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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Adrian Wiestner

PROVIDER: E-GEOD-21029 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

2010-10-01 | GSE21029 | GEO

Transcriptional Profiling of CD133+ Cells in Coronary Artery Disease and Effects of Exercise on Gene Expression

Project description:Bone marrow-derived progenitor cells are under investigation for cardiovascular repair, but may be altered by disease. We identified 82 differentially expressed genes in CD133+ cells from patients with coronary artery disease (CAD) versus controls, of which 59 were found to be up-regulated and 23 down-regulated. These genes were found to be involved in carbohydrate metabolism, cellular development and signaling, molecular transport and cell differentiation. Following completion of an exercise program, gene expression patterns resembled those of controls in 7 of 10 patients. Blood sampled from 4 healthy subjects (H), and from 10 patients with coronary artery disease at baseline (A) and after 3 months (B) of exercise.

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

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

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.

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Critical Role of STAT5 Transcription Factor Tetramerization for Cytokine Responses and Normal Immune Function (RNA)

Project description:Cytokine-activated STAT proteins dimerize and bind to high-affinity motifs, and N-terminal domain-mediated oligomerization of dimers allows tetramer formation and binding to low-affinity tandem motifs, but the functions of dimers versus tetramers are unknown. We generated Stat5a and Stat5b double knock-in (DKI) N-domain mutant mice that form dimers but not tetramers, identified cytokine-regulated genes whose expression required STAT5 tetramers, and defined consensus motifs for dimers versus tetramers. Whereas Stat5- deficient mice exhibited perinatal lethality, DKI mice were viable, indicating that STAT5 dimers were sufficient for survival. Nevertheless, STAT5 DKI mice had fewer CD4+CD25+ T cells, NK cells, and CD8+ T cells, with impaired cytokine-induced proliferation and homeostatic proliferation of CD8+ T cells. DKI CD8+ T cell proliferation following viral infection was diminished and DKI Treg cells did not efficiently control colitis. Thus, tetramerization of STAT5 is dispensable for survival but is critical for cytokine responses and normal immune function. T cells were extracted from spleen of wt and STAT5 double knocked in mice, and treated with IL-2. The cells were collected from 0h (without treatment), 2h, 6h and 17h, and chipped on Affy mouse 430 2.0 arrays.

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Transcriptional Profiling of B19 Virus Nonstructure Protein (NS1) transduced CD36+ Erythoid Progenitor Cells (EPCs)

Project description:B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation. Keywords: RNA CD36+ EPCs were generated from CD34+ stem cells, and transduced with B19V NS1 or control-lentivirus for 12, 24,and 48 hours. Each sample has triplicates. There are 18 samples analyzed.

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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)

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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

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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

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