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The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression

ABSTRACT: The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression

PROVIDER: PRJNA876298 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21404600_1.fastq.gz	Fastqsanger.gz
	SRR21404600_2.fastq.gz	Fastqsanger.gz
	SRR21411200_1.fastq.gz	Fastqsanger.gz
	SRR21411200_2.fastq.gz	Fastqsanger.gz
	SRR21404601_1.fastq.gz	Fastqsanger.gz

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The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [Mesenchymal subsets]

Project description:The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [Mesenchymal subsets]

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The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [CD34+CD38-_MDS]

Project description:The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [CD34+CD38-_MDS]

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The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [Human and Mouse]

Project description:The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [Human and Mouse]

| PRJNA876284 | ENA

Myelodysplastic syndrome marrow stroma shows widespread aberrant hypermethylation that is abrogated by treatment with DNMT inhibitors

Project description:The marrow microenvironment contributes to the pathogenesis of ineffective hematopoiesis in Myelodysplastic Syndromes (MDS). Since mutations and cytogenetic alterations are generally not present in marrow stromal cells, we hypothesized that epigenetic alterations may be responsible for altered stroma functionin MDS. Global DNA methylation of MDS marrow-derived stroma was analyzed by HELP assay and compared to healthy controls. MDS stroma showed aberrant hypermethylation that preferentially occurred outside of CpG islands and involved important signaling pathways.Comparison with stroma derived from 5-Azacytidine (5-Aza) treated MDS patients revealed abrogation of aberrant methylation in treated samples. Integrative expression analysis revealed that the WNT pathway was epigenetically dysregulated in MDS stroma, and the WNT antagonists FRZB and SFRP1 were aberrantly hypermethylated and underexpressed. These epigenetic changes were validated ina co-culture model of stroma and leukemic cells and in an independent set of MDS samples. Importantly, 5-Aza treatment of MDS stroma enhanced hematopoietic activity and erythroid differentiationfrom co-cultured healthy CD34+ cells. These results reveal widespread aberrant epigenetic changes in the MDS marrow microenvironment and demonstrate that DNA methyl transferase inhibitors alter the epigenomic profiles of stromal cells, potentiallycontributing to theirtherapeutic efficacy. The study population consisted of 6 MDS patients and 3 healthy controls. Individual HpaII restriction digest profiles were compared to an internal MspI digest control, to yield differentially methylated fragments for every sample.

2015-05-20 | E-GEOD-60233 | biostudies-arrayexpress

Myelodysplastic syndrome marrow stroma shows widespread aberrant hypermethylation that is abrogated by treatment with DNMT inhibitors

2015-05-20 | GSE60233 | GEO

The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [Mesenchymal subsets]

Project description:Myelodysplastic syndromes (MDS) are a heterogenous group of diseases affecting the hematopoietic stem cell that are curable only by stem cell transplantation. Both hematopoietic cell intrinsic changes and extrinsic signals from the bone marrow niche seem to ultimately lead to MDS. Animal models of MDS indicate that alterations in specific mesenchymal progenitor subsets in the bone marrow microenvironment can induce or select for abnormal hematopoietic cells. Here we identify a subset of human bone marrow (BM) mesenchymal cells marked by the expression of CD271, CD146 and CD106. This subset of human mesenchymal cells is equivalent to those in mice that, when perturbed, results in an MDS-like syndrome. Transcriptional analysis identified epithelial to mesenchymal transition as the most enriched gene set and Osteopontin (SPP1) as the most overexpressed gene. The loss of expression of Spp1 in the microenvironment resulted in an accelerated progression of the transplanted Vav-driven Nup98-HoxD13 MDS model as demonstrated by increased chimerism, increased contribution of mutant cells to the myeloid lineage and a more pronounced anemia when compared to animals with a wild type microenvironment. These data indicate that molecular perturbations can occur in specific bone marrow mesenchymal subsets of MDS patients. However, the niche adaptations to dysplastic clones include Spp1 overexpression that can constrain disease progression. Therefore, niche changes with malignant disease can also serve to protect the host.

2023-08-31 | GSE212638 | GEO

The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [Human and Mouse]

2023-08-31 | GSE212631 | GEO

The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression [CD34+CD38-_MDS]

2023-08-31 | GSE212620 | GEO

The Bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-31 | GSE212639 | GEO

Distinct Transcriptomic and Exomic Abnormalities within Myelodysplastic Syndrome Marrow Cells

Project description:Prior studies using DNA microarray platforms have shown alterations of gene expression profiles (GEPs) of marrow cells in myelodysplastic syndromes (MDS). Using the increased sensitivity and accuracy of high-throughput RNA sequencing (RNA-Seq) for detecting and quantifying mRNA transcripts, our study has demonstrated novel significant differences in GEPs between MDS and normal CD34+ marrow cells with 41 genes identified as disease classifiers. Additionally, two main clusters of GEPs distinguished patients based on their major clinical features, particularly between those whose disease remained stable (sMDS) vs patients whose illness transformed to acute myeloid leukemia within 12 months (tMDS). The genes whose expression was associated with disease outcome were involved in functional pathways and biologic processes highly relevant for MDS. Exomic analysis identified MDS-associated pathogenic mutations in virtually all patients tested. MDS subgroups with spliceosome mutations demonstrated distinct differential isoform usage and expression and consequent dysregulation of distinct biological functions. This combination of clinical, transcriptomic and exomic findings provides valuable molecular insights into the mechanisms underlying MDS and its progression to a more aggressive stage and also facilitates prognostic characterization of MDS patients.

2018-04-09 | GSE111085 | GEO

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