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Expression data from human NHL cell lines treated with agonistic antibodies

ABSTRACT: CD20 is a clinically validated target for Non-Hodgkin’s lymphomas and autoimmune diseases. Interactions of CD20 with the B cell receptor (BCR) and components of the BCR signaling cascade have been reported. In this study we show that antibodies against CD20 or activation of the BCR by specific antibodies induce very similar expression patterns of up- or down-regulated genes in NHL cell lines indicating that CD20 may play a role in BCR signaling and vice versa. We used microarray data to show that antibodies against CD20 or activation of the BCR by specific antibodies induce very similar expression patterns of up- or down-regulated genes in NHL cell lines indicating that CD20 may play a role in BCR signaling and vice versa.

ORGANISM(S): Homo sapiens

PROVIDER: GSE23394 | GEO | 2013/07/23

SECONDARY ACCESSION(S): PRJNA131291

REPOSITORIES: GEO

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Expression data from human NHL cell lines treated with agonistic antibodies

Project description:CD20 is a clinically validated target for Non-Hodgkin’s lymphomas and autoimmune diseases. Interactions of CD20 with the B cell receptor (BCR) and components of the BCR signaling cascade have been reported. In this study we show that antibodies against CD20 or activation of the BCR by specific antibodies induce very similar expression patterns of up- or down-regulated genes in NHL cell lines indicating that CD20 may play a role in BCR signaling and vice versa. We used microarray data to show that antibodies against CD20 or activation of the BCR by specific antibodies induce very similar expression patterns of up- or down-regulated genes in NHL cell lines indicating that CD20 may play a role in BCR signaling and vice versa. Four different cell lines were treated with various antibodies for 4h (3 replicates per treatment), all in all 96 arrays were analysed for 32 samples. Changes were calculated relative to control/reference experiments. Expression patterns of each treatment were compared to determine overlaps.

2013-07-23 | E-GEOD-23394 | biostudies-arrayexpress

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

RNA-seq analysis of paired Non-Hodgkin's lymphoma (NHL) tumor samples at pretreatment and after mosunetuzumab relapse coinciding with the loss of CD20 protein

Project description:CD20 protein-negative diseases were observed for a subset of patients with B-NHL that relapsed after initial responses to mosunetuzumab. For many of these tumors, whole exome (WES) and RNA-seq failed to detect any MS4A1 genetic variants or loss of CD20 mRNA, which could have explained the apparent loss of CD20 protein. For this study, we obtained formalin-fixed paraffin-embedded (FFPE) tumor samples from a similar cohort of four additional patients relapsing after mosunetuzumab, and performed RNA-seq to look for changes in the splicing pattern of CD20.

2023-12-08 | GSE243919 | GEO

ESK1 and MAGE-A4 TCR-like antibody immunoprecipitation in human liver tissue

Project description:We chose to perform a head-to-head immune-enrichment from primary liver tissue resections using both, MAGE-A4 and ESK1 TCR-like antibodies. Since both target antigens MAGE-A4 and WT-1 are not expressed in hepatocytes (Human Protein Atlas, www.proteinatlas.org), the ESK1 enrichment could serve as isotype control for the MAGE-A4 antibody, and vice versa.

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SRC family kinases are involved in the regulation of CD20

Project description:CD20 is an integrate membrane protein expressed on the surface of normal and malignant B-cells. It is an excellent molecular target for monoclonal antibodies (mAbs) that are widely used in the treatment of non-Hodgkin’s lymphomas (NHL) and chronic lymphocytic leukemia (CLL). Anti-CD20-directed therapies are the most effective, successful and widely used therapeutic monoclonal antibodies, routinely incorporated into all phases of conventional treatment, including first-line, maintenance and salvage treatment. Nonetheless, the overall response rates to treatment have been reported to be 46-67% for rituximab, and in patients relapsing after initial rituximab treatment the response rate is ~40%. A number of mechanisms have been proposed to account for this inefficiency, including modulation of surface CD20 levels, occurring due to both transcriptional and posttranscriptional regulations. Our observations strongly imply that the observed CD20 down-regulation relies on transcriptional mechanism and delineate new perspectives in the field of CD20 regulation. Since many of the new therapeutic agents selectively inhibit specific signaling pathways, combining the compounds that target different mechanisms of cell growth and survival is a particularly attractive approach. However, optimal combinations of novel treatment modalities with already existing ones should take into account potential ”off-target” activity yet to be identified that could unexpectedly result in high toxicity and/or impaired outcomes of treatment

