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Affymetrix SNP array data for Primary Effusion Lymphoma samples

ABSTRACT: Primary Effusion Lymphoma (PEL) is a Diffuse-Large B-cell Lymphoma (DLBCL) with poor prognosis. 100% of PEL carry the genome of Kaposi's Sarcoma-associated herpesvirus (KSHV) and approximately half are co-infected with Epstein-Barr virus (EBV). We profiled genomic aberrations in PEL using the Affymetrix 6.0 SNP array. This identified for the first time individual genes that are altered in PEL. 10/13 (76%) samples were deleted for both the fragile site tumor suppressors WWOX and FHIT. Alterations were also observed in: DERL1, ETV1, RASA4, TPK1, TRIM56 and VPS41 genes, which are yet to be characterized for their roles in cancer. Co-infection with EBV was associated with significantly fewer gross genomic aberrations. PEL could be segregated into EBV positive and EBV negative clusters on the basis of host chromosome alterations. The genomic signature of PEL cells in culture was analogous to those explanted from xenograft tumors. This suggests a model in which both host and virus contribute to the PEL phenotype.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25839 | GEO | 2011/06/23

SECONDARY ACCESSION(S): PRJNA135755

REPOSITORIES: GEO

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Affymetrix SNP array data for Primary Effusion Lymphoma samples

Project description:Primary Effusion Lymphoma (PEL) is a Diffuse-Large B-cell Lymphoma (DLBCL) with poor prognosis. 100% of PEL carry the genome of Kaposi's Sarcoma-associated herpesvirus (KSHV) and approximately half are co-infected with Epstein-Barr virus (EBV). We profiled genomic aberrations in PEL using the Affymetrix 6.0 SNP array. This identified for the first time individual genes that are altered in PEL. 10/13 (76%) samples were deleted for both the fragile site tumor suppressors WWOX and FHIT. Alterations were also observed in: DERL1, ETV1, RASA4, TPK1, TRIM56 and VPS41 genes, which are yet to be characterized for their roles in cancer. Co-infection with EBV was associated with significantly fewer gross genomic aberrations. PEL could be segregated into EBV positive and EBV negative clusters on the basis of host chromosome alterations. The genomic signature of PEL cells in culture was analogous to those explanted from xenograft tumors. This suggests a model in which both host and virus contribute to the PEL phenotype. 17 samples (no replicates) were analyzed using Partek Genomic Suite software

2011-06-23 | E-GEOD-25839 | biostudies-arrayexpress

Widespread traces of lytic KSHV in primary effusion lymphoma at single-cell resolution

Project description:Cancer cells of primary effusion lymphoma (PEL) often contain both Kaposi sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). We measured the interplay of human, KSHV, and EBV transcription in a cell culture model of PEL using single-cell RNA sequencing. The data detect widespread trace expression of lytic KSHV genes.

2020-10-13 | GSE154900 | GEO

Affymetrix 500K SNP array data for Primary Effusion Lymphoma samples

Project description:Affymetrix 500K array was used to determine gross genomic aberrations in a panel of Primary Effusion Lymphoma (PEL) cell lines, specifically focusing on chromosome 10, which includes the Phosphatase and Tensin Homolog (PTEN) locus. 10 PEL cell lines were hybridized to the Affymetrix 500K array where non-PEL B-cell lymphoma cell lines BJAB and DG75 were used as controls. The data was analyzed using Partek Genomic Suite software and compared to normal tonsil controls.

2011-06-23 | E-GEOD-28684 | biostudies-arrayexpress

Posttransplant diffuse large B-cell lymphoma: new genetic findings

Project description:Molecular pathogenesis of posttransplant (PT) lymphoproliferative disorder, including the most prevalent diffuse large B cell lymphoma (DLBCL), is largely unknown. We have recently showed that Epstein-Barr Virus (EBV)+ and EBV- PT-DLBCL are biologically different, but gene expression profile of the latter lymphoma is similar to that of immunocompetent (IC) DLBCL. To validate these findings on a genomic level, we performed array CGH analysis of 21 EBV+ and 6 EBV- PT-DLBCL, and 11 control IC-DLBCL. Genomic and transcriptomic data were subsequently integrated. Notably, EBV+ and EBV- PT-DLBCL revealed only one shared recurrent imbalance, while EBV- PT-DLBCL displayed at least 10 aberrations recurrent in IC-DLBCL, among others gain of 3/3q and 18q, and loss of 6q23/TNFAIP3 and 9p21/CDKN2A. EBV+ PT-DLBCL showed distinct aberrations, including the most prevalent gain/amplification of 9p24.1 targeting PDCD1LG2/PDL2. Significant differential representation/expression of 3p13/FOXP1 and 9p21/CDKNA2 in EBV+ PT-DLBCL when compared with EBV- PT-/IC-DLBCL, suggests that the oncogene FOXP1 and the tumor suppressor gene CDKNA2 are not implicated in pathogenesis of EBV+ PT-DLBCL. In summary, genomic profiling of PT-/IC-DLBCL confirmed biological distinctness of EBV+ and EBV- PT-DLBCL, and relationship between EBV- PT-DLBCL and IC-DLBCL. These findings support the hypothesis that EBV- PT-DLBCL are coincidental lymphomas in transplant recipients

2015-06-02 | GSE69440 | GEO

Affymetrix 500K SNP array data for Primary Effusion Lymphoma samples

2011-06-23 | GSE28684 | GEO

Differentially expressed human and viral miRNAs across a panel of B-cell lines, including primary effusion lymphomas

