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Links from GEO DataSets

Items: 20

1.

Cooperative epigenetic remodeling by TET2 loss and NRAS mutation drives myeloid transformation and MEK inhibitor sensitivity [bisulfite-Seq]

(Submitter supplied) Recent studies using next-generation sequencing technology have uncovered mutational landscapes of various myeloid malignancies (Cancer Genome Atlas Research Network, 2013; Yoshida et al., 2011). These genetic data revealed novel classes of mutations that commonly occur in patients with myeloid malignancies, including epigenetic regulators and spliceosomal genes. In addition, co-occurrence and mutual exclusivity of these disease alleles suggest convergent cooperative roles or common biological effects of specific alleles in myeloid leukemogenesis (Shih et al., 2012). more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE96759
ID:
200096759
2.

Cooperative epigenetic remodeling by TET2 loss and NRAS mutation drives myeloid transformation and MEK inhibitor sensitivity

(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
Platform:
GPL17021
27 Samples
Download data: TXT
Series
Accession:
GSE96761
ID:
200096761
3.

Cooperative epigenetic remodeling by TET2 loss and NRAS mutation drives myeloid transformation and MEK inhibitor sensitivity [RNA-Seq]

(Submitter supplied) Recent studies using next-generation sequencing technology have uncovered mutational landscapes of various myeloid malignancies (Cancer Genome Atlas Research Network, 2013; Yoshida et al., 2011). These genetic data revealed novel classes of mutations that commonly occur in patients with myeloid malignancies, including epigenetic regulators and spliceosomal genes. In addition, co-occurrence and mutual exclusivity of these disease alleles suggest convergent cooperative roles or common biological effects of specific alleles in myeloid leukemogenesis (Shih et al., 2012). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
15 Samples
Download data: TXT
Series
Accession:
GSE96758
ID:
200096758
4.

Gene expression profiling in pre-leukemic hematopoietic stem cells carrying both NrasG12D/+ and Tet2+/- mutations

(Submitter supplied) By using a genetically accurate mouse model, we demonstrate that endogenous expression of oncogenic N-RasG12D and Tet2 haploinsufficiency collaborate to accelerate CMML development in mice. Gene expression was compared across all genotypes (WT, Tet2+/-, NrasG12D/+ and double mutants) in bone marrow-derived hematopoietic stem cells (CD150+CD48-Lin-Sca1+cKit+) using RNA-seq. N-RasG12D and Tet2 haploinsufficiency cooperate to induce both unique and overlapping effects on HSC gene expression programs.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE97640
ID:
200097640
5.

Transcriptome of chronic myelomonocytic leukemia

(Submitter supplied) We report the gene expression of human chronic myelomonocytic leukemia by performing whole transcriptome shotgun sequencing of peripheral blood mononuclear cells of patients with chronic myelomonocytic leukemia.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
25 Samples
Download data: TXT
6.

RNA-seq analysis of transcriptomic changes in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice [RNA-seq]

(Submitter supplied) Epigenetic gene regulation and metabolism are highly intertwined, yet little is known whether and how altered epigenetics influences cellular metabolism in cancer progression. Here we show that EZH2 and NRasG12D mutations cooperatively induce progression of myeloproliferative neoplasms to fully penetrant, transplantable and lethal myeloid leukemias in mouse. EZH1, an EZH2 homolog, is indispensable for EZH2-deficient leukemia-initiating cells (LICs) and constitutes an epigenetic vulnerability. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
14 Samples
Download data: TXT
Series
Accession:
GSE132079
ID:
200132079
7.

ChIP-seq analysis of H3K4me3,H3K27ac and H3K27me3 in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

(Submitter supplied) Epigenetic gene regulation and metabolism are highly intertwined, yet little is known whether and how altered epigenetics influences cellular metabolism in cancer progression. Here we show that EZH2 and NRasG12D mutations cooperatively induce progression of myeloproliferative neoplasms to fully penetrant, transplantable and lethal myeloid leukemias in mouse. EZH1, an EZH2 homolog, is indispensable for EZH2-deficient leukemia-initiating cells (LICs) and constitutes an epigenetic vulnerability. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
32 Samples
Download data: BIGWIG
Series
Accession:
GSE132078
ID:
200132078
8.

