Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling of EBV gene in nasal NK/T lymphoma and chronic active EBV infection

ABSTRACT: Nasal T/NK lymphoma is a unique subtype of non-Hodgkin lymphoma (NHL) that is aggressive and incurable closely associated with Epstein-Barr virus (EBV)3. The clonal expansion of EB infected T- or NK cell is also seen in patients with chronic active EBV (CAEBV) infection, suggesting that two diseases might partly share a similar mechanism by which EBV affect host cellular genes. In order to understand the pathogenesis of EBV-associated T/NK lymphoproliferative disorders (LPD) and design new therapies, we employed a novel EBV DNA microarray to compare patterns of EBV expression in SNK/T cells established from EBV-associated T/NK LPD. Keywords: parallel sample

ORGANISM(S): human gammaherpesvirus 4

PROVIDER: GSE2414 | GEO | 2005/09/20

SECONDARY ACCESSION(S): PRJNA91629

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

EBV-Host interaction in nasal NK/T lymphoma and chronic acvtive EBV infection

Project description:Extranodal NK/T-cell, nasal type (hereinafter, nasal T/NK lymphoma), is a distinct clinicopahtologic entity highly associated with EBV. Among nasal T/NK lymphoma, some cases are developed from the long-lasting EBV infection termed chronic active EBV (CAEBV) infection.The clonal expansion of EB infected T- or NK cell are seen in patients with both nasal T/NK lymphoma and CAEBV infection, suggesting that two diseases might partly share the similar mechanism by which EBV affect host cellular genes. Question has thus arisen why a subset of patients with CAEB infection develop into nasal T/NK lymphoma. This study aimed to investigate the virus-host interaction in EBV-associated lymphoma. Keywords = nasak NK/T lymphoma Keywords = chronic active EBV infection Keywords: other

2006-01-11 | GSE2432 | GEO

A Mouse Model of Epstein-Barr virus LMP1 and LMP2A Driven Germinal Center B-cell Lymphoproliferative Disease

Project description:Epstein-Barr virus (EBV) is a major cause of immunosuppression-related lymphomas. EB-driven lymphoproliferative disease complicates up to 20% of transplants, and EBV is a major cause of human immunodeficieciency virus associated lymphomas. Despite successful antiretroviral therapy, the incidence of EBV-associated Hodgkin lymphoma continues to increase in HIV+ individuals. To gain insights into EBV membrane oncoprotein effects on B-cell growth, survival and pathogenesis in vivo, we generated transgenic mouse models, in which knock-in mice transgenically express control GFP or EBV latent membrane proteins (LMP) 1 and 2A under the control of the AICDA promoter. Upon T and NK-cell depletion by antibody cocktail, LMP1 and 2A co-expression drove explosive growth of plasmablastic lymphoma-like cells, which proliferated in the spleen, caused severe end-organ damage and death. RNAseq profiling identified genome-wide LMP1 and 2A effects on B-cell gene expression, including dramatic effects on chemokine and cytokine production. While cells exhibited plasmablast features, LMP1 and 2A co-expression also induced mixed hematopoietic lineage markers, a well described but incompletely understood feature of Hodgkin lymphoma. Collectively, our results identify synergistic effects of EBV membrane oncoprotein expression, and highlight their role in lymphoproliferative diseases of immunocompromised hosts.

2017-03-16 | GSE93827 | GEO

NK-cell associated receptors expression in EBV-positive gamma-delta T cell lines.

Project description:The contribution of chronic antigen stimulation to the occurrence of lymphoproliferative disorder (LPD) with the gamma-delta T-cell lineage is unclear, despite the fact that Epstein-Barr virus (EBV) positive T-cell LPD is derived from antigen-stimulated cytotoxic T-cells. Given the possible association of antigen stimulation with the development of cytotoxic T-cell LPD, we compared gene expression patterns in Epstein-Barr virus (EBV)-positive gamma-delta T-cell lines derived from patients with nasal T-cell lymphoma and chronic active EBV infection and those in gamma-delta T-cells from healthy volunteers. Three EBV-positive gamma-delta T-cells lines, SNT cells (SNT-8, SNT-13 and SNT-15), were used in this study. SNT-8 was established from patients with nasal T-cell lymphoma and SNT-13, -15 were established from patients with chronic active EBV infection (Zhang Y, et al., Br J Cancer 94:599-608, 2006). All the SNT cells exhibits common rearrangement of Vgamma9-JgammaP and Jdelta3 genes. The gamma-delta T-cells obtained from healthy volunteers were expanded ex vivo by 1 microM of zoledronate (ZOL) plus IL-2 for 14 days incubation.

2009-12-09 | GSE13906 | GEO

Transcription profiling of human NK-cell associated receptors expression in EBV-positive gamma-delta T cell lines.

2009-12-18 | E-GEOD-13906 | biostudies-arrayexpress

Chromosomal instability associated with adverse outcome: a case report of patient with Nijmegen breakage syndrome and rapidly developed T-NHL with complex karyotype

Project description:Nijmegen breakage syndrome (NBS) is a rare genetic disorder inherited in an autosomal recessive pattern associated with an increased risk of developing lymphoproliferative disorders, mainly non-Hodgkin lymphoma (NHL) and acute lymphoblastic leukemia (ALL). This work presents a patient previously diagnosed with Nijmegen breakage syndrome who rapidly developed T-NHL despite of constant medical supervision. Cytogenetic karyotype and microarray tests revealed complex aberrations, indicating enhanced chromosomal instability.

