Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

6 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling by array of TET2 wild type and TET2 mutant patients with diffuse large B-cell derived lymphoma

ABSTRACT: Global gene expression in TET2 mutant and Wild type patients. We performed an integrated analysis of global DNA methylation and gene expression data to investigate the effects of DNA hypermethylation on gene expression. Total RNA was isolated from 4 TET2mut and 5 TET2wt were isolated using standard RNAeasy kit protocol (Qiagen). Their gene expression profiles were obtained using the[HuGene-1_0-st] Affymetrix.

ORGANISM(S): Homo sapiens

SUBMITTER: Vasu Punj

PROVIDER: E-GEOD-37363 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Genome-wide profiling identifies a DNA methylation signature that associates with TET2 mutations in diffuse large B-cell lymphoma.

Asmar Fazila F Punj Vasu V Christensen Jesper J Pedersen Marianne T MT Pedersen Anja A Nielsen Anders B AB Hother Christoffer C Ralfkiaer Ulrik U Brown Peter P Ralfkiaer Elisabeth E Helin Kristian K Grønbæk Kirsten K

Haematologica 20130705 12

The discovery that the Ten-Eleven Translocation (TET) hydroxylases cause DNA demethylation has fundamentally changed the notion of how DNA methylation is regulated. Clonal analysis of the hematopoetic stem cell compartment suggests that TET2 mutations can be early events in hematologic cancers and recent investigations have shown TET2 mutations in diffuse large B-cell lymphoma. However, the detection rates and the types of TET2 mutations vary, and the relation to global methylation patterns has ...[more]

PMID: 23831920

Similar Datasets

Transcription profiling by array of TET2 wild type and TET2 mutant patients with diffuse large B-cell derived lymphoma

Project description:Global gene expression in TET2 mutant and Wild type patients. We performed an integrated analysis of global DNA methylation and gene expression data to investigate the effects of DNA hypermethylation on gene expression. Total RNA was isolated from 4 TET2mut and 5 TET2wt were isolated using standard RNAeasy kit protocol (Qiagen). Their gene expression profiles were obtained using the[HuGene-1_0-st] Affymetrix.

2014-11-07 | E-GEOD-37363 | ExpressionAtlas

TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma

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

2013-10-10 | E-GEOD-37365 | biostudies-arrayexpress

NF-kB essential modulator (NEMO) is essential for KSHV-encoded viral FLICE inhibitory protein (vFLIP) K13- induced gene expression and its N-terminal 251 resdidues are sufficent for this process

Project description:We report here that KSHV viral infection targets the NF-kB pathway which is crucial for cell survival. KSHV protein vFLIP K13 is known to directly interact with cellular protein NEMO of the NF-kB pathway. We used gene expression array to suggets that the interaction of K13 with NEMO is important to activate NF-kB pathway. We employed gene array analysis followed by bioinformatics analyses as well as biological pathways to determine the effect of K13 interaction with Nemo in Jurkat cell line system. Total RNA was isolated isolated using standard RNAeasy kit protocol (Qiagen). Their gene expression profiles were obtained using the Affymetrix Human Genome U133A 2.0 Array.

2014-03-27 | E-GEOD-49245 | biostudies-arrayexpress

To integrate functional genomics and craniofacial morphogenesis within FaceBase Consortium

Project description:Congenital malformations in facial bones significantly impact the overall representation of face. Establishing a correlation between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation we will generate gene expression profiles of different facial bones at different time intervals over a period of 5 years to establish their roles in regulating craniofacial development. To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla.

2016-03-24 | E-GEOD-67985 | biostudies-arrayexpress

Celecoxib induced transcriptional alterations in gastric cancer cells

Project description:Celecoxib is recognized to have chemopreventive and anti-cancer property beyond its anti-inflammatory function. Celelcoxib treatment in AGS cells down regulates Wnt/M-NM-2-catenin, STAT3, RXR and ERK/MAPK signaling pathways. Transcriptional profiling after celecoxib shows differential regulation of oncogenic pathway regulated genes. AGS cell were treated with celecoxib in triplicates and incubated for 24 hours. The processed samples were hybridized in M-bM-^@M-^\HuGene-1_0-stM-bM-^@M-^] array and the differentially expressed genes were taken for pathway analysis and transcription factor enrichment analysis.

