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

Transcription profiling of human adult T-cell leukemia/lymphoma (ATL) patients

ABSTRACT: Abstract: Adult T-cell leukemia/lymphoma (ATL) is an aggressive and fatal disease. We have examined 18 ATL patient samples using Affymetrix HG-U133A2.0 arrays. Using the BRB array program, we identified genes differentially expressed in leukemia cells compared to normal lymphocytes. Several unique genes were identified that were overexpressed in leukemia cells including TNFSF11, RGS13, MAFb, CSPG2, C/EBPalpha and TCF4. 200 of the most highly overexpressed ATL genes were analyzed by the PathwayStudio 4.0 program. ATL leukemia cells were characterized by an increase in genes linked to "central" genes CDC2/cyclin B1, SYK/LYN, PCNA and BIRC5. Because of its potential therapeutic importance, we focused our studies on the regulation and function of BIRC5, whose expression was increased in 13 of 14 leukemia samples. TCF4 reporter assays and transfection of DN-TCF4 demonstrated that TCF4 regulates BIRC5 gene expression. Functionally, transfection of ATL cells wi BIRC5 shRNA decreased BIRC5 exprression and cell viability 80%. Clinical treatment of ATL patients with Zenapax or bortezomib decreased BIRC5 expression and cell viability. These experiments represent the first direct experimental evidence that BIRC5 plays an important role in ATL cell viability and provides important insight into ATL genesis and potential targeted therapies. Experiment Overall Design: Gene expression profiles of 7 control and 18 ATL patient samples were analyzed using Affymetrix HG-U133A2.0 arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: John Brady

PROVIDER: E-GEOD-14317 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of ATL patients

Project description:Abstract: Adult T-cell leukemia/lymphoma (ATL) is an aggressive and fatal disease. We have examined 18 ATL patient samples using Affymetrix HG-U133A2.0 arrays. Using the BRB array program, we identified genes differentially expressed in leukemia cells compared to normal lymphocytes. Several unique genes were identified that were overexpressed in leukemia cells including TNFSF11, RGS13, MAFb, CSPG2, C/EBPalpha and TCF4. 200 of the most highly overexpressed ATL genes were analyzed by the PathwayStudio 4.0 program. ATL leukemia cells were characterized by an increase in genes linked to "central" genes CDC2/cyclin B1, SYK/LYN, PCNA and BIRC5. Because of its potential therapeutic importance, we focused our studies on the regulation and function of BIRC5, whose expression was increased in 13 of 14 leukemia samples. TCF4 reporter assays and transfection of DN-TCF4 demonstrated that TCF4 regulates BIRC5 gene expression. Functionally, transfection of ATL cells wi BIRC5 shRNA decreased BIRC5 exprression and cell viability 80%. Clinical treatment of ATL patients with Zenapax or bortezomib decreased BIRC5 expression and cell viability. These experiments represent the first direct experimental evidence that BIRC5 plays an important role in ATL cell viability and provides important insight into ATL genesis and potential targeted therapies. Keywords: disease state analysis

2009-02-01 | GSE14317 | GEO

Expression profiling by array in ATLL

Project description:Previously, we have shown that an AP-1 family member Fra-2, which is hardly expressed in normal mature T cells, is consistently over-expressed in adult T-cell leukemia/lymphoma (ATLL), and together with JunD, upregulates CCR4 and many other genes including proto-oncogenes c-Myb, MDM2, Bcl-6, and SOX4. SOX4 is frequently overexpressed in many solid tumors and considered to be a potential oncogene. To identify downstream target genes of SOX4 and analyze SOX4 oncogenic pathway in ATLL , we compared gene expression profiles of ST1 cells transfected with SOX4 siRNA or control siRNA using the Affymetrix high density oligonucleotide microarray. The ATL-derived cell line ST1 was transfected with control siRNA or SOX4 siRNA using NucleofectorM-BM-. (Lonza, Basel, Switzerland). To determine the high-viability of the cells transfected with siRNAs, the cells were counted after 6 h on FACSCalibur (Becton Dickinson, Mountain View, CA) by gating out cells stained with propidium iodide. The transfection efficiency of RNAs was close to 95%, as determined by using fluorescent siRNA (Qiagen). After 48 h, total RNA samples were prepared and confirmed to be of good quality with the Agilent 2100 Bioanalyzer (Agilent Technologies, Waldbronn, Germany). In addition, quantitative PCR confirmed that SOX4 siRNA effectively reduced SOX4 mRNA in ST1 cells.

2013-05-16 | E-GEOD-38021 | biostudies-arrayexpress

Transcription profiling of human T-lymphocytes from the adaptive immune system from smojers and non smokers

Project description:Cigarette smoke components have a proven negative influence on human health. Adverse metabolic effects have been observed in tissues and single cells. As T-lymphocytes get in contact with affected organs (e.g. lung) or cells (e.g.erythrocytes), as well as with smoke components and bioactive molecules, whose production is influenced by them, we compared the gene exression profiles in these cells of the adaptive immune system of three male heavy smokers and three male non-smokers We combined rapid immuno-precipitation and Affymetrix GeneChipÂ® HG U133A2.0 microarray analysis to analyse the data set. 88 genes were found significantly (T-test) differentially expressed by a factor of 1.5-fold or larger between smokers and non-smokers. Using the gene function groups of the gene ontology consortium to categorize the functions of the differentially expressed genes the group termed âresponse to stimulusâ was found most significantly affected by smoking. Our data indicate a prominent role of cytotoxic T-lymphocytes in response to smoking. Several genes that are typically found in these cells are found regulated although the ratio of cytotoxic and helper T-lymphocytes remained unchanged in smokers. Experiment Overall Design: T-lymphocytes from three non-smokers (control group)and three smokers (case group) were immunoprecipitated from 4ml whole blood. Cells were lysed with Trizol, RNA was worked up using PLG Tubes and the RNeasy Kit. 1Âµg total RNA was processed according to the Affymetrix manual and hybridised on HG U133A 2.0 arrays. Data analysis was done with the GeneSpring software from Agilent. We performed a T-test to extract significantly altered genes from the data set.

