Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA Profiling in Aplastic Anaemia (AA) Reveals Similarities between Secondary Myelodysplastic Syndromes (MDS) Arising from Clonal Progression and de novo MDS

ABSTRACT: MicroRNA Profiling in Aplastic Anaemia (AA) Reveals Similarities between Secondary Myelodysplastic Syndromes (MDS) Arising from Clonal Progression and de novo MDS

PROVIDER: PRJNA1012004 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA Profiling in Aplastic Anaemia (AA) Reveals Similarities between Secondary Myelodysplastic Syndromes (MDS) Arising from Clonal Progression and de novo MDS

Project description:Aplastic anaemia (AA) is a form of bone marrow failure (BMF) resulting in significant cytopenias and may progress with clonal evolution to myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML). MicroRNA expression is dysregulated in MDS/AML but there are limited studies on its role in the pathogenesis of AA. Using stored BM samples (n=81) from 2006-2019 from 52 patients, we demonstrate key differences in miRNA expression between AA patients at diagnosis and de novo MDS patients (n=21). The five most significantly upregulated miRNA in MDS patients (downregulated in AA) were miR-130a-3p, miR-221-3p, miR-126-3p, miR-27b-3p and miR-196b-5p (adj p<0.001). However, at the time of AA clonal progression to secondary MDS/AML, no significant miRNA differences were identified suggesting that the underlying mechanistic pathways are similar between AA progression to MDS/AML and de novo MDS. At diagnosis, miR-127-3p, miR-1271-5p, miR-301b-5p, miR-3934-5p and miR-4531 (adj p=0.081) were upregulated in those whose AA eventually progressed in comparison to those without eventual clonal progression. Using KEGG pathway analysis derived from miRPathDBv2.0, cytokine-cytokine receptor interaction, TGF-, MAP kinase, prolactin, Hippo, neurotrophin and FOXO signalling pathways were enriched in AA patients with clonal progression to MDS/AML; these pathways were similarly enriched in the de novo MDS cohort. These studies highlight the differing miRNA expression profiles in AA and MDS and in AA clonal evolution to MDS/AML.

2023-09-02 | GSE242216 | GEO

Ruxolitinib reduces macrophage pyroptosis in aplastic anaemia

Project description:Ruxolitinib reduces macrophage pyroptosis in aplastic anaemia

| PRJNA1235629 | ENA

Single-cell CNV dataset by Cell Ranger from severe aplastic anaemia patients

Project description:Single Cell CNV experiment was performed in severe aplastic anaemia patients with known chromosome 7 abnormality. The goal of this project is to use single cell CNV to assess whether these abnormalities existed prior to immunosuppressive treatment (baseline) and were just too small to detect it with standard cytogenetics.

2026-05-31 | GSE171207 | GEO

Bulk RNA-seq of aplastic anemia (AA) and healthy donors

Project description:Bulk RNA-seq data of Lin-CD34+ hematopoietic stem and progenitor cells derived from bone marrow of healthy donors and untreated aplastic anemia patients

2021-03-31 | GSE165870 | GEO

Gene expression profile of normal v early MDS v non-MDS anemia bone marrow CD34 cells

2005-08-05 | GSE2779 | GEO

Single cell transcriptome from aplastic anemia (AA) and healthy donors [Full-length RNA-seq]

Project description:Transcriptome analysis of hematopoietic stem and progenitor cells (HSPCs) from aplastic anemia (AA) and healthy donors

2021-03-31 | GSE145531 | GEO

Single cell transcriptome from aplastic anemia (AA) and healthy donors [3' RNA-seq]

Project description:Transcriptome analysis of hematopoietic stem and progenitor cells (HSPCs) and T cells collected from bone marrow and peripheral blood of healthy donors and aplastic anemia patients untreated or response to immunosuppressive therapy.

2021-03-31 | GSE145668 | GEO

Transcription profiling of normal v early MDS v non-MDS anemia bone marrow CD34 cells to identify biomarkers of disease

Project description:Early, low risk IPSS (International Prognostic Scoring System) myelodysplasia (MDS) is a heterogeneous disorder where the molecular and cellular haematopoietic defects are poorly understood. To gain insight into this condition, we analyzed gene expression profiles of marrow CD34+ progenitor cells from normal karyotype, low blast count MDS patients, age-matched controls and patients with non-MDS anaemia. The aim of the study was to further understanding of the cellular defect in MDS and to identify biomarkers of disease Experiment Overall Design: Bone marrow (BM) CD34 cells were purified from patients with MDS, non-MDS anemia and from normal donors. Total RNA was extracted from Tri-reagent and quality verified on by capillary electrophoresis (Agilent). RNA was amplified by the Affymetrix small sample protocol. cRNA was hybridised to Affymetrix U133A chips under standard conditions. Initial data was analysed in MAS 5.0

2007-09-20 | E-GEOD-2779 | biostudies-arrayexpress

Project description:Whole exome sequencing of aplastic anaemia

| PRJNA686657 | ENA

Ruxolitinib reduces macrophage pyroptosis in aplastic anaemia

Project description:Aplastic anaemia (AA) is a disease that shows complex pathogenesis involving multiple immune factors. While immunosuppressive therapies such as cyclosporine can effectively control AA, they may be ineffective in certain patients or those with relapse. Therefore, new treatments are needed. Among the targets for these treatments, the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway regulates inflammatory cytokines and immune activation. Ruxolitinib, a JAK1/2 inhibitor, reduces T-cell activation and the associated inflammatory response and improves AA disease status in mice. However, its mechanism of action is unclear; thus, further research is needed before its clinical use. We previously showed increased pyroptosis in patients with severe AA (SAA) and that macrophage pyroptosis is an important factor in immune activation. The current study investigated the interaction of ruxolitinib with macrophages and whether the drug could treat SAA by improving pyroptosis levels. We induced differentiation of the THP-1 human monocyte cell line into macrophages in vitro and then induced pyroptosis. After constructing a macrophage pyroptosis model, treatment with different concentrations of ruxolitinib was administered. The results showed that ruxolitinib reduced the levels of pyroptosis and inflammatory-related factors. A mouse model of SAA was validated. In conclusion, ruxolitinib may treatment affects SAA by reducing the level of macrophage pyroptosis.

2025-03-18 | GSE291850 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data