Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of microdissected HRS cells is correlated with primary treatment outcome

ABSTRACT: Hodgkin lymphoma is derived from germinal center / post-germinal center B cells. Gene expression profilies of micodissected Hodkin Reed Sternberg cells (n=29) were dichotomized into primary treatment failure (n=14) and primary treatment succeses (n=15). Treament failure was defined as refractory disease or progression at any time after ABVD chemotherapy.

ORGANISM(S): Homo sapiens

SUBMITTER: Christian Steidl

PROVIDER: E-GEOD-39134 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of microdissected HRS cells

Project description:Hodgkin lymphoma is derived from germinal center / post-germinal center B cells. Gene expression profilies of micodissected Hodkin Reed Sternberg cells (n=29) were compared to microdissected germinal centers (n=5)

2012-08-31 | E-GEOD-39133 | biostudies-arrayexpress

Gene expression profiling of cell lines derived from classical Hodgkin lymphoma

Project description:Hodgkin lymphoma is derived from germinal center / post-germinal center B cells. To determine differentially expressed genes between Hodgkin Reed Sternberg cells and their presumed cell of origin we investigated the expression profiles of 5 commonly used Hodgkin lymphoma cell lines as compared to reactive germinal centers.

2010-12-11 | E-GEOD-25986 | biostudies-arrayexpress

Gene expression profiling of Hodgkin lymphoma cell lines

Project description:Hodgkin lymphoma is derived from germinal center / post-germinal center B cells. Gene expression profilies of the Hodgkin lymphoma cell lines were compared to 5 samples of CD77+ centroblasts derived from reactive tonsils

2012-08-31 | E-GEOD-39132 | biostudies-arrayexpress

Gene expression profiling of microdissected HRS cells is correlated with primary treatment outcome

Project description:Hodgkin lymphoma is derived from germinal center / post-germinal center B cells.

2012-08-31 | GSE39134 | GEO

Effect of lestaurtinib on KM-H2 HRS cell line

Project description:Effect of the tyrosine kinase inhibitor (TKI) lestaurtinib on Hodgkin and Reed/Sternberg (HRS) cell line KM-H2 compared to the solvent treated control.

2012-02-21 | E-MEXP-3565 | biostudies-arrayexpress

Fibroblasts in Nodular Sclerosing Classical Hodgkin Lymphoma Are Defined by a Specific Phenotype and Protect Tumor Cells From Brentuximab-Vedotin Induced Injury

Project description:Several studies have described a crosstalk between the tumour cells of cHL, the Hodgkin- and Reed-Sternberg (HRS) cells, and cancer-associated fibroblasts (CAF). However, to date a deep molecular characterization of these fibroblasts is lacking. Aim of the present study therefore was a comprehensive characterization of these fibroblasts.

2020-06-30 | GSE153517 | GEO

Proteome profiling of mouse germinal center B cells

Project description:Productive B cell responses are critical to protect a host from infection. The spleen and lymph nodes are populated by resting follicular B cells, which can enter germinal centers upon antigen encounter. Once in the germinal center, B cells migrate between the dark and light zones, where they undergo somatic hypermutation and selection, respectively. While germinal center B cells have been studied, an intense molecular understanding of these cells/subsets (and the differences between them) is lacking.

2020-04-06 | PXD015524 | Pride

The BCL6 RD2 domain governs commitment of activated B-cells to form germinal centers

Project description:Our data demonstrated that Bcl6 directly binds and represses trafficking receptors S1pr1 and Grp183 by recruiting Hdac2 through the RD2 domain. Deregulation of these genes impairs B-cell migration and may contribute to the Germinal Center failure in Bcl6RD2MUT mice.

2014-09-14 | GSE58365 | GEO

Expression study of the Hodgkin’s lymphoma cell line L-1236 upon CRISPR Cas9-mediated knockout of lymphotoxin alpha (LTA) compared to control

Project description:Persistent NF-κB activation is a hallmark of the malignant Hodgkin/Reed-Sternberg (HRS) cells in classical Hodgkin lymphoma (cHL). Analysis of the cHL cell-secreted key factors for NF-κB activation by chromatography and subsequent mass spectrometry revealed lymphotoxin-α (LTA) as the causative factor for autocrine and paracrine activation of canonical and noncanonical NF-κB in cHL cell lines. Upon CRISPR/Cas9-mediated gene knockout of LTA in the cell line L-1236, we performed expression analysis of LTA knockout versus control cells by using the Affymetrix array, Clariom S human, profiling tool.

2019-05-22 | GSE131559 | GEO

Characterization of human CD30+ B cells and their relationship to Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma

Project description:Small subsets of B cells in the germinal center (GC) and in extrafollicular regions of lymph nodes express the activation marker CD30. Very little is known about the specific features of these cells and their relationship to the CD30-expressing Hodgkin and Reed/Sternberg (HRS) cells of Hodgkin lymphoma. Phenotypic and immunoglobulin V gene analyses revealed that CD30+ GC B lymphocytes represent typical GC B cells, and that CD30+ non-GC B cells are mostly post-GC B cells. However, despite these seemingly distinct identities, both CD30+ subsets share an unexpectedly large overlap in specific transcriptome patterns, and are strikingly different from bulk GC B cells and classical memory and plasma cells, respectively. A main common feature of these CD30+ B cells is a strong MYC signature. CD30+ GC B cells appear to represent the recently described MYC+ GC B cell subset of recirculating centrocytes at the stage of centroblast transition. CD30+ non-GC B cells rather represent highly activated and proliferating memory B cells, differentiating into plasma cells. Notably, CD30+ B cells were more similar in their transcriptome patterns to HRS cells than any other B cell subset investigated, suggesting that HRS cells may either derive from CD30+ B cells or acquired a similar activation signature. In comparison to CD30+ B cells and other lymphomas, HRS cells show a remarkable downregulation of genes regulating cell cycle, genomic stability and polyploidity, providing a potential explanation for the genomic instability and multinuclearity of HRS cells.

2018-06-13 | GSE83441 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data