2008-06-13 | E-GEOD-4806 | biostudies-arrayexpress

SNP array data for adult T-cell leukemia (ATL)

Project description:To identify chromosomal alterations in ATL, SNP array analyses were performed in 19 leukemia cell samples from ATL patients and 9 ATL-related cell lines. ATL displayed complex chromosomal abnormalities, but it contained recurrent chromosomal amplification and deletion, including 14q11 and 14q32, which may be associated with the development of ATL. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from cryopreserved peripheral blood samples and from cell line samples.

2017-06-06 | GSE99667 | GEO

Molecular targets of HIV integrase inhibitor, MK-2048, on ATL cells

Project description:Adult T-cell Leukemia (ATL) is a highly chemoresistant malignancy of peripheral T lymphocytes, associated with retrovirus human T-cell leukemia virus type I (HTLV-1). To elucidate the complex molecular mechanism of anti-Growth effect of the HIV integrase inhibitor, MK-2048 in ATL cells, we attempted to perform gene expression profiling.

2020-01-01 | GSE113265 | GEO

Transcription profiling of four human Adult T-cell leukemia (ATL) cell lines treated with proteasome inhibitor, bortezomib

Project description:Adult T-cell leukemia (ATL) is a fatal neoplasia derived from HTLV-1 infected T lymphocytes exhibiting constitutive activation of NF-kB. To elucidate the complex molecular mechanism of anti-tumor effect of the proteasome inhibitor, bortezomib in ATL cells, we attempted to perform gene expression profiling. Experiment Overall Design: Four ATL cell lines were cultured with or without bortezomib, then analysed.

2008-06-14 | E-GEOD-6034 | biostudies-arrayexpress

Homo sapiens

Project description:Expression data from a malaria vaccine trial (HG-U133A2.0 and U133 Plus 2.0)

| PRJNA117977 | ENA

Knockdown of human TCF4 affects multiple signaling pathways involved in cell survival, epithelial-to-mesenchymal transition and neuronal differentiation

Project description:TCF4 is an important neurodevelopmental transcription factor associated with schizophrenia and Pitt-Hopkins syndrome. In this study, we used genome-wide expression profiling to determine the effects of acute TCF4 knockdown on gene expression in SH-SY5Y neuroblastoma cells. Pathway and enrichment analysis on the differentially expressed genes in TCF4-knockdown cells identified an over-representation of genes involved in TGF-β signaling, epithelial-to-mesenchymal transition (EMT) and apoptosis. Among the most significantly differentially expressed genes were the EMT regulators SNAI2 and DEC1 and the proneural genes NEUROG2 and ASCL1. Altered expression of several mental retardation genes such as UBE3A (AS), ZEB2 (MWS) and MEF2C was also found in TCF4-depleted cells. These data suggest that TCF4 regulates a number of convergent signaling pathways involved in cell differentiation and survival in addition to a subset of clinically important mental retardation genes. To identify TCF4-mediated gene expression changes in SH-SY5Y cells, experiments were conducted with two control (mock and GAPDH KD) and two TCF4 knockdown (KD1 and KD2) groups. Two non-overlapping siRNAs against TCF4 were designed and transfected over a 72h period to induce global knockdown of TCF4 transcripts. In parallel, cells were mock transfected (mock; transfection reagent only) and transfected with an unrelated siRNA against GAPDH (GAPDH KD) in order to control for background gene expression changes due to transfection, presence of dsRNA and activation of the cellular silencing machinery. After transfection, RNA was extracted from all cells, converted to cDNA and labelled for microarray hybridization. Each of the four treatment groups (mock, GAPDH KD, KD1 and KD2) contained three biological replicates which were processed at the same time using the Toray microarray platform.

2013-08-20 | E-GEOD-48367 | biostudies-arrayexpress

Affymetrix SNP array data for acute-type adult T-cell leukemia (ATL) samples

Project description:We recently mapped 605 chromosomal breakpoints in 61 ATL cases by spectral karyotyping and identified chromosome 14q11 as one of the most common chromosomal breakpoint regions. To map the precise location of chromosomal breakpoints at 14q11, we performed single-nucleotide polymorphism (SNP)-based comparative genomic hybridization on leukemia cells from acute-type ATL patients. Copy number analysis of Affymetrix 50K SNP arrays was performed for leukemic cell samples from10 acute-type ATL patients.

2014-01-31 | E-GEOD-54509 | biostudies-arrayexpress

Influence of ATL-type Helios overexpression or WT-Helios/Ikaros knockdown on gene expression profile in Jurkat cells

Project description:It has been known that aberrant isoforms of Ikaros family ptoteins are expressed in malignant cells. We identified that PBMC of ATL (acute T-cell leukemia) patients expresses different patterns of Helios isoforms compared with normal PBMC. In order to investigate the biological impact of ATL-type Helios isoform, we conducted complehensive gene expression analyses in Jurkat cells overexpressing ATL-type Helios. Also, we investigated the influence of WT-Helios or WT-Ikaros knockdown on the gene expression profile and compared with that of the cells with ATL-type Helios overexpression.

2013-03-31 | GSE41796 | 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