ATAC-seq analysis in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

(Submitter supplied) Epigenetic gene regulation and metabolism are highly intertwined, yet little is known whether and how altered epigenetics influences cellular metabolism in cancer progression. Here we show that EZH2 and NRasG12D mutations cooperatively induce progression of myeloproliferative neoplasms to fully penetrant, transplantable and lethal myeloid leukemias in mouse. EZH1, an EZH2 homolog, is indispensable for EZH2-deficient leukemia-initiating cells (LICs) and constitutes an epigenetic vulnerability. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
14 Samples
Download data: BIGWIG
Series
Accession:
GSE132077
ID:
200132077
9.

Epigenomic and transcriptomic analysis of bone marrow LSK cells in WT, G12D, Ezh2-KO, and G12D with Ezh2-KO mice

(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
Platform:
GPL19057
60 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE112995
ID:
200112995
10.

Next gen RNA sequencing of mouse acute myeloid leukemia

(Submitter supplied) Trascriptome analysis of aml samples were performed
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
9 Samples
Download data: TXT
Series
Accession:
GSE87870
ID:
200087870
11.

Global Gene Expression of hematopoietic stem cells expressing endogenous NrasG12D/G12D, NrasG12D/+, Nras+/+

(Submitter supplied) Oncogenic NRAS mutations are frequently identified in human myeloid leukemias. In mice, expression of endogenous oncogenic Nras (NrasG12D/+) in hematopoietic cells leads to expansion of myeloid progenitors, increased long-term reconstitution of bone marrow cells, and a chronic myeloproliferative neoplasm (MPN). However, acute expression of NrasG12D/+ in a pure C57BL/6 background does not induce hyperactivated GM-CSF signaling or increased proliferation in myeloid progenitors. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL4134
8 Samples
Download data: TXT
Series
Accession:
GSE46948
ID:
200046948
12.

Wild-Type Nras Lacks Tumor Suppressor Activity and Nras Oncogene Dosage Strongly Modulates Hematopoietic Transformation

(Submitter supplied) Contemporary treatment of pediatric acute myeloid leukemia (AML) requires the assignment of patients to specific risk groups. To explore whether expression profiling of leukemic blasts could accurately distinguish between the known risk groups of AML, we analyzed 130 pediatric and 20 adult AML diagnostic bone marrow or peripheral blood samples using the Affymetrix U133A microarray. Class discriminating genes were identified for each of the major prognostic subtypes of pediatric AML, including t(15;17)[PML-RARalpha], t(8;21)[AML1-ETO], inv(16) [CBFbeta-MYH11], MLL chimeric fusion genes, and cases classified as FAB-M7. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
108 Samples
Download data: CEL
Series
Accession:
GSE43176
ID:
200043176
13.

Discovery of novel recurrent mutations and rearrangements in early T-cell precursor acute lymphoblastic leukaemia by whole genome sequencing

(Submitter supplied) Acute lymphoblastic leukaemia with early T-cell precursor immunophenotype (ETP ALL) is a highly aggressive subtype of ALL of unknown aetiology. To gain insights into the genetic basis of this disease, we performed whole genome sequencing of tumour and normal DNA of 12 children with ETP ALL. Analysis of structural and sequence variants in this discovery cohort, and mutation recurrence screening in a panel of 51 ETP and 43 non ETP ALL samples identified a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling, including IL7R, NRAS, KRAS, FLT3, BRAF, JAK1 and JAK3 in ETP ALL. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
575 Samples
Download data: CEL
Series
Accession:
GSE33315
ID:
200033315
14.

