE82116
ID:
200082116
16.

A major chromatin regulator determines resistance of tumor cells to T cell–mediated killing

(Submitter supplied) Many human cancers are resistant to immunotherapy, for reasons that are poorly understood. We used a genome-scale CRISPR-Cas9 screen to identify mechanisms of tumor cell resistance to killing by cytotoxic T cells, the central effectors of antitumor immunity. Inactivation of >100 genes—including Pbrm1, Arid2, and Brd7, which encode components of the PBAF form of the SWI/SNF chromatin remodeling complex—sensitized mouse B16F10 melanoma cells to killing by T cells. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: BW
Series
Accession:
GSE131674
ID:
200131674
17.

A Major Chromatin Regulator Determines Resistance of Tumor Cells to T cell Mediated Killing

(Submitter supplied) Many human cancers are resistant to immunotherapy for reasons that are poorly understood. We used a genome-scale CRISPR/Cas9 screen to identify mechanisms of tumor cell resistance to killing by cytotoxic T cells, the central effectors of anti-tumor immunity. Inactivation of >100 genes sensitized mouse B16F10 melanoma cells to killing by T cells, including Pbrm1, Arid2 and Brd7, which encode components of the PBAF form of the SWI/SNF chromatin remodeling complex. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
24 Samples
Download data: CSV
Series
Accession:
GSE107670
ID:
200107670
18.

Multiplex CRISPR/Cas9-Based Genome Editing of Mouse Hematopoietic Stem Cells Recapitulates Acute Erythroid Leukemia and Identifies Therapeutic Targets

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL21103 GPL24247
110 Samples
Download data: TXT
Series
Accession:
GSE147344
ID:
200147344
19.

Multiplex CRISPR/Cas9-Based Genome Editing of Mouse Hematopoietic Stem Cells Recapitulates Acute Erythroid Leukemia and Identifies Therapeutic Targets [Bisulfite-Seq]

(Submitter supplied) Acute erythroid leukemia (AEL) is a high-risk leukemia with a distinct mutational spectrum. Here, we examined the cooperativity of loss of function alterations in leukemogenesis and tested the therapeutic tractability of each model of AEL. Using CRISPR/Cas9 genome editing, we generated six pools of lentiviral vectors with different combinations of guide RNAs and transduced Cas9-eGFP-mouse mouse hematopoietic stem and progenitor cells (HSPCs) that were used in transplant assays. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL21103
49 Samples
Download data: TXT
Series
Accession:
GSE147343
ID:
200147343
20.

Multiplex CRISPR/Cas9-Based Genome Editing of Mouse Hematopoietic Stem Cells Recapitulates Acute Erythroid Leukemia and Identifies Therapeutic Targets [RNA-Seq]

(Submitter supplied) Acute erythroid leukemia (AEL) is a high-risk leukemia with a distinct mutational spectrum. Here, we examined the cooperativity of loss of function alterations in leukemogenesis and tested the therapeutic tractability of each model of AEL. Using CRISPR/Cas9 genome editing, we generated six pools of lentiviral vectors with different combinations of guide RNAs and transduced Cas9-eGFP-mouse mouse hematopoietic stem and progenitor cells (HSPCs) that were used in transplant assays. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
61 Samples
Download data: TXT
Series
Accession:
GSE147265
ID:
200147265
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