Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from EBER1-overexpressing Hodgkin lymphoma cell lines KM-H2 and L428

ABSTRACT: Epstein-Barr virus (EBV)- encoded RNAs (EBERs) are aboundance in all EBV lantency, it was found that EBERs may contribute to the oncogenesis. To study the role of EBV-encoded small RNAs (EBERs) in Hodgkin lymphoma, we transfected Hodgkin lymphoma cell lines, KMH2 and L428, with EBER1 and screen with microarrays to verify what is the possible role of the EBER1 in Hodgkin lymphoma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE12427 | GEO | 2010/02/13

SECONDARY ACCESSION(S): PRJNA113739

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profile of classical Hodgkin lymphoma according to Epstein-Barr infection status

Project description:Transcriptional profiling of Human Hodkin Lymphoma lineages infected or not by Epstein Baar Virus (EBV). We compared EBV infected lineage L591 and not EBV infected lineages L428, L1236 and KMH2. Goal was to determine presence versus absence of EBV infection on global gene expression of Hodkin Lymphoma cell lines. EBV infected Hodkin Lymphoma lineage L591 vs 3 Hodkin Lymphoma lineages not EBV infected L428, L1236 and KMH2. Dye Swap and direct comparisom between L591 (EBV infected) and the three others not infected cell lines.

2011-12-31 | E-GEOD-21586 | biostudies-arrayexpress

Gene expression profile of classical Hodgkin lymphoma according to Epstein-Barr infection status

2011-12-31 | GSE21586 | GEO

Transcription profiling of Hodgkin Lymphoma- and Anaplastic Large Cell Lymphoma-derived cell lines

Project description:To identify genes and pathways involved in the pathogenesis of Hodgkin Lymphoma (HL) and Anaplastic Large Cell Lymphoma (ALCL) , we used the Ontario Cancer Institute (OCI) Human 27k arrays (UNH Homo sapiens 19K8 array), to study the expression profiling in pairs of HL-derived cell lines (KMH2 and L428) and ALCL-derived cell lines (DEL and SR-786).

2009-03-31 | E-MEXP-1132 | biostudies-arrayexpress

JAK/STAT blockade in cHL

Project description:Here we investigated the effects of JAK/STAT pharmacological inhibition on cHL cell models using ruxolitinib, a JAK 1/2 inhibitor. We use five classical Hodgkin lymphoma cell lines: L428, L1236, L540, KMH2, L591

2021-10-15 | GSE185818 | GEO

Hodgkin lymphoma

Project description:This SuperSeries is composed of the following subset Series: GSE25986: Gene expression profiling of cell lines derived from classical Hodgkin lymphoma GSE25987: Gene expression profiling of Hodgkin lymphoma cell line KMH2: Comparison of CIITA-BX648577 knockdown cultures with non-silencing controls GSE25989: Copy number analysis of Hodgkin lymphoma cell lines KM-H2 and L-428 Refer to individual Series *** This submission represents the microarray gene expression and microarray copy number components of the study

2010-12-11 | E-GEOD-25990 | biostudies-arrayexpress

LY294002 induced gene expression changes in Hodgkin lymphoma cell line KMH2.

Project description:In this study, we investigated the effect of LY294002 on gene expression in Hodgkin lymphoma cell line KMH2 cells.

2017-09-11 | GSE89759 | GEO

BATF3siRNA induced gene expression changes in Hodgkin lymphoma cell line L428.

Project description:In this study, we investigated the effect of BATF3 silecing on gene expression in Hodgkin lymphoma cell line L428.

2017-09-11 | GSE89760 | GEO

PAX5 overexpression is not enough to reestablish the mature B-cell phenotype in classical Hodgkin lymphoma

Project description:In lymphomas derived from mature B cells the expression of the transcription factor PAX5 is maintained whereas classical Hodgkin lymphoma displays significantly reduced PAX5 expression despite its derivation from mature B cells. To elucidate the functional role of PAX5 in classical Hodgkin lymphoma, we re-established the PAX5 expression in the Hodgkin cell line L428 with and without epigenetic modulation. To this end, we stably transfected the Hodgkin cell line L428 with an inducible PAX5 expression construct. Although the overexpressed PAX5 was transcriptionally active as demonstrated by synthetic reporter constructs, no induction of the B-cell phenotype was achieved. PAX5 chromatin immunoprecipitation with subsequent next generation sequencing in B-cell lines and the PAX5 overexpressing L428 cell line showed different binding patterns. Since epigenetic restrictions might affect PAX5 binding, combined DNA demethylation and histone acetylation was performed. However, no re-expression of B-cell genes was observed also under these conditions. Thus, PAX5 is not sufficient for the re-activation of the B-cell program in Hodgkin cells despite epigenetic opening of the chromatin. This clearly indicates that the repression of the B-cell identity of the Hodgkin cells is caused and secured by complex molecular mechanisms. 2 Burkitt lymphoma cell lines (Raji, Namalwa), the Hodgkin lymphoma cell line L428 and the PAX5-producing L428 (L428-PAX5) with or without 5-aza-2M-bM-^@M-2-deoxycytidine/Trichostatin A treatment were analysed in triplicate.

2013-07-30 | E-GEOD-44244 | biostudies-arrayexpress

Analyzing primary Hodgkin and Reed-Sternberg cells to capture the molecular and cellular pathogenesis of classical Hodgkin lymphoma

Project description:The pathogenesis of classical Hodgkin lymphoma (cHL), the most common lymphoma in the young, is still enigmatic, largely because its Hodgkin and Reed-Sternberg (HRS) tumor cells are rare in the involved lymph node and therefore difficult to analyze. Here, by overcoming this technical challenge and performing for the first time a genome-wide transcriptional analysis of microdissected HRS cells in comparison to other B-cell lymphomas, cHL lines and normal B-cell subsets, we show that they differ extensively from the usually studied cHL cell lines, that the lost B-cell identity of cHLs is not linked to the acquisition of a plasma cell-like gene expression program, and that Epstein-Barr virus infection of HRS cells has a minor transcriptional influence on the established cHL clone. Moreover, although cHL appears a distinct lymphoma entity overall, HRS cells of its histological subtypes diverged in their similarity to other related lymphomas. Unexpectedly, we identified two molecular subgroups of cHL associated to differential strengths of the transcription factor activity of the NOTCH1, MYC and IRF4 proto-oncogenes. Finally, HRS cells display deregulated expression of several genes potentially highly relevant to lymphoma pathogenesis, including silencing of the apoptosis-inducer BIK and of INPP5D, an inhibitor of the PI3K-driven oncogenic pathway. The present study complements the GSE12453 and GSE14879 records by adding the following 10 samples: 5 primary tumor samples and 5 cell line samples. The 5 primary tumor samples represent 1000-2000 neoplastic cells microdissected from frozen biopsies of 5 cases of primary mediastinal B-cell lymphoma (PMBL). The 5 cell line samples represent 500-1000 living neoplastic cells isolated by fluorescence-activated cell sorting from growing cultures of the classical Hodgkin lymphoma (cHL) cell lines L1236, L428, KMH2 and HDLM2 and the lymphocyte-predominant Hodgkin lymphoma (lpHL) cell line DEV.

2012-09-17 | E-GEOD-40160 | biostudies-arrayexpress

Expression changes induced by PTPN1 knockdown in KM-H2 cells

Project description:Gene expression data for shRNA PTPN1 knockdown vs. Non-silencing in the classical Hodgkin lymphoma-derived cell line KM-H2

2014-01-17 | GSE54157 | GEO