GEO DataSets

(Submitter supplied) Transcriptional profiling of mouse mesenchymal stem/progenitor cells (MSPC) comparing control Ptpn11+/+ MSPC with Ptpn11E76K/+ MSPC. By obtaining 20 million reads of sequence from two pair, we confirmed our cytokine/chemokine array data and quantitative ELISA data from both mouse and patient-derived specimens. CCL3, CCL12, CCL4, and CXCL12 (SDF-1) were aberrantly produced by Ptpn11 mutated MSPCs

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

2 Samples

Download data: TXT

(Submitter supplied) Activating mutations in PTPN11 gene are the most frequent in JMML patients. Here we explore the transcriptome of HSPC (hematopoietic stem and progenitor cells) sorted from sporadic JMML patients with PTPN11 mutation and from healthy age matched donnors. Bulk transcriptome of sorted HSPC reveals an inflammatory gene expression signature which may represent a future target for JMML therapy.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

36 Samples

Download data: TXT

(Submitter supplied) Hematopoietic stem and progenitor cells derived from a zebrafish model of Noonan syndrome, carrying a patient-associated Shp2-D61G mutation, display an expansion of monocyte/macrophage progenitors with an inflammatory gene expression signature.

Organism:

Danio rerio

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20828

6 Samples

Download data: CSV, TSV

(Submitter supplied) To gain insights into which pathways might be dysregulated in JMML, we compared the transcriptome profiles among hiPSC and sorted CD33+ myeloid cells from control and patient samples. NS/JMML-derived CD33+ myeloid cells showed dysregulation in major biological processes. Moreover, a consistent expression pattern among sets of genes related to pluripotency and myeloid regulation was observed in the control, NS and NS/JMML CD33+ myeloid cells further supporting generally successful myelopoiesis.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

21 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; Expression profiling by array

Platforms:

GPL6246 GPL11002

6 Samples

Download data: CEL

(Submitter supplied) Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common acquired mutation of Janus kinase 2 (JAK2) gene in HSCs that renders this kinase constitutively active, leading to uncontrolled cell expansion. The bone marrow (BM) microenvironment might contribute to the clinical outcomes of this common event. We previously showed that BM nestin+ mesenchymal stem cells (MSCs) innervated by sympathetic nerve fibres regulate normal HSCs. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

4 Samples

Download data: CEL

(Submitter supplied) Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common acquired mutation of Janus kinase 2 (JAK2) gene in HSCs that renders this kinase constitutively active, leading to uncontrolled cell expansion. The bone marrow (BM) microenvironment might contribute to the clinical outcomes of this common event. We previously showed that BM nestin+ mesenchymal stem cells (MSCs) innervated by sympathetic nerve fibres regulate normal HSCs. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11002

2 Samples

Download data: TXT

(Submitter supplied) Multipotent stromal cells (MSC) and their osteoblastic lineage cell (OBC) derivatives are part of the bone marrow (BM) niche and contribute to hematopoietic stem cell (HSC) maintenance. During myeloproliferative neoplasm (MPN) development, MSCs are stimulated to overproduce functtionally altered OBCs, which accumulate in the BM cavity as myelofibrotic cells. These MPN-expanded OBCs, in turn, impair the maintenance of normal HSCs but not of leukemic stem cells. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5024

Platform:

GPL6246

10 Samples

Download data: CEL

Analysis of osteoblastic lineage cells (OBC) from Scl-tTA::TRE-BCR/ABL (BA) double-transgenics withdrawn from doxycycline at 5 weeks of age to induce myeloproliferative neoplasia (MPN). MPN development drives OBC expansion. Results provide insight into molecular features of MPN-expanded OBCs.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 genotype/variation sets

Platform:

GPL6246

Series:

GSE48438

10 Samples

Download data: CEL

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

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL20301 GPL18573

31 Samples

Download data: TXT

(Submitter supplied) We report on the characterization of JMML hematopoietic stem and progenitor cells (HSPCs). In order to characterize the single cell heterogeneity in comparison to normal cord blood we preformed droplet based single cell RNA-seq of FACS sorted CD34+ cells using the 10x genomics platform. We identified distinct clustering of unique JMML HSPC populations in relation to cord blood control.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

4 Samples

Download data: TXT

(Submitter supplied) We report on the characterization of JMML hematopoietic stem and progenitor cells (HSPCs). In order to molecularly characterize these populations we preformed bulk RNA-seq on purified cord blood and JMML HSCs, GMPs, and JMML double positives (+/+). We identified a conserved molecular hierarchy in JMML with high stem cell gene expression in HSCs, high progenitor and cell cycle gene expression in GMPs. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

27 Samples

Download data: TXT

(Submitter supplied) Mutations that decrease activity of the tyrosine phosphatase, SHP2 (encoded by PTPN11), causes Noonan syndrome with multiple lentigines or NSML (also called LEOPARD syndrome), while the gain-of-function mutations promotes several malignancies. Precisely how a spectrum of maladies ranging from developmental disorders to cancer are regulated by varying a solitary phosphatase activity is not clearly understood. more...

Organism:

Homo sapiens; Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL24247 GPL24676

8 Samples

Download data: NARROWPEAK