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Viral microRNA expression in two nasal NK T cell lymphoma cell lines

ABSTRACT: We have used microarray profiling to examine the expression of viral microRNAs (miRNAs) in two independently derived nasal natural killer T cell lymphoma (NKTCL) cell lines, SNK6 and SNT16. The goal of the study was to investigate the role of the viral miRNAs in the genesis and maintenance of NKTCLs.

ORGANISM(S): Merkel cell polyomavirus Human gammaherpesvirus 8 JC polyomavirus Betapolyomavirus macacae Murid gammaherpesvirus 4 Homo sapiens Human immunodeficiency virus 1 Human betaherpesvirus 5 Macacine gammaherpesvirus 4 Human alphaherpesvirus 2 Gallid alphaherpesvirus 3 Betapolyomavirus hominis Human alphaherpesvirus 1 Gallid alphaherpesvirus 2 Macaca mulatta rhadinovirus human gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE30695 | GEO | 2011/11/28

SECONDARY ACCESSION(S): PRJNA144411

REPOSITORIES: GEO

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Viral microRNA expression in two nasal NK T cell lymphoma cell lines

Project description:We have used microarray profiling to examine the expression of viral microRNAs (miRNAs) in two independently derived nasal natural killer T cell lymphoma (NKTCL) cell lines, SNK6 and SNT16. The goal of the study was to investigate the role of the viral miRNAs in the genesis and maintenance of NKTCLs. This experiment includes a total of 2 samples, one from SNK6 cells and the other from SNT16 cells.

2011-11-28 | E-GEOD-30695 | biostudies-arrayexpress

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miRNA expression profiles in nasal NK-cell lymphoma

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MicroRNA microarray analysis in nasal NK/T-cell lymphoma cell lines

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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

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MicroRNA microarray analysis in nasal NK/T-cell lymphoma cell lines

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Exome sequencing identifies somatic mutations of DDX3X in natural killer/T-cell lymphoma

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Bovine nasal swabs viral metagenome

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Transcription profiling by array of human non anaplastic T-cell lymphoma biopsies and cell lines

Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net) | Affymetrix HG-U133 Plus 2.0 : 7 NKTCL biopsies, 2 NKTCL cell lines (SNK6, SNT8), 16 PTCL NOS biopsies, 2 NK cells samples | Biopsies and cell lines of NK/T-cell lymphoma, nasal-type (NKTCL) were subject to combined gene expression profiling and array-based comparative genomic hybridization analyses. Compared to PTCL, NOS, NKTCL had higher transcript levels for NK-cell markers and cytotoxic molecules, especially granzyme H, a novel sensitive biomarker of NKTCL. Compared to normal NK cells, tumors were closer to activated than resting cells and overexpressed several genes related to vascular biology, EBV-induced genes and PDGFRA. Notably, PDGFR? and its phosphorylated form were confirmed at the protein level, and in vitro the MEC04 NKTCL-cell line was sensitive to imatinib. Deregulation of the AKT, JAKSTAT and NF-?B pathways suggested by bioinformatical analysis, was corroborated by nuclear expression of phosphorylated AKT, STAT3 and RelA in NKTCL, and several deregulated genes in these pathways mapped to regions of recurrent copy number aberrations (AKT3 (1q44), IL6R (1q21.3), CCL2 (17q12), TNFRSF21 (6p12.3)). Several features of NKTCL uncovered by this analysis (overexpression of VEGFA and its receptor KDR by the tumor cells, overexpression of MET-HGF) suggest deregulation of angiogenic pathways. Integrative analysis also identified a novel putative tumor suppressor HACE1 in the frequently deleted 6q21 region. This study highlights emerging oncogenic pathways in NKTCL and identifies novel diagnostic and therapeutic targets. | Submitter : Aurelien de Reynies <reyniesa@ligue-cancer.fr> | Project leader : Philippe Gaulard <philippe.gaulard@hmn.aphp.fr>

2009-12-31 | E-TABM-702 | biostudies-arrayexpress

Single-Cell Transcriptome Analysis Identifies Key Components of Tumor Microenvironment for Extranodal Natural Killer/T-cell lymphoma

Project description:Extranodal natural killer/T-cell lymphoma (NKTCL) is an aggressive Epstein-Barr virus (EBV)-associated lymphoma with heterogeneous tumor behaviors and clinical outcomes. Here, we profiled tumor microenvironment (TME) of NKTCL through single-cell transcriptome analysis of 137,304 cells from 10 tumor-blood pairs. We identified six malignant subtypes with diverse transcriptional signatures, among which LMP1+ NK_C9_CXCL13 was characterized with oncogenic and immunosuppressive potentials as well as an axial role in malignant transformation. Moreover, ligand-receptor analyses and multiplex immunofluorescent staining assays revealed intensive interactions among malignant NK, tumoral myeloid, and T cells, fostering immunosuppressive TME in NKTCL. Furthermore, co-culture assays revealed that malignant cells induced the development of immunosuppressive and pro-tumorigenic tumor-associated macrophages (TAMs) through high expression of CSF1 and hampered the recruitment of normal NK cells through broad secretion of a dipeptidylpeptidase DPP4 in NKTCL. Lastly, we revealed the inter-patient heterogeneity of NKTCL with distinct EBV transcription and TAM infiltration in multiple patient cohorts, of which high and low were favorable prognostic indicators for NKTCL patients, respectively. Collectively, for the first time to our knowledge, our study dissects the heterogeneous composition of NKTCL TME at single-cell resolution, which provides insights into understanding the pathogenic mechanisms of NKTCL and developing novel therapeutic strategies against NKTCL.

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