CD20+ B cell expression profile
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Arcadio Rubio García
PROVIDER: E-MTAB-4852 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:For the complete cure of tumors, it is essential to eliminate cancer-initiating cells (CICs). Immunohistochemically, most tumor cells were CD20 and/or CD138 positive in clinical samples of lymphoplasmacytic lymphoma (LPL), and CD20- CD138- cells were hardly detected. Therefore, useful positive markers expressing in a candidate of CICs of LPL are necessary. First, we performed gene expression microarray analysis between CD20- CD138- and CD20+ CD138+ subpopulations using sorted Waldenstrom macroglobulinemia cell line (MWCL-1).
2016-02-17 | GSE73756 | GEO
Project description:For the complete cure of tumors, it is essential to eliminate cancer-initiating cells (CICs). Immunohistochemically, most tumor cells were CD20 and/or CD138 positive in clinical samples of lymphoplasmacytic lymphoma (LPL), and CD20- CD138- cells were hardly detected. Therefore, useful positive markers expressing in a candidate of CICs of LPL are necessary. First, we performed gene expression microarray analysis between CD20- CD138- and CD20+ CD138+ subpopulations using sorted Waldenstrom macroglobulinemia cell line (MWCL-1). Two dye-swap experiment was performed onto Human GE 4Ã44K V2 arrays (G4845A; Agilent Technologies).
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Project description:Background: Mutant BRAF targeted therapies remain a standard of care for the treatment of metastatic malignant melanoma (MM); however high initial response rates are tempered by the persistence of residual MM cells that eventually lead to disease recurrence and mortality. Since MM recurrence during targeted therapy can present with the simultaneous occurrence of multiple tumour nodules at the original body sites, we hypothesised the presence of an intrinsically resistant MM cell sub-population. Objectives: Identify an MM cell subpopulation that is intrinsically resistant to targeted therapy and so may be responsible for MM recurrence. Methods: Using melanoma cell lines, we define culture conditions for reproducible 3D growth of melanospheres to investigate putative cancer stem cell populations. We undertook RNA sequencing and bioinformatic analysis to characterise cell populations between adherent and non-adherent culture, and cells expressing or not expressing CD20. Furthermore, we define an in vitro assay to evaluate killing of melanoma cancer stem cells as a therapeutic test using combination therapies targeting driver mutation and CD20 marker. Results: We have described culture conditions that promote MM cells to form melanospheres with a reproducible colony forming efficiency of 0.3% to 1.3%. RNA sequencing of melanosphere versus conventional MM cell cultures (n=6), irrespective of the BRAF mutation status, showed that melanosphere formation was associated with growth and differentiation transcriptional signatures resembling MM tumours. Importantly, melanosphere formation also led to the emergence of a CD20+ MM cell subpopulation, similar to that observed in primary human MM tumours. CD20+ MM cells were resistant to BRAF inhibitor therapy, and consistent with this finding demonstrated a Forkhead box protein M1 (FOXM1) transcriptomic profile (n=6). Combining BRAF inhibitor and anti-CD20 antibody treatment led to the additional killing of previously resistant CD20+ BRAF mutant MM cells. Conclusions: In MM patients that harbour a CD20+ sub-population, combined therapy with BRAF inhibitor and anti-CD20 antibody could potentially kill residual MM cells and so prevent disease recurrence.
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2014-09-01 | E-GEOD-54201 | biostudies-arrayexpress
Project description:Rituximab alone or in combination with chemotherapeutics is the first-line therapy for variety of lymphoproliferative disorders including low- and high grade non-Hodgkin’s lymphomas (NHL). Although the complete response rate is quite impressive, vast majority of patient presents recurrent disease. The association between CD20 expression and clinical outcome in patients strongly suggests that reduced CD20 expression leads to inferior response to RCHOP (rituximab, cyclophosphamide, vincristine, doxorubicin and prednisone). In order to understand how loss of CD20 leads to development of RCHOP resistance, we developed rituximab resistant DOHH2 model in vivo by chronic exposure to rituximab. Characterization of several resistant in vivo xenografts revealed one model that maintained resistance to an acute dose of rituximab and demonstrated loss of CD20. Further characterization of the model demonstrated a loss of CD20 is associated with over expression of BCL2 and BIM. In vivo efficacy studies showed resistant line is insensitive to acute dose of RCHOP and treatment with an inhibitor of BCL2 (ABT199) in combination with chemotherapy resulted in better efficacy than RCHOP alone. We have identified an in vivo model of DLBCL where loss of CD20 and over expression of anti-apoptotic protein BCL2 leads to RCHOP resistance. These data suggest the addition of BCL2 inhibitor to chemotherapy might be effective in treating CD20 negative lymphomas.
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Project description:We report the single-cell RNA sequencing data obtained from BCL1 lymphoma-bearing mice treated with either isotype control, anti-CD20 mAb, anti-CD27 mAb or anti-CD20+anti-CD27 mAb together
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Project description:B cell identity and function is dependent on the proteins residing in the B cell surfaceome and their respective nanoscale organization. Here we show that CD20 is a gatekeeper for B cell identity and function due to its control of the functional nanoscale organization of receptors within the B surfaceome and the resting state of B lymphocytes. CRISPR/Cas-based ablation of CD20 in Ramos B cells revealed that IgM class B cell antigen receptor (IgM-BCR) and the co-receptor CD19 are functionally interlinked in the absence of CD20. The resulting IgM-BCR/CD19 signalling synapse leads to transient B cell activation and the loss of B cell identity. Re-expression of CD20 involving an aptamer-controlled riboswitch restores resting-state B cell nanoscale organization and function. Treatment of naive human B cells with the anti-CD20 antibody Rituximab leads to transient B cell activation and formation of transiently activated IgM-BCR/CD19 signalling synapses providing new insights into the molecular mode of action of Rituximab. The loss of B cell identity due to CD20-deficiency is accompanied by a PAX5 to BLIMP-1 transcriptional switch and increased plasma cell development. This cellular B cell differentiation towards plasma B cells is mechanistically accompanied by a metabolic shift towards oxidative phosphorylation.
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Project description:Transcriptome analysis of RNA samples from human PBMCs of anti-CD20 therapy in multiple sclerosis patients. Anti-CD20 is a highly effective therapy for multiple sclerosis (MS), a disease with multiple abnormalities in function of B and T cells and innate immune cells. Anti-CD20 therapy depletes B cells, which alters antibody production and has diverse effects on B cell immunity. These changes potentially affect immunity beyond B cells in MS. We determined if anti-CD20 therapy effects non-B-cell, as well as B-cell, gene expression and serum protein levels. We found anti-CD20 therapy reduced expression of 413 total genes and 185 B-cell-regulated genes at 2 weeks vs. pre-therapy. Expression of 19 (15%) of these B cell genes returned towards baseline by 6 months, including genes for the B cell activation protein, CD79A, and for immunoglobulin A, D, and G heavy chains. Expression pathways for Th17 and CD4 regulatory T cell (Treg) development, differentiation, and proliferation also quieted. In contrast, expression increased in Th1 and myeloid cell antiviral, pro-inflammatory, and toll-like receptor (TLR) gene pathways.
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