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3D culture of AIDS-NHL cells influences gene expression related to B-cell development, proliferation and survival

ABSTRACT: Full title: Three-dimensional culture of AIDS-NHL cells influences gene expression related to B-cell development, proliferation and survival The AIDS-NHL-derived cell line, UMCL01-101, representing diffuse large B-cell lymphoma of immunoblastic morphology (AIDS-IBL), was grown in conventional, static suspension culture or three-dimensionally (3D) in the Rotating Wall Vessel (RWV) bioreactor. The objective was to assess the impact on gene expression of growth as a three-dimensional tissue assembly. Global gene expression analysis was performed on UMCL01-101 cells grown under either condition using Affymetrix microarray.

ORGANISM(S): Homo sapiens

PROVIDER: GSE18826 | GEO | 2010/03/01

SECONDARY ACCESSION(S): PRJNA121157

REPOSITORIES: GEO

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3D culture of AIDS-NHL cells influences gene expression related to B-cell development, proliferation and survival

Project description:Full title: Three-dimensional culture of AIDS-NHL cells influences gene expression related to B-cell development, proliferation and survival The AIDS-NHL-derived cell line, UMCL01-101, representing diffuse large B-cell lymphoma of immunoblastic morphology (AIDS-IBL), was grown in conventional, static suspension culture or three-dimensionally (3D) in the Rotating Wall Vessel (RWV) bioreactor. The objective was to assess the impact on gene expression of growth as a three-dimensional tissue assembly. Global gene expression analysis was performed on UMCL01-101 cells grown under either condition using Affymetrix microarray. UMCL01-101 cells were cultured in the Rotating Wall Vessel bioreactor to form 3D assemblies, or in conventional suspension culture, for 15 days. RNA was prepared from triplicate samples under each growth condition and submitted for microarray analysis.

2010-03-07 | E-GEOD-18826 | biostudies-arrayexpress

AIDS-related Kaposi's sarcoma

Project description:Kaposi's Sarcoma (KS) is a proliferation of aberrant vascular structures lined by spindle cells, and is caused by a gammaherpes virus (HHV8/KSHV). Its course is aggravated by co-infection with HIV-1, where the timing of infection with HIV-1 and HHV8 is important for the clinical outcome. METHODS: In order to better understand the pathogenesis of KS, we have analysed tissue from two AIDS-KS lesions, and from normal skin by serial analysis of gene expression (SAGE). Semi-quantitative RT-PCR was then used to validate the results. RESULTS: The expression profile of AIDS-related KS (AIDS-KS) reflects an active process in the skin. Transcripts of HHV8 were found to be very low, and HIV-1 mRNA was not detected by SAGE, although it could be found using RT-PCR. Comparing the expression profile of AIDS-KS tissue with publicly available SAGE libraries suggested that AIDS-KS mRNA levels are most similar to those in an artificially mixed library of endothelial cells and leukocytes, in line with the description of KS lesions as containing spindle cells with endothelial characteristics, and an inflammatory infiltrate. At least 64 transcripts were found to be significantly elevated, and 28 were statistically downregulated in AIDS-KS compared to normal skin. Five of the upregulated mRNAs, including Tie 1 and sialoadhesin/CD169, were confirmed by semi-quantitative PCR to be elevated in additional AIDS-KS biopsies. Antibodies to sialoadhesin/CD169, a known marker of activated macrophages, were shown to specifically label tumour macrophages. CONCLUSION: The expression profile of AIDS-KS showed 64 genes to be significantly upregulated, and 28 genes downregulated, compared with normal skin. One of the genes with increased expression was sialoadhesin (CD169). Antibodies to sialoadhesin/CD169 specifically labelled tumour-associated macrophages, suggesting that macrophages present in AIDS-KS lesions belong to a subset of human CD169+ macrophages. Keywords: other

2003-07-16 | GSE514 | GEO

Transcription profiling of human non-Hodgkins lymphoma (NHL) cell lines

Project description:We profiled 40 NHL cell lines to determine gene expression patterns and molecular subtypes. Experiment Overall Design: RNA profiles of NHL cell lines.

