GEO DataSets

(Submitter supplied) PcG proteins form the polycomb repressive complexes (PRC) 1 and 2, functioning as transcriptional repressors through histone modifications. They have been implicated in the maintenance of self-renewing somatic and cancer stem cells. PcG genes have been characterized as tumor suppressor genes as exemplified by somatic inactivating mutations of EZH2, a gene encoding histone methyltransferase in PRC2, in myeloid malignancy. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL13912

12 Samples

Download data: TXT

(Submitter supplied) Recent studies have showed that loss-of-function mutations of EZH2, a catalytic component of polycomb repressive complex 2, are often associated with RUNX1 mutations in myelodysplastic syndrome (MDS) patients. We established a novel MDS model mouse by transducing a RUNX1S291fs mutant in hematopoietic stem cells followed by deletion of Ezh2 and found that Ezh2 loss significantly promoted RUNX1S291fs-induced MDS.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

8 Samples

Download data: TXT

(Submitter supplied) The polycomb group (PcG) proteins function in gene silencing through histone modifications. They form chromatin-associated multiprotein complexes, termed polycomb repressive complex (PRC) 1 and PRC2. These two complexes work in a coordinated manner in the maintenance of cellular memories through transcriptional repression of target genes. EZH2 is a catalytic component of PRC2 and trimethylates histone H3 at lysine 27 to transcriptionally repress the target genes. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10333

4 Samples

Download data: TXT

(Submitter supplied) How specific genetic lesions contribute to transformation of non-malignant myeloproliferative neoplasms (MPN) and myelodysplastic syndromes (MDS) to secondary acute myeloid leukemia (sAML) are poorly understood. The JARID2 gene is lost by chromosomal deletions in a proportion of MPN/MDS patients who progress to sAML. In this study, genetic mouse models and patient-derived xenografts (PDX) demonstrated that Jarid2 acts as a tumor suppressor in chronic myeloid disorders. more...

Organism:

Mus musculus

Type:

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

Platform:

GPL21493

32 Samples

Download data: BW, TXT

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

2 Samples

Download data: BIGWIG, NARROWPEAK

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

Organism:

Mus musculus

Type:

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

4 related Platforms

74 Samples

Download data: BIGWIG, BW, NARROWPEAK

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...

Organism:

Mus musculus

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL13112

24 Samples

Download data: BW

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

20 Samples

Download data: BW, NARROWPEAK

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24247

16 Samples

Download data: NARROWPEAK

(Submitter supplied) The p300 lysine acetyltransferase (KAT) can function as an oncogene or a tumor suppressor in hematologic malignancies. We have identified a tumor suppressor role for p300 in myelodysplastic syndrome (MDS) driven by Tet2 deficiency. Compared to Tet2-null hematopoietic stem and progenitor cells (HSPCs), HSPCs lacking both p300 and Tet2 (double knock out, DKO) displayed enhanced proliferation and impaired differentiation. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

12 Samples

Download data: XLSX

(Submitter supplied) Bmi1 is a component of polycomb repressive complex 1 and its role in the inheritance of the stemness of adult somatic stem cells has been well characterized. Bmi1 maintains the self-renewal capacity of adult stem cells, at least partially, by repressing the Ink4a/Arf locus that encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf 14. Deletion of both Ink4a and Arf in Bmi1-deficient mice substantially restored the defective self-renewal capacity of HSCs and neural stem cells.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL, CHP

(Submitter supplied) Bmi1 is a component of polycomb repressive complex 1 and its role in the inheritance of the stemness of adult somatic stem cells has been well characterized. Bmi1 maintains the self-renewal capacity of adult stem cells, at least partially, by repressing the Ink4a/Arf locus that encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf 14. Deletion of both Ink4a and Arf in Bmi1-deficient mice substantially restored the defective self-renewal capacity of HSCs and neural stem cells.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

7 Samples

Download data: CEL, CHP

(Submitter supplied) TET2 is a close relative of TET1, an enzyme that converts 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in DNA. The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies. Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML). more...

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL8490

81 Samples

Download data: TXT

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

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing; Expression profiling by array

Platforms:

GPL16791 GPL22448

16 Samples

Download data: BEDGRAPH, NARROWPEAK, TXT

(Submitter supplied) Improved understanding of mechanisms regulating myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cell (HSPC) growth and self-renewal is critical for developing MDS therapy. We revealed a novel regulatory axis that SIRT1-deficiency induced TET2 hyperacetylation promotes MDS HSPC functions, and provide an approach to target MDS HSPCs by activating SIRT1 deacetylase.

Organism:

Homo sapiens

Type:

Methylation profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: BEDGRAPH, NARROWPEAK

(Submitter supplied) Improved understanding of mechanisms regulating myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cell (HSPC) growth and self-renewal is critical for developing MDS therapy. We revealed a novel regulatory axis that SIRT1-deficiency induced TET2 hyperacetylation promotes MDS HSPC functions, and provide an approach to target MDS HSPCs by activating SIRT1 deacetylase. Four Groups: Group1: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for SIRT1); Group2: MDS-L cells transduced with lentiviral vector containing interference squence targeting SIRT1 (SIRT shRNA); Group 3: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for TET2); Group 4: MDS-L cells transduced with lentiviral vector containing interference squence targeting TET2 (TET2 shRNA).

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL22448

10 Samples

Download data: TXT

(Submitter supplied) To identify genes that are influenced by the catalytic and non-catalytic functions of Tet2 in hematopoietic stem and progenitor cells (HSPCs), we analyzed the gene expression profiles of Tet2 catalytic mutant (Tet2 Mut), Tet2 knockout (Tet2 KO) and wild-type HSPCs (or LSK, Lin–Sca-1+c-Kit+) and multi-potent progenitor (or MPP, Lin–) cells by RNA-seq.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

12 Samples

Download data: TXT

(Submitter supplied) Mutations in the RNA splicing complex member SRSF2 are found frequently in myelodysplastic syndrome and related malignancies such as chronic myelomonocytic leukemia. These mutations cluster on proline 95, with P95H the most frequent. How SRSF2P95H mutations modify hematopoiesis and promote MDS/MPN development is not clear. We have established a conditionally activatable Srsf2P95H/+ knock-in allele which, when expressed within the hematopoietic stem cell populations caused profound myeloid bias, at the expense of erythroid and lymphoid cells, and a reduced frequency and competitive repopulation of HSCs. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21273

6 Samples

Download data: GCT, ODF, XLSX

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

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Other

Platforms:

GPL19057 GPL21273

14 Samples

Download data: TXT, VCF

(Submitter supplied) Mutations in the RNA splicing complex member SRSF2 are found frequently in myelodysplastic syndrome and related malignancies such as chronic myelomonocytic leukemia. These mutations cluster on proline 95, with P95H the most frequent. How SRSF2P95H mutations modify hematopoiesis and promote MDS/MPN development is not clear. We have established a conditionally activatable Srsf2P95H/+ knock-in allele which, when expressed within the hematopoietic stem cell populations caused profound myeloid bias, at the expense of erythroid and lymphoid cells, and a reduced frequency and competitive repopulation of HSCs. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

2 Samples

Download data: XLSX