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Gene expression changes in subclones of a Burkitt lymphoma cell line with different patterns of EBV latent infection

ABSTRACT: In this study we have investigated the gene expression profiles of three different types of subclone all generated by single cell cloning of the same parental EBV positive Burkitt lymphoma cell line Awia-BL. These included EBV negative clones which have lost the virus episome, EBV positive clones with a conventional Latency I form of infection and EBV positive clones with an atypical Wp-restricted form of infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42867 | GEO | 2013/01/22

SECONDARY ACCESSION(S): PRJNA183683

REPOSITORIES: GEO

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Gene expression changes in subclones of a Burkitt lymphoma cell line with different patterns of EBV latent infection

Project description:In this study we have investigated the gene expression profiles of three different types of subclone all generated by single cell cloning of the same parental EBV positive Burkitt lymphoma cell line Awia-BL. These included EBV negative clones which have lost the virus episome, EBV positive clones with a conventional Latency I form of infection and EBV positive clones with an atypical Wp-restricted form of infection. Gene expression was compared between two different EBV negative clones (both performed in biological duplicate), four different Latency I clones and four different Wp-restricted clones using HG U133 Plus 2.0 gene chip arrays.

2013-01-22 | E-GEOD-42867 | biostudies-arrayexpress

Gene expression in EBV-positive versus EBV-loss clones derived from endemic Burkitt lymphoma cell lines

Project description:Whilst the association of Epstein-Barr virus (EBV) with Burkitt lymphoma (BL) has long been recognized, the precise role of the virus in BL pathogenesis is not fully resolved. EBV can be lost spontaneously from some BL cell lines, and these EBV-loss lymphoma cells reportedly have a survival disadvantage. We have generated an extensive panel of EBV-loss clones from multiple BL backgrounds and examined their phenotype comparing them to their isogenic EBV-positive counterparts. Whilst loss of EBV from BL cells is rare, it is consistently associated with an enhanced predisposition to undergo apoptosis and reduced tumorigenicity in vivo. We investigated whether there were common gene expression changes between EBV-positive and loss clones derived for four endemic Burkitt lyphoma cell lines that could explain the apoptosis sensitivity of clones that had lost EBV.

2018-01-25 | GSE100458 | GEO

circRNA microarray of the Epstein-Barr virus positive Burkitt's lymphoma cell line Akata

Project description:Epstein-Barr virus positive Burkitt's lymphoma cell line Akata (+) and it's EBV-depleted subclone Akata (-) were analyzed for human circRNA expression.

2022-12-19 | GSE206824 | GEO

Expression data from Burkitt Lymphoma cell lines followed by expression or inhibition of ebv-BART6-3p microRNA

2016-03-02 | GSE63665 | GEO

Homo sapiens

Project description:Gene expression in EBV-positive versus EBV-loss clones derived from endemic Burkitt lymphoma cell lines

| PRJNA391866 | ENA

Expression data from Burkitt Lymphoma cell lines followed by expression or inhibition of ebv-BART6-3p microRNA

Project description:Epstein-Barr virus is associated with several human malignancies, including Burkitt Lymnphoma. The virus encodes more than 40 microRNAs, which participate in its possible pathogenetic role. We used microarrays to study the effect of the expression of an Epstein-Barr virus-encoded microRNA (ebv-BART6-3p) on the global gene expression profile of Burkitt Lymphoma cell lines. In order to determine the BART6-3p targets, EBV-negative Akata 2A8 or EBV-positive Akata cells were transiently transfected (in duplicates) with synthetic BART6-3p mimic or inhibitor (100 nM; Custom synthesized by Dharmacon- Thermo Scientific, Germany), respectively. For each treatment, a further transfection with corresponding negative control was performed as well (10 nM; I-300145-01, Dharmacon- Thermo Scientific, Germany). The transfection of 5,000,000 cells per treatment was performed by Amaxa nucleofector apparatus (Amaxa, Cologne-Germany), using the program G23 and the transfection solution V according to the manufacturerâs instructions. Transfection efficiency was assessed by means of a further treatment (2Âµg of pmaxGFP) and detection of both fluorescence and cell viability by flow cytometry. Twenty four hours post-transfection, cells were harvested and RNA was extracted using Trizol, and transfection efficiency was further confirmed by evaluating the expression level of BART6-3p using q-PCR by means of Taqman probes, employing RNU43 as housekeeping miRNA (Applied Biosystems, Cologne, Germany). RNA was further hybridized to HuGene-2.0-st array (Affymetrix, Santa Clara, CA) according to the manufacturer's instructions.