TET2 mutations are associated with specific methylation profiles in patients with Chronic Myelomonocytic Leukemia

(Submitter supplied) Chronic myelomonocytic leukemia (CMML) has recently been associated with a high incidence of diverse mutations in genes implicated in epigenetic mechanisms such as TET2 or EZH2. We have performed genome-wide methylation arrays and mutational analysis of TET2, IDH1, IDH2, EZH2 and JAK2 in a group of 24 patients with CMML. 249 genes were differentially methylated between CMML patients and controls. Using Ingenuity pathway analysis enrichment in a gene network centered in PLC, JNK and ERK, a recently described pathway involved in CMML was found, suggesting the potential role of epigenetics in the regulation of these pathways. more...
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL8490
32 Samples
Download data: TXT
Series
Accession:
GSE31600
ID:
200031600
15.

Mutant SETBP1 enhances NRAS-driven MAPK pathway activation to promote aggressive leukemia

(Submitter supplied) Mutations in SET binding protein 1 (SETBP1) are associated with poor outcomes in myeloid leukemias. In the Ras-driven leukemia, juvenile myelomonocytic leukemia, SETBP1 mutations are enriched in relapsed disease. We demonstrate that SETBP1 enhances the NRAS gene expression signature, driving upregulation of mitogen-activated protein kinase (MAPK) signaling and downregulation of differentiation pathways.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE158379
ID:
200158379
16.

Expression data from loss-of-TET2 and/or JAK2V617F mutant Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

(Submitter supplied) Recent studies have shown that both TET2 mutation and JAK2V617F mutation are frequent in myeloproliferative neoplasms patients. The pathophysiological roles of each mutation have been elucidated in murine models, but the cooperative effect of the two mutations has not been elucidated yet. In this study, we examined the function of the cooperative effect of loss-of-TET2 function and JAK2V617F mutation in murine hematopoiesis.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10787
4 Samples
Download data: TXT
Series
Accession:
GSE62302
ID:
200062302
17.

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

(Submitter supplied) Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4287
Platform:
GPL1261
14 Samples
Download data: CEL
Series
Accession:
GSE27816
ID:
200027816
18.
Full record GDS4287

Effect of Tet2 loss in bone marrow progenitors

Analysis of sorted bone marrow progenitor populations (LSK, CMP, GMP) deficient in ten-eleven translocation 2 (TET2). Tet2 loss causes increased hematopoietic stem cell self-renewal and myeloid transformation. Results provide insight into the molecular mechanisms underlying myeloid malignancies.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 4 cell type, 2 genotype/variation sets
Platform:
GPL1261
Series:
GSE27816
14 Samples
Download data: CEL
19.

Tet2-/-Flt3ITD and WT stem and progenitor cells

(Submitter supplied) The study was a comparison of gene expression using RNA-seq. We analyzed the stem and progenitor cells from WT and Vav-cre+ Tet2fl/fl Flt3-ITD (T2F3) mice. We isolated stem cells LSK (lin- sca+ kit+) and granulocyte-macrophage progenitors GMP (lin- sca- kit+ fcgr+ cd34+) cells from bone marrow. Comparisons were made across genotypes WT vs. T2F3 and cell types LSK vs. GMP.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18635
12 Samples
Download data: TXT
Series
Accession:
GSE57244
ID:
200057244
20.

FLT3-ITD mutations and TET2 loss synergistically alter global DNA methylation in AML

(Submitter supplied) Studies of AML patient samples have shown that specific combinations of AML disease alleles confer an adverse outcome, however, in vivo models do not exist for the majority of common, poor-prognosis genotypes. Here we show that TET2/FLT3 mutations can cooperate to induce AML in vivo using a genetically engineered mouse model, and that this model has a defined stem-cell population with a characteristic transcriptional and epigenetic profile. more...
Organism:
Homo sapiens; Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
15 Samples
Download data: TXT
Series
Accession:
GSE57114
ID:
200057114
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