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RNA sequencing/Gene expression studies of G⍺13 signaling in lymphoma [scRNA-seq]

ABSTRACT: We determined that loss of G⍺13 signaling promotes oncogenic signaling in aggressive B-cell lymphomas. We sought to measure gene expression change in control and G⍺13-deficient germinal center (GC) B cells by RNA-sequencing

ORGANISM(S): Mus musculus

PROVIDER: GSE253434 | GEO | 2024/01/17

REPOSITORIES: GEO

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RNA sequencing/Gene expression studies of G⍺13 signaling in lymphoma [RNA-seq]

Project description:We determined that loss of G⍺13 signaling promotes oncogenic signaling in aggressive B-cell lymphomas. We sought to measure gene expression change in aggressive B-cell lymphoma cells by RNA-sequencing following G⍺13 stimulation.

2024-01-17 | GSE253433 | GEO

Small-RNA expression in normal and malignant mature B cells

Project description:Small-RNA profiles were generated for normal mature germinal center (GC) B cells and GC-derived lymphomas.

2014-06-01 | GSE56354 | GEO

Small-RNA expression in normal and malignant mature B cells

Project description:Small-RNA profiles were generated for normal mature germinal center (GC) B cells and GC-derived lymphomas. Normal and tumor samples are derived from different donors.

2014-06-01 | E-GEOD-56354 | biostudies-arrayexpress

Molecular Determinants of Sensitivity to Polatuzumab Vedotin in Diffuse Large B Cell Lymphoma

Project description:Polatuzumab Vedotin (Pola-V) is an antibody-drug conjugate directed to the CD79B subunit of the B cell receptor (BCR). When combined with conventional immunochemotherapy, Pola-V improves outcomes in DLBCL. To identify molecular determinants of sensitivity to Pola-V, we used CRISPR-Cas9 screening for genes that modulated the toxicity of Pola-V for lymphomas or the surface expression of its target, CD79B. Our results reveal a striking impact of CD79B glycosylation on Pola-V epitope availability on the lymphoma cell surface and on Pola-V toxicity. Genetic, pharmacological, and enzymatic approaches that remove terminal sialic acid residues from N-linked glycans enhanced lymphoma killing by Pola-V. Pola-V toxicity was also modulated by KLHL6, a ubiquitin ligase that targets CD79B for degradation in normal and malignant germinal center B cells, explaining its recurrent inactivation in germinal center-derived lymphomas. Our findings suggest precision medicine strategies to optimize Pola-V as a lymphoma therapeutic.

2024-07-12 | PXD043670 | Pride

MEF2B LC-MS in normal and malignant germinal center B cells.

Project description:The MEF2B transcription factor is frequently mutated in germinal center (GC)-derived B-cell lymphomas. Its N-terminal mutations drive lymphomagenesis by escaping interaction with transcriptional repressors, while the function of C-terminal mutations remains to be elucidated. Here, we show that MEF2B C-tail is physiologically phosphorylated at specific residues and phosphorylation at S324 is impaired by lymphoma-associated mutations. Lack of phosphorylation at S324 enhances the interaction of MEF2B with the SWI/SNF chromatin remodeling complex, leading to higher transcriptional activity. In addition, these mutants show an increased protein stability due to impaired interaction with the CUL3/KLHL12 ubiquitin complex. Mice expressing a phosphorylation-deficient lymphoma-associated MEF2B mutant display GC enlargement and develop GC-derived lymphomas, when crossed with Bcl2 transgenic mice. These results unveil converging mechanisms of action for a diverse spectrum of MEF2B mutations, all leading to its dysregulation and GC B-cell lymphomagenesis. These assorted mechanisms provide additional opportunities for the development of targeted therapeutic approaches.

2024-08-26 | PXD043998 | Pride

Gene expression profiling of Hodgkin Lymphoma and Non-Hodgkin Lymphoma cell lines for the NF-kB family of trasncription factors followinf each one depletion by shRNA.

Project description:NF-kB transcription factors regulate different sets of genes in distinct germinal center derived B-cell lymphomas

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MicroRNA-28 replacement for non-Hodgkin lymphoma therapy

Project description:Our studies identify the role of mIR-28 in germinal center response and its therapeutic potential for the treatment of non-Hodgkin lymphomas

2017-05-03 | GSE81236 | GEO

SWI/SNF Chromatin Remodeling Complex Orchestrates Sequential Binding of Key Transcription Factors in B Cells and Restricts Aggressive Lymphoma [human ChIP-seq]

Project description:ARID1A, a subunit of the canonical BAF nucleosome remodeling complex, is commonly mutated in lymphomas. Our study shows that ARID1A orchestrates B-cell fate during the germinal center (GC) response, facilitating cooperative and sequential binding of PU.1 and NF-kB at crucial genes for cytokine and CD signaling. The absence of ARID1A tilts GC cell-fate towards immature IgM+CD80-PDL2- memory B-cells, known for their potential to re-enter new GCs. When combined with BCL2 oncogene, ARID1A haploinsufficiency hastens the progression of aggressive follicular lymphomas in mice. Remarkably, follicular lymphoma patients with ARID1A-inactivating mutations preferentially display an immature memory B-cell-like state with increased transformation risk to aggressive disease. These observations offer mechanistic understanding into the emergence of both indolent and aggressive lymphomas in ARID1A-mutant patients through formation of immature memory-like clonal precursors. Lastly, we demonstrate that ARID1A mutation induces synthetic lethality to SMARCA2/4 inhibition, paving the way for potential precision therapy for high-risk patients.

2024-03-22 | GSE262093 | GEO

SWI/SNF Chromatin Remodeling Complex Orchestrates Sequential Binding of Key Transcription Factors in B Cells and Restricts Aggressive Lymphoma [mouse RNA-Seq]

2024-02-02 | GSE254595 | GEO

SWI/SNF Chromatin Remodeling Complex Orchestrates Sequential Binding of Key Transcription Factors in B Cells and Restricts Aggressive Lymphoma [mouse ATAC-Seq]

2024-02-02 | GSE254594 | GEO