2016-03-02 | E-GEOD-63665 | biostudies-arrayexpress

Expression data from Epstein-Barr virus -positive and negative Akata Burkitt's Lymphoma Clones

Project description:Transition of Akata Burkitt lymphoma (BL) cells from a malignant to nonmalignant phenotype upon loss of Epstein-Barr virus (EBV) genomes in vitro is evidence for a viral contribution to tumor maintenance despite the tightly restricted pattern of EBV gene expression in BL. Akata cells retaining virus manifest increased resistance to apoptosis under growth limiting conditions, although ambiguity exists regarding the exact mechanisms involved. By examining global cellular gene expression differences in Akata subclones that had either retained or lost EBV, we identified spermidine/spermine N1-acetyltransferase (SSAT), an inducible acetylating enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes up-regulated upon loss of EBV. Keywords: Disease state analysis We used Affymetrix microarrays to examine variations in global gene expression between the paired EBV-positive (1B6) and EBV-negative (2A8) Akata Burkitt's lymphoma clones. EBV-negative Akata clones were generated by treatment with hydroxyurea, an inhibitor of ribonucleotide reductase that forced rapid loss of EBV episomes and compared to their EBV-positive counterparts. Logarithmically growing EBV-negative and positive Akata EBV clones were seeded at 2.5x10^5 cells/ml in RPMI1640 supplemented with 10% fetal bovine serum, 2mM glutamine, and 100units/ml penicillin/streptomycin. The next day, the cells were incubated for 4 hours in media containing 1% fetal bovine serum (low serum), 2mM glutatmine and 100units/ml penicillin/streptomycin to begin selection of the Akata tumor phenotype. The short incubation time was intended to minimize cell death and other potential downstream effects of low serum treatment, while at the same time initiating expression changes contributing to the tumorigenic phenotype.

2010-01-19 | E-GEOD-19761 | biostudies-arrayexpress

Genomics of Endemic Burkitt Lymphoma

Project description:This genomic landscape of Burkitt lymphoma represents a multimodal sequencing of tumors and control tissues and individuals to better understand the etiology, and molecular pathogenesis of Burkitt lymphoma including the roles of the associated Plasmodium falciparum malaria and EBV infections. Comprehensive sequencing set includes genomic, transcriptomic, and epigenomic datasets in concert with variable clinical phenotypes and outcome information such as anatomical presentation site, in-hospital survival rates, and EBV genome type. The initial deposit represents polyA RNA-seq from tumor specimens from 28 cases of endemic BL and 2 cases of sporadic BL. For initial transcriptome analysis see: Kaymaz et al. Comprehensive Transcriptome and Mutational Profiling of Endemic Burkitt Lymphoma Reveals EBV Type-specific Difference. Molecular Cancer Research: MCR, January. doi:10.1158/1541-7786.MCR-16-0305. For general overview of cohort study see: Buckle et al. Factors influencing survival among Kenyan children diagnosed with endemic Burkitt lymphoma between 2003 and 2011: A historical cohort study. Int J Cancer. 15:1231, 2016.

| phs001282 | dbGaP

Burkitt Lymphoma beyond MYC translocation:N-MYC and DNA methyl transferases dysregulation

Project description:Identification of miRNA differentially expressed between MYC-translocation positive and and MYC-translocation negative Burkitt Lymphoma and their impact on gene expression profile Study of microRNA profile of MYC-translocation positive and MYC-translocation negative Burkitt Lymphoma cases in order to uncover possible differences at the molecular level

2015-08-05 | E-GEOD-71471 | biostudies-arrayexpress

Comprehensive immunophenotypic characterization of Burkitt-like lymphoma with 11q aberration by flow-cytometry

Project description:Recently, a subset of MYC-translocation negative aggressive B-cell lymphomas resembling Burkitt lymphoma (BL) characterized by proximal gains and distal losses in the long arm of chromosome 11 has been described. In the 2016 revision of the WHO classification these MYC-translocation negative lymphomas have been introduced as new provisional entity designated “Burkitt-like lymphoma with 11q aberration” (MNBLL 11q). Here, we show a comprehensive flow-cytometry analysis of 10 MNBLL 11q cases, well characterized genetically and pathologically. Twenty-three cases of MYC-positive BL, including three cases carrying both MYC rearrangements and 11q aberration, served as controls. All MNBLL 11q were CD20+/CD10+/BCL6+/BCL2- /MUM1- /MYC+/EBV negative , presented a high proliferation rate and showed a three-year overall survival (80%) similar to BL patients, with no recurrence after the end of treatment. MNBLL 11q immunophenotype was similar to that of MYC-positive BL without and with 11q, except for less frequent CD38higher expression (10% MNBLL 11q vs 91% MYC-positive BL, p<0.001), less frequent diminished CD45 expression (90% vs 23%, p=0.001), and CD16/CD56 co-expression (60% vs 0%, p<0.001). Our findings suggest subtle but important differences in MNBLL 11q immunophenotypes and MYC-positive BLs, which could not only aid in the differential diagnosis but also in the understanding of the pathogenesis of MNBLL 11q.

2019-07-30 | GSE93002 | GEO

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