Genome-Wide Expression Profiling of cultured B-CLL cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE18192 | GEO | 2010/09/21
SECONDARY ACCESSION(S): PRJNA119503
REPOSITORIES: GEO
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Project description:Increased survival of primary B-CLL cells cultured in high cell density: Evidence for activation of pathways also induced by stromal cells. Expression profiles of B-CLL cells before and after three different survival-inducing culture conditions: (1) stromal cell coculture [HCo], (2) stromal cell conditioned medium [CM], (3) high cell density cultures [CD]. Controls without survival-inducing culture conditions are included [0]. Peripheral blood samples were obtained from B-CLL patients.
2010-09-21 | E-GEOD-18192 | biostudies-arrayexpress
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-M-NM-2II and the subsequent activation of NF-M-NM-:B in bone marrow stromal cells is a prerequisite to support the survival of malignant B-cells. PKC-M-NM-2 knockout mice are insusceptible to CLL-transplantations, underscoring the in vivo significance of the PKC-M-NM-2II- NF-M-NM-:B signaling pathway in the tumor microenvironment. Upregulated stromal PKC-M-NM-2II 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) We compared mouse BMSC cells from Nemo knockout cells (Nemo+CRE) and Nemo wild type cells (Nemo-CRE) co-cultured for 5 days with leukemic B-cells microarray analysis on Affymetrix MG-430_2.0 arrays..
2013-03-08 | E-GEOD-36415 | biostudies-arrayexpress
Project description: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.
2019-07-14 | GSE80355 | GEO
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
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
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-M-NM-2II and the subsequent activation of NF-M-NM-:B in bone marrow stromal cells is a prerequisite to support the survival of malignant B-cells. PKC-M-NM-2 knockout mice are insusceptible to CLL-transplantations, underscoring the in vivo significance of the PKC-M-NM-2II- NF-M-NM-:B signaling pathway in the tumor microenvironment. Upregulated stromal PKC-M-NM-2II 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 gene expression changes induced by co-culturing with leukemic B-cells (CLL) in EL08-1D2 cells. We compared EL08-1D2 cells co-cultured for 5 days with leukemic B-cells to EL08-1D2 mono-cultured cells by microarray analysis on Affymetrix MG-430_2.0 arrays.
2013-03-08 | E-GEOD-36414 | biostudies-arrayexpress
Project description:Survival of primary CLL cells is mediated by mesenchimal stromal cells in vitro. The goal of this study is to compare the gene expression profile of primary CLL cells in monoculture to that one following cell-cell contact with MSCs
2019-05-20 | GSE99724 | GEO
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
Project description:Aberrant expression of TNFR-1 is induced in CLL cells in the lymphoid microenvironment and stimulation of TNFR-1 increases CLL cell viability.
2017-07-06 | GSE100801 | GEO
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 gene expression changes induced by co-culturing with leukemic B-cells (CLL) in EL08-1D2 cells.
2013-03-08 | GSE36414 | GEO