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Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization [Expression Array]

ABSTRACT: To determine what DNA methylation and gene expression changes occur following EBV transformation. B-cells were isolated from 3 donors. Resting, CD40 activated and EBV transfromed cells from each donor was analyzed. Each sample was assayed using Affymetrix expression arrays and whole genome bisulfite sequenicng. Additional time points during transformation and activation were sequenced as well, but not assayed for expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49628 | GEO | 2013/09/17

SECONDARY ACCESSION(S): PRJNA214516

REPOSITORIES: GEO

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Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization [Bisulfite-seq]

2013-09-17 | GSE49627 | GEO

Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization [Expression Array]

Project description:To determine what DNA methylation and gene expression changes occur following EBV transformation. B-cells were isolated from 3 donors. Resting, CD40 activated and EBV transfromed cells from each donor was analyzed. Each sample was assayed using Affymetrix expression arrays and whole genome bisulfite sequenicng. Additional time points during transformation and activation were sequenced as well, but not assayed for expression. B-cells were isolated from 3 donors. Resting, CD40 activated and EBV transfromed cells from each donor was analyzed.

2013-09-17 | E-GEOD-49628 | biostudies-arrayexpress

Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization [Bisulfite-seq]

2013-09-17 | E-GEOD-49627 | biostudies-arrayexpress

Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization.

Project description:Altered DNA methylation occurs ubiquitously in human cancer from the earliest measurable stages. A cogent approach to understanding the mechanism and timing of altered DNA methylation is to analyze it in the context of carcinogenesis by a defined agent. Epstein-Barr virus (EBV) is a human oncogenic herpesvirus associated with lymphoma and nasopharyngeal carcinoma, but also used commonly in the laboratory to immortalize human B-cells in culture. Here we have performed whole-genome bisulfite sequencing of normal B-cells, activated B-cells, and EBV-immortalized B-cells from the same three individuals, in order to identify the impact of transformation on the methylome. Surprisingly, large-scale hypomethylated blocks comprising two-thirds of the genome were induced by EBV immortalization but not by B-cell activation per se. These regions largely corresponded to hypomethylated blocks that we have observed in human cancer, and they were associated with gene-expression hypervariability, similar to human cancer, and consistent with a model of epigenomic change promoting tumor cell heterogeneity. We also describe small-scale changes in DNA methylation near CpG islands. These results suggest that methylation disruption is an early and critical step in malignant transformation.

| S-EPMC3912409 | biostudies-literature

Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization

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

2013-09-17 | E-GEOD-49629 | biostudies-arrayexpress

Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-09-17 | GSE49629 | GEO

The Epstein-Barr virus induced tumor suppressor miR-34a is growth promoting in EBV-infected B cells

Project description:Epstein-Barr virus (EBV) infection of primary human B cells drives their indefinite proliferation into lymphoblastoid cell lines (LCLs). B cell immortalization depends on expression of viral latency genes as well as the regulation of host genes. Given the important role of miRNAs in regulating fundamental cellular processes, in this study we assayed changes in host miRNA expression during primary B cell infection by EBV. We observed and validated dynamic changes in several miRNAs from early proliferation through immortalization; oncogenic miRNAs were induced and tumor suppressor miRNAs were largely repressed. However, one miRNA described as a p53-targeted tumor suppressor, miR-34a, was strongly induced by EBV infection and expressed in many EBV and KSHV-infected lymphoma cell lines. The EBV latent membrane protein 1 (LMP1) was sufficient to induce miR-34a requiring downstream NFκB activation, but independent of functional p53. Furthermore, over-expression of miR-34a was not toxic in several B lymphoma cell lines and inhibition of miR-34a impaired the growth of EBV transformed cells. This study identifies a pro-growth role for a tumor suppressive miRNA in oncogenic virus-mediated transformation highlighting the importance of studying miRNA function in different cellular contexts.

2012-04-20 | GSE36926 | GEO

CRISPR/Cas9 Screens Reveal Epstein-Barr virus Synthetic Lethal Targets

Project description:Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma and immunosuppression-related lymphomas. These B-cell malignancies arise by distinct transformation pathways and utilize divergent viral and host expression programs. To identify host dependency factors elicited by EBV latent-infection states, we performed parallel genome-wide CRISPR/Cas9 screens in Burkitt lymphoma (BL) and lymphoblasotid cell lines (LCL). Our results highlighted 57 BL and 87 LCL genes selectively critical for their growth and survival. LCL hits were enriched for EBV-induced genes, including viral super-enhancer targets and multiple kinases. We uncovered key CD19/CD81 roles in EBV membrane protein-driven PI3K/AKT activation and mechanisms by which EBV evades tumor suppressor responses to its growth program. LMP1-induced cFLIP was critical for LCL defense against TNFa-mediated programmed cell death, while EBV-induced BATF/IRF4 were critical for LCL BIM suppression and MYC induction. EBV super-enhancer targeted IRF2 protected LCLs against BLIMP1 responses. Collectively, our results identify host/pathogen interaction-driven synthetic lethal targets for therapeutic intervention.

2017-05-11 | GSE93681 | GEO

Metabolic stress is a barrier to Epstein-Barr virus mediated B-cell immortalization

Project description:Early after infection, Epstein-Barr Virus (EBV) induces a transient period of hyper-proliferation that is suppressed by the activation of the DNA damage response and a G1/S phase growth arrest. This growth arrest prevents long-term outgrowth of the majority of infected cells. We developed a method to isolate and characterize infected cells that arrest after this early burst of proliferation. We used microarray analysis to uncover changes in gene expression that could give us a better understanding of the pathways that attenuate immortalization. Human PBMCs were labeled with CellTrace Violet and infected with the B95-8 strain of EBV. At 4 days post-infection, the cells were labeled with a second proliferation dye, CFSE. Cells that proliferated are called PP and those that initially proliferated and then arrested are called PA. Total mRNA was isolated from sorted PA and PP cells using an RNeasy kit . The RNA was processed using an Ambion MessageAmp Premier Package and hybridized to a Human Genome U133 Plus. 2.0 Chip by the Duke Center for Genomic and Computational Biology Microarray Core. The resultant CEL files were RMA normalized (Partek) and the data was analyzed with GenePattern and GSEA v2.

2015-12-19 | E-GEOD-76137 | biostudies-arrayexpress

Epstein-Barr virus maintains lymphomas via its miRNAs

Project description:Epstein‐Barr virus (EBV) has evolved exquisite controls over its host cells, human B lymphocytes, not only directing these cells during latency to proliferate and thereby expand the pool of infected cells, but also to survive and thereby persist for the lifetime of the infected individual. Although these activities ensure the virus is successful, they also make the virus oncogenic, particularly when infected people are immunosuppressed. Here we show, strikingly, that one set of EBV’s miRNAs both sustain BL (Burkitt’s lymphoma) cells in the absence of other viral oncogenes and promote the transformation of primary B lymphocytes. Burkitt’s Lymphoma cells were engineered to lose EBV and found to die by apoptosis and could be rescued by constitutively expressing viral miRNAs in them. Two of these EBV miRNAs were found to target Caspase 3 to inhibit apoptosis at physiological concentrations.

2013-04-30 | GSE44769 | GEO

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