GEO DataSets

(Submitter supplied) Cancer cells frequently depend on chromatin regulatory activities to maintain a malignant phenotype. Here, we show that leukemia cells require the mammalian SWI/SNF chromatin remodeling complex for their survival and aberrant self-renewal potential. While Brg1, an ATPase subunit of SWI/SNF, is known to suppress tumor formation in several cancer types, we found that leukemia cells instead rely on Brg1 to support their oncogenic transcriptional program, which includes Myc as one of its key targets. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

21 Samples

Download data: TXT

(Submitter supplied) Cancer cells frequently depend on chromatin regulatory activities to maintain a malignant phenotype. Here, we show that leukemia cells require the mammalian SWI/SNF chromatin remodeling complex for their survival and aberrant self-renewal potential. While Brg1, an ATPase subunit of SWI/SNF, is known to suppress tumor formation in several cancer types, we found that leukemia cells instead rely on Brg1 to support their oncogenic transcriptional program, which includes Myc as one of its key targets. more...

Organism:

Mus musculus

Type:

Other

Platform:

GPL16417

6 Samples

Download data: WIG

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other

Platforms:

GPL6246 GPL16417 GPL13112

42 Samples

Download data: CEL, TXT, WIG

(Submitter supplied) Cancer cells frequently depend on chromatin regulatory activities to maintain a malignant phenotype. Here, we show that leukemia cells require the mammalian SWI/SNF chromatin remodeling complex for their survival and aberrant self-renewal potential. While Brg1, an ATPase subunit of SWI/SNF, is known to suppress tumor formation in several cancer types, we found that leukemia cells instead rely on Brg1 to support their oncogenic transcriptional program, which includes Myc as one of its key targets. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: WIG

(Submitter supplied) Cancer cells frequently depend on chromatin regulatory activities to maintain a malignant phenotype. Here, we show that leukemia cells require the mammalian SWI/SNF chromatin remodeling complex for their survival and aberrant self-renewal potential. While Brg1, an ATPase subunit of SWI/SNF, is known to suppress tumor formation in several cancer types, we found that leukemia cells instead rely on Brg1 to support their oncogenic transcriptional program, which includes Myc as one of its key targets. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

9 Samples

Download data: CEL

(Submitter supplied) We demonstrate that CBFb-SMMHCmaintains leukemia viability by inhibiting RUNX1 repression of MYC expression. Upon pharmacologic inhibition of CBF-SMMHC/RUNX1 binding, RUNX1 increases its association with three MYC distal downstream enhancers and represses MYC expression.

Organism:

Homo sapiens

Type:

Other

Platform:

GPL20301

4 Samples

Download data: TXT

(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; Other

Platforms:

GPL11154 GPL20301

20 Samples

Download data: BW, NARROWPEAK, TXT

(Submitter supplied) We recently reported the discovery of a small molecule inhibitor, AI-10-49 which can specially inhibit the protein-protein interaction between RUNX1 tumor suppressor and CBFβ-SMMHC oncogene. We also demonstrated that AI-10-49 can re-establish the RUNX1 transcriptional program in inv(16) cells and can extend the survival of inv(16) leukemic mice. To identify the changes in chromatin accessibility associated with AI-10-49, we performed ATAC-seq analysis in ME-1 cells [human inv(16) leukemia cell line] treated with AI-10-49.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

4 Samples

Download data: BW, NARROWPEAK

(Submitter supplied) We recently reported the discovery of a small molecule inhibitor, AI-10-49 which can specially inhibit the protein-protein interaction between RUNX1 tumor suppressor and CBFβ-SMMHC oncogene. We also demonstrated that AI-10-49 can re-establish the RUNX1 transcriptional program in inv(16) cells and can extend the survival of inv(16) leukemic mice. To identify the epigenetic changes as well as RUNX1 binding associated with AI-10-49, we performed genome wide analysis of H3K27ac histone mark as well as RUNX1 bindings in ME-1 cells [human inv(16) leukemia cell line] treated with AI-10-49.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL20301

6 Samples

Download data: BW, NARROWPEAK

(Submitter supplied) We recently reported the discovery of a small molecule inhibitor, AI-10-49 which can specially inhibit the protein-protein interaction between RUNX1 tumor suppressor and CBFβ-SMMHC oncogene. We also demonstrated that AI-10-49 can re-establish the RUNX1 transcriptional program in inv(16) cells and can extend the survival of inv(16) leukemic mice. To identify the transcriptional changes associated with AI-10-49, we performed RNA-seq analysis in ME-1 cells [human inv(16) leukemia cell line] treated with AI-10-49.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: CSV, DIFF

(Submitter supplied) Identification of gene expression changes in wild type versus mutant mouse hearts where Brg1 and Brm were knocked out in adult cardiomyocytes.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL21163

8 Samples

Download data: TXT

(Submitter supplied) To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the transcription factor MAX.Human SCLC cell lines waere analyzed for mutations at the MAX locus. Those cell lines that were found mutated in MAX and showed no MAX protein expression were used as a models to restore the expression of MAX transcription factor, and Identify MAX signature on Human SCLC.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17077

12 Samples

Download data: TXT

(Submitter supplied) Global Transcriptional analysis of BRG1 in lung cancer cells

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

12 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL570 GPL16699

24 Samples

Download data: CEL, TXT

(Submitter supplied) We explored the role of SMARCA4 and the two Brahma associated factors SMARCD2 and DPF2 in leukaemia. We observed the selective requirement for these factors for leukemic cell expansion, as well as extended survival of mice transplanted with leukaemic cells with reduced expression of these genes. Gene expression profiling revealed largely similar alterations with the down-regulation of each of these three factors, suggesting a concerted function in transformed blood cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL16699

12 Samples

Download data: TXT

(Submitter supplied) Pharmacological inhibition of the SMARCA4 bromodomain inhibited human leukemic cell proliferation, phenocopying SMARCA4 knockdown in these cells. We performed microarray analysis of global gene expression changes in MV4-11 cells after 6 days of PFI-3 treatment and after SMARCA4 knock-down. With this analysis we identified several genes whose expression was similarly up- or down-regulated upon inhibitor treatment and SMARCA4 depletion.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

12 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

4 related Platforms

30 Samples

Download data: BW, TSV, TXT

(Submitter supplied) BRG1 S1382 phospho-mutations led to altered gene activation in neurons in response to neuronal activation

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL28457

14 Samples

Download data: MATRIX, TSV

(Submitter supplied) BRG1 deletion led to impaired gene activation in neurons in response to neuronal activation

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21493

4 Samples

Download data: TXT

(Submitter supplied) CHIP-seq analysis of BRG1 binding sites in cultured cortical neurons revealed a depolarization induced BRG1 binding to neuronal inducible enahncers.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

4 Samples

Download data: BW, TXT