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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.

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Gene expression data in obinuzumab treated Karpas-1106P PMBL cell line

Project description:Primary Mediastinal large B-cell lymphoma (PMBL) is a rare form of non-Hodgkin lymphoma (NHL) representing 2% of mature B-cell NHL in patients less than 18 years of age.We compared the gene expression profiling between fully humanized anti-CD20 targeted monoclonal antibody recognizing a unique CD20 type II epitope, obinutuzumab and IgG or PBS treated Karpas Primary Mediastinal B-cell lymphoma (PMBL) cell line. -

2016-12-01 | GSE75605 | GEO

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

Casein kinase II suppresses autophagy by activating Filamin-NHL containing TRIM proteins

Project description:Autophagy is a tightly regulated process integral to cellular homeostasis and innate immunity. As such, dysregulation of autophagy is associated with cancer, neurodegenerative disorders, and infectious diseases. While many factors have been characterized that promote autophagy, key players preventing excessive autophagy are less well understood. Here, we identify Casein kinase II (CK2) as a negative regulator of autophagy. Pharmacological inhibition of CK2 activity or siRNA-mediated depletion of CK2 increased basal autophagic flux in cell lines and primary human lung cells. Vice versa, ectopic expression of CK2 reduced autophagic flux. Mechanistically, CK2 interacts with tripartite motif (TRIM) family members TRIM2, TRIM3 and TRIM71 at their shared C-terminal NHL domain. This interaction was required for autophagy inhibition by CK2. TRIM3 was highly phosphorylated by CK2 at serine 661, and a phosphorylation-defective mutant of TRIM3 was unable to reduce autophagy induction. Targeting of the CK2-TRIM axis promoted autophagy during influenza A virus (IAV) and measles virus (MeV) infection. In line with this, inhibition of CK2 enhanced autophagy-dependent restriction of IAV, MeV and human immunodeficiency virus 1 (HIV-1). Thus, our results identify the CK2-TRIM2/3/71 axis as a key regulatory pathway that limits autophagy. Targeting this axis may allow therapeutic induction of autophagy against viral infections and diseases associated with dysregulated autophagy.

2023-05-16 | MSV000091956 | MassIVE

Immunoglobulin expression in the endoplasmic reticulum shapes the metabolic fitness of B lymphocytes

Project description:The major function of B lymphocytes is to sense antigens and to produce protective antibodies after activation. This function requires the expression of a B-cell antigen receptor (BCR), and evolutionary conserved mechanisms seem to exist that ensure that B cells without a BCR do not develop nor survive in the periphery. Here, we show that the loss of BCR expression on Burkitt lymphoma cells leads to decreased mitochondrial function and impaired metabolic flexibility. Strikingly, this phenotype does not result from the absence of a classical Syk-dependent BCR signal but rather from compromised ER expansion. We show that the reexpression of immunoglobulins (Ig) in the absence of the BCR signaling subunits Igα and Igβ rescues the observed metabolic defects. We demonstrate that immunoglobulin expression is needed to maintain ER homeostasis not only in lymphoma cells but also in resting B cells. Our study provides evidence that the expression of BCR components, which is sensed in the ER and shapes mitochondrial function, represents a novel mechanism of metabolic control in B cells.

2020-04-21 | MTBLS186 | MetaboLights

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