Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis of impact of culture conditions on gene expression of primary leukemic cells from chronic lymphocytic leukemia (CLL)

ABSTRACT: Proliferation and survival of CLL cells is highly dependent on the interaction of the tumor cells with different populations of accessory cells, incl. mesenchymal bone marrow stromal cells. In this project interactions between CLL cells and transformed bone-marrow derived fibroblast cell lines were studied. Gene expression was analyzed in CLL cells that were cocultured for different time periods with human (HS-5) or murine (M2-10B4) transformed fibroblasts, as compared to CLL cells from the same patient sample that were cultured in DMEM medium or conditioned medium in which HS-5 cells had been growing.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE80355 | GEO | 2019/07/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Unveiling key players in the Chronic Lymphocytic Leukemia (CLL)-microenvironment interplay

Project description:Novel dendritic cells (DCs) population in murine bone marrow (BM) that support CLL malignancy

2021-08-01 | GSE119115 | GEO

RNA-Seq analysis of LYN deficient HS-5 stroma cells cocultured with primary human CLL cells

Project description:LYN kinase is a tyrosine kinase, that regulates cellular homeostasis in a context-specific manner. Our group could show, that its expression in the leukemic microenvironment of chronic lymphocytic leukemia contributes to disease progression (Nguyen PH et al.; Cancer Cell; 2016). To analyze the effect of LYN kinase on the leukemia supportive phenotype of the bone marrow stromal cell line HS-5, we generated single cell clones of LYN deficient stroma cells. These cells were analyzed in a Multi-Omic approach, including ARNA-Seq of stromal cells after 72h of coculture with primary human chronic lymphocytic leukaemia (CLL) samples.

2023-02-10 | E-MTAB-12629 | biostudies-arrayexpress

The lymph node microenvironment promotes B-cell receptor signaling, NF-κB activation, and tumor proliferation in chronic lymphocytic leukemia (CLL)

Project description:To elucidate effects of tumor host interactions in vivo in CLL, purified tumor cells were obtained concurrently from blood, bone marrow and/or lymph node and analyzed by gene expression profiling. Keywords: RNA Comparision of gene expression profiling in matched pairs of peripheral blood (PB) vs. bone marrow (BM) or lymph nodes (LN) derived CLL cells

2010-10-01 | E-GEOD-21029 | biostudies-arrayexpress

RNA-Seq analysis of LYN deficient HS-5 stroma cells cocultured with primary human CLL cells

Project description:RNA-Seq analysis of LYN deficient HS-5 stroma cells cocultured with primary human CLL cells

| PRJEB59836 | ENA

Effect of NF-kappaB activation in bone marrow stromal cells co-cultured with CLL cells

Project description:Tumor cell survival critically depends on heterotypic communication with benign cells in the microenvironment. Here we describe a novel survival signaling pathway activated in stromal cells by contact to B-cells from chronic lymphocytic leukemia (CLL) patients. The expression of PKC-βII and the subsequent activation of NF-κB in bone marrow stromal cells is a prerequisite to support the survival of malignant B-cells. PKC-β knockout mice are insusceptible to CLL-transplantations, underscoring the in vivo significance of the PKC-βII- NF-κB signaling pathway in the tumor microenvironment. Upregulated stromal PKC-βII in biopsies from CLL, breast- and pancreatic- cancer patients suggest that this pathway may commonly be activated in a variety of malignancies. We used microarrays to determine Nemo/ IKK-gamma dependent gene expression changes in bone marrow stromal cells (BMSCs) induced by co-culturing with leukemic B-cells (CLL)

2013-03-08 | GSE36415 | GEO

Notch2 in mesenchymal stromal cells regulates canonical Wnt signalling in CLL cells

Project description:We used microarrays to investigate differential gene expression in mouse bone marrow derived mesenchymal stromal cells, proficient or deficient for Notch2, cultured for 5 days in the presence or absence with primary CLL cells from 6 patients

2019-05-20 | GSE99614 | GEO

Whole genome transcriptional analysis of leukemic CLL cells purified from bone marrow of xeno-transplanted mice

