Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Age-related epigenetic drift in the pathogenesis of MDS and AML part 1

ABSTRACT: Genomic DNA is isolated from bone marrow (MDS patient) and whole blood (normal control). We used MCAM to identify genes that have methylation changes. Two-condition experiment, MDS patient vs. normal control.

ORGANISM(S): Homo sapiens

SUBMITTER: Yue Lu

PROVIDER: E-GEOD-46063 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Project description:Genomic DNA is isolated from spleen (RUNX1 model and normal control) and bone marrow (NHD13 model and normal control). We used MCAM to identify genes that have methylation changes. Two-condition experiment, MDS model mouse vs. normal control.

2014-01-09 | E-GEOD-46065 | biostudies-arrayexpress

Project description:Genomic DNA is isolated from bone marrow (MDS patient) and whole blood (normal control). We used MCAM to identify genes that have methylation changes.

2014-01-09 | GSE46063 | GEO

2014-01-09 | GSE46065 | GEO

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-09 | E-GEOD-46067 | biostudies-arrayexpress

Project description:The myelodysplastic syndrome (MDS) is a clonal hematologic disorder that frequently evolves to acute myeloid leukemia (AML). Its pathogenesis remains unclear, but mutations in epigenetic modifiers are common and the disease often responds to DNA methylation inhibitors. We analyzed DNA methylation in the bone marrow and spleen in two mouse models of MDS/AML, the NUP98-HOXD13 (NHD13) mouse and the RUNX1 mutant mouse model. Methylation array analysis showed an average of 512/3445 (14.9%) genes hypermethylated in NHD13 MDS, and 331 (9.6%) genes hypermethylated in RUNX1 MDS. Thirty-two percent of genes in common between the two models (2/3 NHD13 mice and 2/3 RUNX1 mice) were also hypermethylated in at least two of 19 human MDS samples. Detailed analysis of 41 genes in mice showed progressive drift in DNA methylation from young to old normal bone marrow and spleen; to MDS, where we detected accelerated age-related methylation; and finally to AML, which markedly extends DNA methylation abnormalities. Most of these genes showed similar patterns in human MDS and AML. Repeat element hypomethylation was rare in MDS but marked the transition to AML in some cases. Our data show consistency in patterns of aberrant DNA methylation in human and mouse MDS and suggest that epigenetically, MDS displays an accelerated aging phenotype.

| S-EPMC3975058 | biostudies-literature

Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukaemia (AML)

Project description:A 10K cDNA microarray was used to compare neutrophil RNA from 21 MDS patient and 2 AML patients to pooled neutrophil RNA from 7 healthy controls.

2005-01-09 | E-GEOD-971 | biostudies-arrayexpress

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

2014-01-09 | GSE46067 | GEO

Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukaemia (AML)

Project description:A 10K cDNA microarray was used to compare neutrophil RNA from 21 MDS patient and 2 AML patients to pooled neutrophil RNA from 7 healthy controls. Keywords: repeat sample

2005-01-10 | GSE971 | GEO

Genome-wide DNA methylation in MDS/secondary AML and de novo AML

Project description:An increasing body of work reveals aberrant hypermethylation of genes occurring in and potentially contributing to the pathogenesis of myeloid malignancies. Several of these diseases, such as myelodysplastic syndromes (MDS), are responsive to DNA methyltransferase inhibitors. In order to determine the extent of promoter hypermethylation in such tumors we compared the distribution of DNA methylation of 14,000 promoters in MDS and secondary AML patients enrolled in a phase I trial of 5-azacytidine and the histone deacetylase inhibitor entinostat against de novo AML patients and normal CD34+ bone marrow cells. The MDS and secondary AML patients displayed more extensive aberrant DNA methylation involving thousands of genes than did the normal CD34+ bone marrow cells or de novo AML blasts. Aberrant methylation in MDS and secondary AML tended to affect particular chromosomal regions, occurred more frequently in Alu poor genes, and included prominent involvement of genes involved in the WNT and MAPK signaling pathways. DNA methylation was also measured at days 15 and 29 after the first treatment cycle. DNA methylation was reversed at day 15 in a uniform manner throughout the genome, and this effect persisted through day 29, even without continuous administration of the study drugs. Keywords: DNA methylation profiling Direct comparison of DNA methylation in bone marrow samples from patients with Myelodysplastic syndrome or secondary Acute Myeloid Leukemia (AML) at baseline and after in vivo treatment with 5-azacytidine + etinostat. A comparison to de novo normal karyotype AML was also performed. Two control groups were included: one consisting of 8 CD34+ bone marrow samples from healthy donors and a second one consisting of matched CD34+ and CD34- fractions from the bone marrows of 4 healthy donors.

2010-05-15 | E-GEOD-17328 | biostudies-arrayexpress

Genome-wide DNA methylation in MDS/secondary AML and de novo AML

2009-08-05 | GSE17328 | GEO