2020-04-07 | GSE148229 | GEO

Spontaneous EBV-reactivation during in vitro B-cell differentiation: a model for polymorphic EBV-driven lymphoproliferations studied with targeted single cell expression analysis

Project description:Epstein Barr Virus (EBV) driven B-cell neoplasms arise from reactivation of latently infected B-cells. In a subset of patients EBV drives a polymorphous lymphoproliferative disorder (LPD) in which B-cell differentiation is retained. Spontaneous EBV reactivation following B-cell mitogen stimulation provides a potential model of polymorphic EBV-driven LPD. We have developed an in vitro model of plasma cell (PC) differentiation from peripheral blood memory B-cells. To assess the frequency and phenotypes of EBV-associated populations derived during differentiation we analyzed 8 differentiations at the PC stage, with a targeted single cell gene expression panel. We identified subpopulations of EBV-gene expressing cells with PC and/or B-cell expression features in differentiations from all tested donors. EBV-associated cells varied in frequency ranging from 3-28% of cells. Most EBV-associated cells expressed PC genes such as XBP1 or MZB1 and in all samples these included a quiescent PC fraction lacking cell cycle gene expression. With increasing EBV-associated cells, populations with B-cell features became prominent, co-expressing germinal centre (GC) and activated B-cell gene patterns. The presence of highly proliferative EBV-associated cells was linked to retained MS4A1/CD20 expression and IGHM and IGHD co-expression, while IGHM only and class-switched cells were enriched in quiescent PC fractions. Thus, patterns of gene expression in primary EBV reactivation are consistent with recently proposed models relating EBV-mediated transformation in lymphoblastoid cell lines to features of GC B-cells, and suggest a particular association between spontaneously developing EBV-expansions and IgM+ IgD+ non-switched B-cells.

2023-06-14 | GSE232418 | GEO

Deregulated expression of HDAC9 in B cells promotes development of lymphoproliferative disease and lymphoma in mice [Bcell subsets]

Project description:Histone deacetylase 9 (HDAC9) is expressed in B cells, and its overexpression has been observed in B-lymphoproliferative disorders, including B-cell non-Hodgkin lymphoma (B-NHL). We examined HDAC9 protein expression and copy number alterations in primary B-NHL samples, identifying high HDAC9 expression among various lymphoma entities and HDAC9 copy number gains in 50% of diffuse large B-cell lymphoma (DLBCL). To study the role of HDAC9 in lymphomagenesis, we generated a genetically engineered mouse (GEM) model that constitutively expressed an HDAC9 transgene throughout B-cell development under the control of the immunoglobulin heavy chain (IgH) enhancer (Eμ). Here, we report that the Eμ-HDAC9 GEM model develops splenic marginal zone lymphoma and lymphoproliferative disease (LPD) with progression towards aggressive DLBCL, with gene expression profiling supporting a germinal center cell origin, as is also seen in human B-NHL tumors. Analysis of Eμ-HDAC9 tumors suggested that HDAC9 might contribute to lymphomagenesis by altering pathways involved in growth and survival, as well as modulating BCL6 activity and p53 tumor suppressor function. Epigenetic modifications play an important role in the germinal center response, and deregulation of the B-cell epigenome as a consequence of mutations and other genomic aberrations are being increasingly recognized as important steps in the pathogenesis of a variety of B-cell lymphomas. A thorough mechanistic understanding of these alterations will inform the use of targeted therapies for these malignancies. These findings strongly suggest a role for HDAC9 in B-NHL and establish a novel GEM model for the study of lymphomagenesis and, potentially, preclinical testing of therapeutic approaches based on histone deacetylase inhibitors.

2016-11-17 | GSE89955 | GEO

Deregulated expression of HDAC9 in B cells promotes development of lymphoproliferative disease and lymphoma in mice [HDAC9 transgenic]

2016-11-17 | GSE89954 | GEO

Kinome profiling of Non-Hodgkin Lymphoma identifies Tyro3 as a therapeutic target in PEL

Project description:Non-Hodgkin lymphomas (NHL) make up the majority of lymphoma diagnoses and represent a very diverse set of malignancies. We sought to identify kinases uniquely upregulated in different NHL subtypes. Using Multiplexed Inhibitor Bead-mass spectrometry (MIB/MS), we found Tyro3 was uniquely upregulated and important for cell survival in primary effusion lymphoma (PEL), which is a viral lymphoma infected with Kaposi’s sarcoma-associated herpesvirus (KSHV).

2019-07-11 | PXD012087 | Pride

Expression of EBV miRNAs in numerous EBV-positive cell lines

Project description:EBV-positive cell lines were assayed for expression of EBV miRNAs. The names of the miRNAs are from miRBase from Fall 2007. Microarray probes are tandem complements of the mature miRNA sequence. We assayed Burkitt's lymphoma (BL), Nasopharyngeal carcinoma, post-transplant lymphoproliferative disease (PTLD), primary effusion lymphoma, and lymphoblastoid cell lines. We also assayed primary B cells that were infected with the B95-8 strain of EBV, which was found to express EBV miRNAs as early as 20 hours post infection. We have found PTLD and BLs from HIV-positive donors both express EBV miRNAs. These types of cell lines have not previously been found to express viral miRNAs. We have found that cells that support type I and type II latency express only the BART miRNAs, whereas cells that support type III latency express BART and BHRF1 miRNAs. Furthermore, BL cell lines that spontaneously lose EBV express levels of the viral miRNAs that are at least 5-fold lower than cell lines that do not lose EBV.

2008-12-01 | GSE12014 | 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