2014-04-01 | E-GEOD-54657 | biostudies-arrayexpress

14-3-3 protects AMPK phosphorylated TET2 from dephosphorylation by PP2A

Project description:Ten-eleven translocation-2 (TET2) is a member of the methylcytosine dioxygenase family of enzymes implicated in cancer and in aging due to its role as a global epigenetic modifier. TET2 has a large N-terminal domain followed by a catalytic C-terminal. Previous reports have demonstrated that the catalytic domain remains active independent of the N-terminal domain. As such, the function of the N-terminus of this large protein remains poorly characterized. Here, we identify that several isoforms of the 14-3-3 family of proteins bind TET2. 14-3-3s bind TET2 when phosphorylated at serine 99 (S99). AMPK-mediated phosphorylation at S99 promotes TET2 stability and increases global DNA 5-hydroxymethylcytosine. 14-3-3s’ interaction with TET2 serves to protect S99 phosphorylation. Disruption of this interaction leads to both reduced TET2 phosphorylation and decreased protein stability. Furthermore, we identify that the protein phosphatase 2A (PP2A) can interact with TET2 and dephosphorylates S99. Collectively, our study provides novel insights into the role of the N-terminal domain in TET2 regulation. Moreover, they demonstrate the dynamic nature of TET2 protein regulation that could have therapeutic implications for disease states resulting from reduced TET2 levels and/or activity.

2020-01-13 | PXD016160 | Pride

TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma (DNA methylation)

Project description:Genome wide DNA methylation profiling of patient samples with TET2 mutations and Wild type TET2 status . The Illumina Infinium HumanMethylation 450_15017482_v.1.1 was used to obtain DNA methylation profiles across approximately 482,421 CpGs in fresh frozen lymphoma samples. Samples include 19 TET2 wild type and 12 TET2 mutant samples. Bisulphite converted DNA from the 31 samples were hybridised to the Illumina Infinium HM450K Human Methylation Beadchip v1.2

2013-10-10 | E-GEOD-37362 | biostudies-arrayexpress

Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription

Project description:This SuperSeries is composed of the following subset Series: GSE26018: Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuEx-1_0-st] GSE26019: Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuGene-1_0-st] GSE26038: Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuEx-1_0-st, transcript] GSE26040: Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks Refer to individual Series

2011-03-31 | E-GEOD-26020 | biostudies-arrayexpress

Gene expression data from non-infected and M. hyorhinis-infected gastric cancer cell lines using Affymetrix genechip (HuGene-1_0-st)

Project description:Chronic infection of M. hyorhinis is postulated to be associated with cancer cell migration and invasion. To explore the mechanisms of M. hyorhinis-promoted invasiveness, we performed Affymetrix genechip (HuGene-1_0-st) analysis to examine differential gene expression profiles between non-infected and infected gastric cancer cells. We used microarrays to detail global programme of gene expression and identified distinct classes of upregulated genes after M. hyorhinis infection of gastric cancer cell lines.

2013-11-22 | GSE52638 | GEO

Context Dependent Effects of Ascorbic Acid Treatment in TET2 Mutant Myeloid Neoplasia

Project description:Loss-of-function TET2 mutations (TET2MT) are common in myeloid neoplasia. TET2, a DNA dioxygenase, requires 2-oxoglutarate and Fe(II) to oxidize 5-methylcytosine. TET2MT thus result in hypermethylation and transcriptional repression. Ascorbic acid (AA) increases dioxygenase activity by facilitating Fe(III)/Fe(II) redox reaction and may alleviate some biological consequences of TET2MT by restoring dioxygenase activity. Here, we report the utility of AA in the prevention of TET2MT MN, clarify the mechanistic underpinning of the TET2-AA interactions, and demonstrate that the ability of AA to restore TET2 activity in cells depends on N- and C-terminal lysine acetylation and nature of TET2MT. Consequently, pharmacologic modulation of acetyltransferases and histone deacetylases may regulate TET dioxygenase-dependent AA effects. Thus, our study highlights the contribution of factors that may enhance or attenuate AA effects on TET2 and provides a rationale for novel therapeutic approaches including combinations of AA with class I/II HDAC inhibitor or sirtuin activators in TET2MT leukemia.

2020-09-09 | PXD020550 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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