GEO DataSets

(Submitter supplied) The JAK2V617F mutation has been detected in ~50% cases of MF. Elevated expression of high mobility group AT hook 2 (HMGA2) also has been frequently observed in patients with MF. Interestingly, upregulation of HMGA2 expression has been found in association with the JAK2V617F mutation in significant cases of MF. However, the contribution of HMGA2 in the pathogenesis of MF remains elusive. To determine the effects of concurrent expression of HMGA2 and JAK2V617F mutation in hematopoiesis, we transduced bone marrow cells from Jak2V617F knock-in mice with lentivirus expressing Hmga2 and performed bone marrow transplantation. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

6 Samples

Download data: TXT

(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

Platforms:

GPL16570 GPL19057

12 Samples

Download data: CEL, WIG

(Submitter supplied) Inactivating EZH2 mutations have been associated with myelofibrosis (MF). Moreover, EZH2 mutations co-exist with the JAK2V617F mutation in a significant cases of MF. To determine the effects of concomitant loss of EZH2 and JAK2V617F mutation in hematopoiesis, we generated Ezh2-deficient Jak2V617F-expressing mice. To identify the Ezh2 target genes that are regulated by H3K27me3 in MF, we performed H3K27me3 ChIP-sequencing in sorted LSK cells from control, MxCre;Jak2VF/+ and MxCre;Jak2VF/+ EZH2-/- mice.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

3 Samples

Download data: WIG

(Submitter supplied) Inactivating EZH2 mutations have been associated with myelofibrosis (MF). Moreover, EZH2 mutations co-exist with the JAK2V617F mutation in a significant cases of MF. To determine the effects of concomitant loss of EZH2 and JAK2V617F mutation in hematopoiesis, we generated Ezh2-deficient Jak2V617F-expressing mice. To gain insights into the mechanisms by which Ezh2 deficiency promotes the development of MF in Jak2V617F knock-in mice, we performed microarray gene expression analysis on sorted LT-HSC from control, MxCre;Jak2VF/+ and MxCre;Jak2VF/+ EZH2-/- mice.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

9 Samples

Download data: CEL

(Submitter supplied) TGF-β1 signaling pathway of bone marrow of the Gata1low mouse model of myelofibrosis

Organism:

Mus musculus

Type:

Expression profiling by RT-PCR

Platform:

GPL16739

4 Samples

Download data: TXT

(Submitter supplied) TGF-β1 signaling pathway of spleen of the Gata1low mouse model of myelofibrosis

Organism:

Mus musculus

Type:

Expression profiling by RT-PCR

Platform:

GPL16739

4 Samples

Download data: TXT

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

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

12 Samples

Download data: TXT

(Submitter supplied) Loss-of-function mutations in EZH2 are associated with worse outcomes in patients with primary myelofibrosis (PMF). To understand how EZH2 insufficiency is involved in the pathogenesis of PMF, we generated mice compound for Ezh2 conditional deletion and a JAK2V617F transgene.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

4 Samples

Download data: TXT

(Submitter supplied) Loss-of-function mutations in EZH2 are associated with worse outcomes in patients with primary myelofibrosis (PMF). To understand how EZH2 insufficiency is involved in the pathogenesis of PMF, we generated mice compound for Ezh2 conditional deletion and a JAK2V617F transgene.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

8 Samples

Download data: TXT

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

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL19057 GPL13112

64 Samples

Download data: TSV

(Submitter supplied) Comparison of mRNA expression profiles of LT-HSCs with or without mutations in JAK2 and Ezh2 by RNA sequencing. LT-HSC mRNA was extracted from six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) 10 weeks after tamoxifen injection. Our study represents the first detailed analysis of mRNA expression profile of LT-HSC with or without mutations in JAK2 and Ezh2 , with biologic replicates, generated by RNA-seq technology. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

