Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

30 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells (gene expression)

ABSTRACT: We analyzed the methylation pattern of a well characterized leukemia cell line, named K562. Furthermore, we decided to investigate how the malignant epiegenome change during the reprogramming process We used Affymatrix expression microarrays analysis to investigate the relation between expression and methylation in leukemia and reprogrammed leukemia (LiPS). We show that the erasure of the epigenetic aberrancies have functional consequences on leukemia phenotype

ORGANISM(S): Homo sapiens

SUBMITTER: Touati Benoukraf

PROVIDER: E-GEOD-33226 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells

Project description:This SuperSeries is composed of the following subset Series: GSE33226: Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells (gene expression) GSE33230: Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells (sequencing) Refer to individual Series

2012-10-01 | E-GEOD-33231 | biostudies-arrayexpress

Expression data from WT HL60 cells

Project description:We used the microarray analysis to detail the gene expression profile from the leukemic cell line HL-60 Relationship between DNMT1-RNA interactions, DNA methylation and gene expression

2012-12-01 | E-GEOD-32153 | biostudies-arrayexpress

C/EBPa gene signature

Project description:We defined the C/EBPa signature characterized by a set of genes which are upregulated upon C/EBPa activation. In order to identify the C/EBPa signature, we performed microarray gene expression analysis of K562 cells stably expressing p42-C/EBPa-ER after activating the C/EBPa construct to translocate to the nucleus for 6 hours with beta-estradiol. The gene expression profile was performed in K562 p42-C/EBPa-ER expressing cells treated with beta-estradiol (n=4) or EtOH vehicle control (n-4) for 6 hours. Induction of nuclear localization of C/EBPa-ER fusion protein was achieved by addition of 1 uM beta-estradiol as indicated into the culture medium.

2013-04-01 | E-GEOD-43998 | biostudies-arrayexpress

Genome wide DNA methylation analysis of leukemia and reprogrammed leukemia cells (sequencing)

Project description:We analyzed the methylation pattern of a well characterized leukemia cell line, named K562. Furthermore, we decided to investigate how the malignant epiegenome change during the reprogramming process We used RRBS analysis to investigate the methylation pattern in leukemia and reprogrammed leukemia (LiPS).We show that the erasure of the epigenetic aberrancies have functional consequences on leukemia phenotype

2012-10-01 | E-GEOD-33230 | biostudies-arrayexpress

Expression data of Dnmt1 haploinsufficient leukemia stem cells and bulk leukemia

Project description:Leukemia stem cells (LSCs) are an attractive target in treatment of many types of blood cancers. There remains an incomplete understanding of the epigenetic mechanisms driving LSC formation and maintenance, and how this compares to the epigenetic regulation of normal hematopoietic stem cells (HSCs). To investigate novel mechanisms underlying the dependence of MLL-AF9 leukemia stem cells on Dnmt1, we used genome-wide expression profiling to examine changes in gene expression in Dnmt1 haploin sufficient L-GMPs as well as more differentiated leukemia cells (the bulk population of leukemia cells) compared to their control counterparts. Bone marrow LSK (Lin- Sca-1+ c-Kit+) cells were isolated from Dnmtfl/+ Mx-Cre+ or control Dnmtfl/fl mice. These cells were transduced with MLL-AF9-IRES-GFP retrovirus for 2 days, then GFP+ cells were sorted and transplanted into C57BL/6 syngeneic sublethally irradiated (600 rad) recipients. After 2 weeks, Dnmt1 haploinsufficiency was achieved in the leukemia cells by seven injections of poly(I)poly(C). Upon development of terminal stage acute myeloid leukemia, populations of L-GMPs or bulk GFP+ leukemia cells were FACS sorted from leukemic spleens, RNA was extracted, amplified and hybridized to Affymetrix 430A 2.0 microarrays to compare changes in gene expression. There are 2 biological replicates of Dnmtfl/+ Mx-Cre+ and control L-GMPs and bulk leukemia cells.

2012-03-14 | E-GEOD-31626 | biostudies-arrayexpress

Expression data from AMPK deficient MLL-AF9 leukemia initiating cells and whole leukemia cells

Project description:Deletion of AMPK significantly extended the onset of leukemogenesis and depleted leukemia initiating cells (LICs). To identify how AMPK regulates LICs, we performed gene expression profiling of LICs isolated from AMPK wild type leukemic mice or AMPK-deficient leukemic mice. 4 groups were analyzed; 1) Whole leukemia (GFP+) from AMPK WT ( AMPKfl/fl) mice, 2) Whole leukemia (GFP+) from AMPK-deficient ( AMPK?/?l) mice, 3) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK WT ( AMPKfl/fl) mice, 4) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK-deficient ( AMPK?/?l) mice.