Project description:The development and progression of CLL are dependent upon a complex microenvironmental network of cellular and molecular signals. As an example the in vitro survival of CLL cells is supported by nurse-like cells, which have been identified as a CLL-specific tumor-associated macrophage (TAM) population. However little is known regarding the role of TAMs in CLL development and progression. In the CLL xenograft model based on the engraftment of MEC1 human CLL cell line into Rag2-/-Î³c-/-, we analyzed the whole-genome transcriptome of leukemic B cells, exposed in vivo to TAMs, isolated from the bone marrow. We found an enrichment of genes involved in inflammation and interaction between TAMs and leukemic cells. Rag2-/-Î³c-/- were injected intravenously with MEC1 cells and sacrificed at early stage of leukemia (n=3). RNA was isolated from: i) in vitro pre-injected human CD19+ MEC1 cells and ii) human CD19+ MEC1 cells purified from murine bone marrow by magnetic separation and processed for illumina whole-genome gene expression direct-hybridization assay

2016-02-16 | E-GEOD-57787 | biostudies-arrayexpress

CLL: CD38+CD49d+ vs. CD38-CD49d-

Project description:CD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38+CD49d+ vs. CD38-CD49d- CLL cells, we demonstrated overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also upregulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38+CD49d+ but not CD38-CD49d- cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors for CCL3 and CCL4, were found in CLL-derived monocyte-macrophages. Consistently, CCL3 increased monocyte migration, and CD68+ macrophage infiltration was particularly high in BMB from CD38+CD49d+ CLL. Conditioned media from CCL3-stimulated macrophages induced endothelial cells to express VCAM-1, the CD49d ligand, likely through TNFα over-production. These effects were apparent in BMB from CD38+CD49d+CLL, where lymphoid infiltrates were characterized by a prominent meshwork of VCAM-1+ stromal/endothelial cells. Lastly, CD49d engagement by VCAM-1-transfectants increased viability of CD38+CD49d+ CLL cells. Altogether, CD38 and CD49d can be thought of as a part of a consecutive chain of events ultimately leading to improved survival of CLL cells.

2009-03-03 | GSE14560 | GEO

Stromal cells support the survival of human primary chronic lymphocytic leukemia (CLL) cells

Project description:In chronic lymphocytic leukemia (CLL), the tumor cells receive survival support from stromal cells through direct cell contact, soluble factors and extracellular vesicles. The tyrosine protein kinase Lyn, is aberrantly expressed in the malignant and stromal cells in CLL tissue. We therefore studied the role of Lyn in the EV-based communication and tumor support. We compared the Lyn-dependent EV release, uptake and functionality using Lyn-proficient and deficient stromal cells and primary CLL cells. Lyn-proficient cells caused a significantly higher EV release and EV uptake as compared to Lyn-deficient ones. Also, they induced stronger support of primary CLL cells. Proteomic comparison of the EVs from Lyn-proficient and deficient stromal cell highlighted 72 significantly differentially expressed proteins, many of which belonging to the extracellular matrix organization, such as collagen, nidogen, fibronectin and endosialin (CD248). CD248, a marker of certain tumors and of cancer associated fibroblast (CAF) was significantly depleted in Lyn-deficient HS-5 cells. A knockdown of CD248 in Lyn+ HS-5 cells resulted in a diminished B-CLL cells survival feeding capacity compared to wildtype or scrambled control cells. The presented data provide preclinical evidence, that the tyrosine kinase Lyn crucially influences the EV-based communication between stromal and primary B-CLL cells by raising the EV release and their concentration of functional molecules, such as endosialin.

2023-01-12 | PXD036932 | Pride

T-Cells from CLL patients

Project description:T cells may have a role in sustaining the leukemic clone in chronic lymphocytic leukemia (CLL). In this study, we have examined the ability of T cells from CLL patients to support the survival of the leukemic B cells in vitro. Additionally, we compared global gene expression of T cells from indolent CLL patients with healthy individuals and multiple myeloma (MM) patients. Apoptosis of purified CLL cells was inhibited in vitro when cocultured with increasing numbers of autologous T cells (p<0.01) but not with normal donors. The anti-apoptotic effect exceeded that of the antiapoptotic cytokine IL-4 (p=0.02) and was greater with CD8+ T cells than with CD4+ cells (p<0.05). The effect depended mainly on cell-cell contact although a significant effect was observed in transwell experiments (p<0.05). Additionally, about 356 genes involved in different cellular pathways were deregulated in T cells of CLL patients compared to healthy individuals and MM patients. The results of gene expression profiling was verified for 7 genes (KLF6, TRAF1, CCL4, CCL5, RANTES, XCL1 and XCL2) using qRT-PCR and immunoblotting. Our results demonstrate that CLL-derived T cells can prevent apoptosis of leukemic cells and have altered expression of genes that may facilitate survival of the leukemic clone.

2011-03-24 | GSE28107 | 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