2009-05-16 | E-GEOD-15329 | biostudies-arrayexpress

Multicenter AIDS Cohort Study

Project description:Multicenter AIDS Cohort Study

| PRJNA671263 | ENA

Multicenter AIDS Cohort Study

Project description:Multicenter AIDS Cohort Study

| PRJNA671262 | ENA

Gene expression profiling of human non-Hodgkins lymphoma (NHL) cell lines

Project description:We profiled 40 NHL cell lines to determine gene expression patterns and molecular subtypes. Keywords: NHL, cancer, cell lines

2009-05-11 | GSE15329 | GEO

Affymetrix SNP 6.0 profiles of 10 Human B-NHL lines

Project description:B-cell Non Hodgkin Lymphoma are a heterogenous group chracterized by a variety of genetic changes, including translocations, deletions and amplifications. Here we analyzed 10 B-NHL lines by Affymetrix SNP 6.0 to detect copy number changes. Specifically, we aim to identify cell lines suitable for testing the consequences of acute reintroduction of candidate tumor suppressor genes as they harbor deletions which include the candidate gene(s). 10 BNHL cell lines were grown in standard cell culture conditions. Genomic DNA was exptracted from frozen pellets and analyzed for copy number variations with Affymetrix SNP 6.0 Arrays

2012-04-02 | E-GEOD-36967 | biostudies-arrayexpress

Gene expression analysis of B-NHL from λMYC, λMYC/IµHABCL6, λMYC/AIDKO and λMYC/IµHABCL6/AIDKO mouse models

Project description:Most human B cell lymphomas (B-NHL) are derived from germinal centers (GCs), the structure where B-cells undergo class switch recombination (CSR) and somatic hypermutation (SHM) and are selected for high-affinity antibody production. The pathogenesis of B-NHL is associated with distinct genetic lesions, including chromosomal translocations and aberrant somatic hypermutation, which appear to arise from mistakes occurring during CSR and SHM. To ascertain the role of CSR and SHM in lymphomagenesis, we crossed three oncogene-driven (MYC, BCL6, MYC/BCL6) mouse models of B cell lymphoma with mice lacking activation-induced cytidine deaminase (AID), the enzyme required for both processes. We show that AID deficiency prevents BCL6-dependent, GC-derived B-NHL, while it has no impact on the formation of MYC-driven, pre-GC lymphomas. Accordingly, abrogation of AID is associated with the disappearance of both CSR- and SHM-mediated structural alterations, including cMYC-IgH chromosomal translocations and aberrant SHM. These results demonstrate that AID is required for GC-derived lymphomagenesis, providing direct support to the notion that errors in AID-mediated antigen-receptor gene modification events represent major contributors to the pathogenesis of human B-NHL. Keywords: Phenotypic characterization of tumors developing in oncogene-driven mouse models of lymphomas

2007-11-01 | GSE9249 | GEO

Global expression of mouse hepatocytes cultured as monolayers or as three-dimensional aggregates

Project description:Three-dimensional (3D) culture of hepatocytes leads to improved and prolonged synthetic and metabolic functions, but the underlying molecular mechanisms were unknown. In order to investigate the molecular mechanisms underlying 3D cell-cell interactions in maintaining hepatocyte differentiated functions ex vivo, microarray analyses were performed on primary mouse hepatocytes cultured either as monolayers on tissue culture dishes (TCD) or as 3D aggregates in rotating wall vessel (RWV) bioreactors.

2013-12-23 | GSE53054 | GEO

Activity of the novel BTK inhibitor TG-1701 is associated with the disruption of the Ikaros signaling pathway in responder B-NHL patients and with sensitization to anti-CD20 therapy in B-NHL xenografts

Project description:Covalent Bruton's tyrosine kinase inhibitors (BTKis) have transformed the treatment of B-cell non-Hodgkin lymphoma (B-NHL), including chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL), but their activity has been limited by off-target toxicity and acquired drug resistance. TG-1701 is a novel irreversible and highly specific BTKi being presently under study in a phase 1 clinical trial in patients with relapsed/refractory B-NHL alone and in combination with ublituximab, a CD20 antibody, and umbralisib, a dual PI3Kδ and CK1ε inhibitor. Here we show, for the first time that phosphoproteomic analysis of CLL patients receiving a BTKi (TG-1701) led to a non-supervised clustering that matched the clinical outcomes and separated a group of “responders” from a group of “non-responders”. This clustering was based on a selected list of 96 phosphosites, with Ikaros-Ser442/445 phosphorylation as a potential marker for TG-1701 efficacy. RNA-seq analysis followed by qPCR and western blot validation further revealed that TG-1701 treatment blunted the Ikaros gene signature only in responder patients, as well as in BTKi-sensitive, but not BTKi-insensitive, B-NHL cell lines and xenografts. Importantly, and in contrast with ibrutinib, TG-1701 did not impair FcγR-driven antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP) triggered by the anti-CD20 antibodies rituximab and ublituximab in a multicellular MCL co-culture system. In addition, TG-1701 cooperated with ublituximab coupled to umbralisib (also referred as the U2 regimen) in reducing the tumor growth in both ibrutinib-sensitive and ibrutinib-insensitive mouse models of MCL. Altogether, these data validate phosphoproteomic as a broken thread to omics analysis in the clinic and support the use of TG-1701-U2 combination in R/R B-NHL patients, irrespective of prior response to ibrutinib.

2021-09-22 | PXD023231 | Pride

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