Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

34 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile of the human leukemia cell line Reh after treatment with bortezomib, valproic acid or a combination of both.

ABSTRACT: New therapy options are required for relapsed B-cell precursor ALL patients in order to improve survival and reduce adverse acute and late effects. We observed a synergistic anti-leukemic activity of concomitant treatment with bortezomib and valproic acid in BCP-ALL cells. In this experiment we aimed to identify the pathways modulated after concomitant treatment with bortezomib and valproic acid. Reh cells treated with either bortezomib, valproic acid, or the combination of both normalized to a untreated control.

ORGANISM(S): Homo sapiens

SUBMITTER: Shabnam Shalapour

PROVIDER: E-GEOD-41951 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profile of the human leukemia cell line Reh after treatment with bortezomib, valproic acid or a combination of both.

Project description:New therapy options are required for relapsed B-cell precursor ALL patients in order to improve survival and reduce adverse acute and late effects. We observed a synergistic anti-leukemic activity of concomitant treatment with bortezomib and valproic acid in BCP-ALL cells. In this experiment we aimed to identify the pathways modulated after concomitant treatment with bortezomib and valproic acid.

2013-02-01 | GSE41951 | GEO

Expression data from ETV6-RUNX1-positive Reh leukemic cells after overexpression of miR-125b, miR-100 and miR-99a levels in different combinations

Project description:Combined overexpression of miR-125b with miR-99a and/or miR-100 induced VCR resistance in ETV6-RUNX1-positive leukemic cells Reh. We used microarrays to detail the global changes in gene expression of Reh cells upon enforced expression of miR-125 per se compared with combination of overexpression of miR-125b, miR-100 and/or miR-99a MiR-99a and/or miR-100 were transiently overexpressed in stable miR-125b-expressing and stable scrambled miR-control-expressing Reh cells. Cellular resistance to VCR was determined by MTT assay after incubating the cells with 9 ng/mL VCR for 3 days. Changes in the gene expression pattern of Reh cells induced by miRNAs overexpression were measured using Affymetrix Arrays.

2013-06-27 | E-GEOD-46362 | biostudies-arrayexpress

Expression and ChIP-chip data from REH and SEM leukemia cell lines

Project description:MLL-fusion proteins are potent inducers of cancer in hematopoietic cells, where they are known to cause changes in global gene expression. How MLL-fusion proteins interact with the genome has not been established, so we have limited understanding of the pathway by which these proteins generate aberrant gene expression programs. Here we describe how the MLL-AF4 protein occupies the genome in human leukemia cells and its striking effects on chromatin states. We find that the MLL-AF4 fusion protein selectively occupies regions of the genome that contain developmental regulatory genes important for hematopoietic stem cell identity and self-renewal. These MLL-AF4 bound regions have grossly altered chromatin structure, with histone modifications catalyzed by Trithorax Group (TrxG) proteins and Dot1 extending across unusually large domains. This indicates that a key feature of MLL-associated leukemogenesis is aberrant targeting of chromatin modifiers to regions of the genome controlling hematopoietic development. Our results define the direct targets of the MLL-fusion protein, reveal the global role of epigenetic misregulation in leukemia, and identify new targets for therapeutic intervention in human cancer. Keywords: cell type comparison This dataset includes expression data for two replicates each of SEM and REH leukemia cell lines and ChIP-chip data targeting RNAP2, H3K4me3, H3K79me2, ENL, AF4-C, and MLL-N in SEM and REH leukemia cell lines.

2008-12-14 | E-GEOD-13313 | biostudies-arrayexpress

Identification of ETV6 bound protein by affinity purification of ETV6-HA fusion protein in REH cells

Project description:To determine the protein partners of ETV6, we expressed ETV6 and HA-tagged ETV6 in Reh pre-B leukemic cells. Anti-HA magnetic beads were used for affinity purification of ETV6-HA (and ETV6 control) from the nuclear and cytoplasmic fraction. Following purification on-beads digest and LC-MS/MS experiments were performed at the Proteomics platform of the CHU de Quebec Research Center, Quebec, Canada.