Project description:To identify differentially expressed human and viral miRNAs across a panel of B-cell lines, including several primary effusion lymphomas (PEL). Gammaherpesvirus and host cell microRNAs (miRNAs) together modulate gene expression in normal and malignant cells. Using microRNA microarrays, we determined the expression of mature viral and host cellular miRNAs in a series of B cell tumours that include Kaposiâs Sarcoma-associated herpesvirus (KSHV) infected Primary Effusion Lymphoma (PEL) and Epstein-Barr virus (EBV) infected Burkittâs lymphoma (BL) cell lines. We show that 35 host miRNAs were constitutively expressed in all the B cell lymphomas and differences in viral miRNA expression were evident between herpesvirus positive tumour types. Furthermore, we show that in PEL, miR-221 and miR-222 expression is defective due to a lack of transcript expression rather than mutation in the miRNA encoding loci. Absence of miR-221 and miR-222 resulted in the enhanced expression of the known target gene p27 (CDKN1B) and reintroduction of miR221 in PEL reduces p27 protein expression. miRNA expression profiling of a panel of 25 B-cell line samples.

2015-12-05 | E-GEOD-18437 | biostudies-arrayexpress

microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP [Illumina]

Project description:Primary effusion lymphoma (PEL) is caused by Kaposi's sarcoma-associated herpesvirus (KSHV) and frequently also harbors Epstein-Barr virus (EBV). The expression of KSHV- and, often, EBV-encoded microRNAs (miRNAs) in PELs suggests a role for these miRNAs in viral latency and lymphomagenesis. Here we report the direct and transcriptome-wide identification of miRNA target sites for all miRNAs expressed in PEL cell lines. The resulting dataset revealed that KSHV miRNAs directly target more than 2000 cellular mRNAs encoding proteins that function in pathways with relevance to KSHV pathogenesis. Moreover, ~50% of these mRNAs are also targeted by EBV miRNAs, via distinct binding sites. In addition to a known viral analog of miR-155, we show that KSHV encodes a viral miRNA that mimics cellular miR-142-3p function. In summary, these experiments identify an extensive list of mRNAs targeted by KSHV miRNAs and indicate that these are likely to strongly influence viral replication and pathogenesis. small RNA sequencing, 3 samples Ago2 (EIF2C2) PAR-CLIP, 2 samples

2011-11-16 | E-GEOD-32109 | biostudies-arrayexpress

Convergence of KSHV Reactivation with EBV latency and cellular growth mediated by the Notch signaling pathway in co-infected cells.

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiologic agent of primary effusion lymphoma (PEL). All PEL cell lines are infected with KSHV, and 70% are co-infected with Epstein-Barr Virus (EBV). KSHV reactivation from latency requires promoter-specific transactivation by the KSHV Rta protein through interactions with RBP-Jk (CSL), the cellular DNA binding component of the Notch signal transduction pathway. EBV transformation of primary B cells requires EBV nuclear antigen (EBNA)-2 to interact with RBP-Jk to direct the latent viral and cellular gene expression program. Although KSHV Rta and EBV EBNA-2 both require RBP-Jk for transactivation, previous studies have suggested that RBP-Jk-dependent transactivators do not function identically. We have found that the EBV latent protein LMP-1 is expressed in less than 5% of KSHV+/EBV+ PEL cells, but is induced in an Rta-dependent fashion when KSHV reactivates. KSHV Rta transactivates the EBV latency promoters in an RBP-Jk-dependent fashion and forms a ternary complex with RBP-Jk on the promoters. In B cells that are conditionally transformed by EBV alone, we show that KSHV Rta complements a short-term EBNA2 growth deficiency in an autocrine/paracrine manner. Complementaton of EBNA2-deficiency by Rta depends on RBP-Jk and LMP-1, and Rta transactivation is required for optimal growth of KSHV+/EBV+ PEL lines. Our data suggest that Rta can contribute to EBV-driven cellular growth by transactivating RBP-Jk-dependent EBV latency genes. However, our data also suggest that EBNA2 and Rta induce distinct alterations in the cellular proteomes that contribute to growth of infected cells.

2010-12-31 | GSE21375 | GEO

Differentially expressed human and viral miRNAs across a panel of B-cell lines, including primary effusion lymphomas

Project description:To identify differentially expressed human and viral miRNAs across a panel of B-cell lines, including several primary effusion lymphomas (PEL). Gammaherpesvirus and host cell microRNAs (miRNAs) together modulate gene expression in normal and malignant cells. Using microRNA microarrays, we determined the expression of mature viral and host cellular miRNAs in a series of B cell tumours that include Kaposi’s Sarcoma-associated herpesvirus (KSHV) infected Primary Effusion Lymphoma (PEL) and Epstein-Barr virus (EBV) infected Burkitt’s lymphoma (BL) cell lines. We show that 35 host miRNAs were constitutively expressed in all the B cell lymphomas and differences in viral miRNA expression were evident between herpesvirus positive tumour types. Furthermore, we show that in PEL, miR-221 and miR-222 expression is defective due to a lack of transcript expression rather than mutation in the miRNA encoding loci. Absence of miR-221 and miR-222 resulted in the enhanced expression of the known target gene p27 (CDKN1B) and reintroduction of miR221 in PEL reduces p27 protein expression.

2015-12-05 | GSE18437 | GEO

microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP [Illumina]

2011-11-16 | GSE32109 | GEO

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