2015-01-01 | E-GEOD-64602 | biostudies-arrayexpress

Frequent derepression of the mesenchymal transcription factor gene in acute myeloid leukemia (mouse)

Project description:Murine CD45.1+ CD117+ BM cells were co-transduced pairwise with retroviral vectors expressing Hoxa9, Meis1, Foxc1 or a control empty vector. Ninety-six hours later 10^6 drug resistant cells were transplanted into CD45.2+ irradiated congenic recipients. To investigate the consequences of FOXC1 expression on the transcriptome in murine AML, we performed exon array analysis using flow sorted CD117+Gr1+ leukemia cells recovered from sick mice (Hoxa9/control; Moxa9/Meis1; or Hoxa9/FOXC1 leukemias; 3 mice per cohort). Nine exon arrays total; 3 arrays for each cohort (Hoxa9/control; Moxa9/Meis1; or Hoxa9/FOXC1), each from a separate mouse.

2015-09-17 | E-GEOD-66253 | biostudies-arrayexpress

The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9 leukemia stem cells (expression data)

Project description:Using a mouse model of human MLL-AF9 leukemia, we identified the lysine-specific demethylase KDM1A (LSD1 or AOF2) as an essential regulator of leukemia stem cell (LSC) potential. KDM1A acts at genomic loci bound by MLL-AF9 to sustain expression of the associated oncogenic program, thus preventing differentiation and apoptosis. In vitro and in vivo pharmacologic targeting of KDM1A using tranylcypromine analogues active in the nanomolar range phenocopied Kdm1a knockdown in both murine and primary human AML cells exhibiting MLL translocations. By contrast, the clonogenic and repopulating potential of normal hematopoietic stem and progenitor cells was spared. Our data establish KDM1A as a key effector of the differentiation block in MLL leukemia which may be selectively targeted to therapeutic effect. To investigate the genetic program regulated by KDM1A in murine MLL-AF9 AML cells enriched for LSCs, we compared the transcriptome of KIT+Gr1+ control and Kdm1a KD cells using exon arrays soon after initiation of KD. At this time, there was no immunophenotypic evidence of differentiation in Kdm1a KD cells. Exonic expression values were condensed into gene-level expression summaries, which represent the mean expression value of the probe sets targeting the length of a given protein coding gene. Three separate samples from two different animals were used. Kdm1a KD samples were compared with control samples. Total six arrays.

2012-03-28 | E-GEOD-36347 | biostudies-arrayexpress

The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9 leukemia stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE36346: The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9 leukemia stem cells (ChIP-Seq data) GSE36347: The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9 leukemia stem cells (expression data) Refer to individual Series

2012-03-28 | E-GEOD-36348 | biostudies-arrayexpress

Novel IDH1 Mutant Inhibitors for Treatment of Acute Myeloid Leukemia (expression)

Project description:Neomorphic mutations in isocitrate dehydrogenase 1 (IDH1) are driver mutations in acute myeloid leukemia (AML) and other cancers. We report the development of new allosteric inhibitors of mutant IDH1. Crystallographic and biochemical results demonstrated that compounds of this chemical series bind to an allosteric site and lock the enzyme in a catalytically inactive conformation, thereby enabling inhibition of different clinically relevant IDH1 mutants. Treatment of IDH1 mutant primary AML cells uniformly led to a decrease in intracellular 2-HG, abrogation of the myeloid differentiation block and induction of granulocytic differentiation at the level of leukemic blasts and more immature stem-like cells, in vitro and in vivo. Molecularly, treatment with the inhibitors led to a reversal of the DNA cytosine hypermethylation patterns caused by mutant IDH1 in AML patients’ cells. Our study provides proof-of-concept for the molecular and biological activity of novel allosteric inhibitors for targeting different mutant forms of IDH1 in leukemia. To obtain insight into the molecular mechanism for the induction of granulocytic differentiation and cell death following inhibition of IDH1 mutant protein in primary AML cells, we performed gene expression microarrays following treatment with either GSK321 IDH1 inhibitor or Controls (DMSO or GSK990 inactive inhibitor). Primary IDH1 mutant acute myeloid leukemia (AML) mononuclear (MNC) cells were treated in suspension cultures in differentiating media for 6 days with 3 microM GSK990 or GSK321 and an equal volume of DMSO. Followed by microarray analysis after RNA extraction.

2015-09-21 | E-GEOD-72152 | biostudies-arrayexpress

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