2022-01-26 | PXD031001 | Pride

Homo sapiens isolate:REH

Project description:REH MultiOmics

| PRJNA600820 | ENA

Expression, ChIP-chip, and ChIP-Seq data from REH and SEM leukemia cell lines [ChIP-Seq]

Project description:MLL-fusion proteins are potent inducers of cancer in hematopoietic cells, where they are known to cause changes in global gene expression. How MLL-fusion proteins interact with the genome has not been established, so we have limited understanding of the pathway by which these proteins generate aberrant gene expression programs. Here we describe how the MLL-AF4 protein occupies the genome in human leukemia cells and its striking effects on chromatin states. We find that the MLL-AF4 fusion protein selectively occupies regions of the genome that contain developmental regulatory genes important for hematopoietic stem cell identity and self-renewal. These MLL-AF4 bound regions have grossly altered chromatin structure, with histone modifications catalyzed by Trithorax Group (TrxG) proteins and Dot1 extending across unusually large domains. This indicates that a key feature of MLL-associated leukemogenesis is aberrant targeting of chromatin modifiers to regions of the genome controlling hematopoietic development. Our results define the direct targets of the MLL-fusion protein, reveal the global role of epigenetic misregulation in leukemia, and identify new targets for therapeutic intervention in human cancer. This dataset includes expression data for two replicates each of SEM and REH leukemia cell lines, ChIP-chip data targeting RNAP2, H3K4me3, H3K79me2, ENL, AF4-C, and MLL-N in SEM and REH leukemia cell lines, and ChIP-Seq data of H3K79me2, H3K4me3, ans WCE in SEM and REH cell lines. This Series contains the ChIP-Seq data only. The expression and ChIP-chip data are provided in GEO Series GSE13313.

2012-05-31 | E-GEOD-38338 | biostudies-arrayexpress

Inducible PAX5 expression in a human B lymphoblastic leukemia cell line

Project description:Hypomorphic mutations of the transcription factor PAX5 occur in one third of B-progenitor acute lymphoblastic leukemias (B-ALLs). To identify PAX5-regulated genes in B-ALL, here we employ inducible expression of PAX5 in a human B-ALL cell line (REH) that harbors a loss-of-function mutation in PAX5. In this model, inducing PAX5 expression is associated with competitive disadvantage. Comparison of REH cell lines with Dox-inducible expression of PAX5-IRES-GFP, or control GFP alone. GFP positive cells were isolated by FACS.

2014-06-18 | E-GEOD-57480 | biostudies-arrayexpress

Reciprocal leukemia-stroma VCAM-1/VLA-4-dependent activation 1 of NF-ÎºB mediates chemoresistance

Project description:Bone marrow (BM) mesenchymal stromal cells (BM-MSC) upregulate their NF-ÎºB signaling to protect leukemia cells from chemotherapy-induced apoptosis. To elucidate molecular mechanisms by which leukemia-stroma interactions within the BM microenvironment could confer chemoresistance to leukemia cells, we used genome-wide gene expression profiling (GEP) to examine human normal BM-MSC that had been co-cultured with the pre-B ALL REH cells and then separated by flow cytometry (FACS). GEP results for co-cultured cells of each type were compared to GEP results for cells of the corresponding type cultured alone, and taken through the same FACS purification procedure, to identify changes in gene expression profiles caused by co-culture.

2014-05-19 | E-GEOD-55533 | biostudies-arrayexpress

Gene expression changes in REH following CDC42 inhibition

Project description:ARHGEF4 expression is associated with t(12;21) acute lymphoblastic leukaemia (ALL). Our study investigated the substrate specificity of ARHGEF4, a member of the diffuse B-cell lymphoma (DBL) family of guanine nucleotide exchange factors (GEFs), in t(12;21) ALL REH cells. ARHGEF4 was found to activate the small guanine nucleotide binding protein (GTPase) CDC42. In order to determine the function of CDC42 in t(12;21) ALL cells, we performed RNAseq analysis on REH cells treated for 24 hours with DMSO vehicle control in comparison to 25uM ML141, a CDC42 inhibitor.

2020-06-20 | GSE152836 | GEO

H3K27ac ChIP-Seq in REH and 697

Project description:H3K27ac ChIP-Seq data of the B-ALL cell lines REH and 697 were obtained to find active regions in the genome and to correlate that with expression profiling of lncRNAs in these cell lines.

2016-09-26 | GSE79870 | 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