35 Samples

Download data: TSV

(Submitter supplied) Comparison of mRNA expression profiles of MEPs with or without mutations in JAK2 and Ezh2 by RNA sequencing. MEPs mRNA was extracted from six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) 10 weeks after tamoxifen injection. Our study represents the first detailed analysis of mRNA expression profile of MEP with or without mutations in JAK2 and Ezh2 , with biologic replicates, generated by RNA-seq technology. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

29 Samples

Download data: TSV

(Submitter supplied) In this dataset, we determine the global gene expression in human induced pluripotent stem (iPS) cell-derived CD61+ megakaryocytes carrying homozygous JAK2 V617F mutation or the JAK2 wildtype gene.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

6 Samples

Download data: CSV

(Submitter supplied) The JAK2 mutation V617F is detectable in a majority of patients with Ph-negative myeloproliferative neoplasms (MPN). Enforced expression of JAK2 V617F in mice induces myeloproliferation and bone marrow (BM) fibrosis suggesting a causal role for the JAK2 mutant in the pathogenesis of MPN. However, little is known about mechanisms and effector molecules contributing to JAK2 V617F-induced myeloproliferation and fibrosis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

6 Samples

Download data: CEL

(Submitter supplied) Transcriptomics analysis was performed on FACS purified HSPC subsets from SclCre;V617F mice and WT mice bone marrow. The goal of this study is to identify the molecular signatures that are specific to the mutant JAK2 expressing HSPC subsets. We found that mutant JAK2 activation caused dysregulated expression of large numbers of genes in primitive HSPC subsets. Furthermore, this analysis revealed molecular identity and developmental proximity of HSC CD41+/- cells within the HSPC hierarchy.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

23 Samples

Download data: CSV

(Submitter supplied) Increased energy requirement and metabolic reprograming is a hallmark of cancer cells. We found that mouse models of myeloproliferative neoplasms (MPN) expressing mutant JAK2 displayed systemic metabolic changes including hypoglycemia and adipose atrophy. Modulation of nutrient availability modified MPN manifestations and survival. Hypoglycemia in MPN mice correlated with hyperactive erythropoiesis and was due to a combination of elevated glycolysis and increased oxidative phosphorylation. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

9 Samples

Download data: TSV

(Submitter supplied) Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm whose severity and treatment complexity is attributed to the presence of bone marrow (BM) fibrosis and alterations of stroma impairing the production of normal blood cells. Despite the recently discovered mutations including the JAK2V617F mutation in about half of patients, the primitive event responsible for the clonal proliferation is still unknown. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5802

Platform:

GPL4133

12 Samples

Download data: TXT

Analysis of bone marrow mesenchymal stromal cells from primary myelofibrosis (PMF) patients. PMF is a Philadelphia chromosome-negative, chronic myeloproliferative neoplasm. Results provide insight into molecular mechanisms underlying myelofibrosis pathology.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 disease state sets

Platform:

GPL4133

Series:

GSE44426

12 Samples

Download data: TXT

(Submitter supplied) Myelofibrosis (MF) is the deadliest form of myeloproliferative neoplasm (MPN). Pim1 expression is significantly elevated in MPN/MF hematopoietic progenitors. So, we investigated the role of Pim1 in myelofibrosis. We show that genetic ablation of Pim1 blocked the development of myelofibrosis induced by Jak2V617F and MPLW515L. Pharmacologic inhibition of Pim1 with a second-generation Pim kinase inhibitor TP-3654 significantly reduced leukocytosis, splenomegaly and attenuated bone marrow fibrosis in Jak2V617F and MPLW515L mouse models of MF. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

6 Samples

Download data: CSV

(Submitter supplied) Mesenchymal stromal cells are a critical component of the bone marrow hematopoietic stem cell niche. In myelofibrosis, these cells are the major source of fibrosis in the bone marrow. We performed gene expression analysis using microarrays to systematically elucidate the mechanisms leading to fibrogenic conversion of these cells.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

6 Samples

Download data: CEL