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NF-κB-induced expression of T-bet suppresses the proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia

ABSTRACT: NF-κB-induced expression of T-bet suppresses the proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia

PROVIDER: PRJEB62867 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11526218_1.fastq.gz	Fastqsanger.gz
	ERR11526218_2.fastq.gz	Fastqsanger.gz
	ERR11526219_1.fastq.gz	Fastqsanger.gz
	ERR11526219_2.fastq.gz	Fastqsanger.gz
	ERR11526220_1.fastq.gz	Fastqsanger.gz

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NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia

Project description:NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia

| PRJNA980572 | ENA

NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia [scRNA-seq]

Project description:NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia [scRNA-seq]

| PRJNA980578 | ENA

NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia [scATAC-seq]

Project description:NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia [scATAC-seq]

| PRJNA980577 | ENA

NF-κB-induced expression of T-bet suppresses the proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia

Project description:Tbx21-/- TCL1 cells were generated to explore the effect of T-bet expression in malignant B cells. Single-cell suspensions from spleens of Tbx21 knockout and control TCL1 mice were prepared and splenocytes were enriched in TCL1 cells, resulting in a purity above 97% of CD5+ CD19+ cells. RNA sequencing libraries were prepared using the Illumina TruSeq Stranded mRNA Kit and sequenced on the Illumina NovaSeq 6000.

2024-01-31 | E-MTAB-13030 | biostudies-arrayexpress

NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia [scRNA-seq]

Project description:The T-box transcription factor T-bet is encoded by Tbx21 and was identified to play a role in aging and tissue localization of B cells. T-bet expression was detected in malignant B cells but its potential role in B-cell malignancies remains largely unexplored. We used single cell RNA sequencing (scRNA-seq) and the assay for transposase accessible chromatin using sequencing (scATAC-seq) to analyze the regulatory role of T-bet in TCL1 leukemia.

2024-06-01 | GSE234225 | GEO

NF-κB-induced expression of T-bet suppresses proliferation of malignant B cells and is associated with good prognosis in chronic lymphocytic leukemia [scATAC-seq]

2024-06-01 | GSE234224 | GEO

Distinct gene expression profile between ARID1Ahigh and good prognosis and ARID1Alow and poor prognosis groups

Project description:Cancer tissue specimens from ARID1Ahigh and good prognosis and ARID1Alow and poor prognosis of patients with advanced gastric cancer were extracted and analyzed.

2018-02-06 | GSE110078 | GEO

Distinct gene expression profile between ARID1Ahigh and good prognosis and ARID1Alow and poor prognosis groups

Project description:Distinct gene expression profile between ARID1Ahigh and good prognosis and ARID1Alow and poor prognosis groups

| PRJNA432896 | ENA

BET bromodomain inhibitors attenuate transcription of a subset of IL-1-induced NF-κB target genes that promote inflammation in β-cells

Project description:Cytokine-stimulated transcription of NF-κB target genes is linked to the development of multiple inflammatory and autoimmune diseases. Inhibitors of bromodomain and extraterminal domain (BET) epigenetic reader proteins attenuate inflammatory gene transcription and delay the onset of several inflammatory diseases, including autoimmune diabetes. Our previous studies showed that BET bromodomain inhibitors disrupt the interaction between BET family member BRD4 and NF-κB transcription factor p65 in β-cells, thus attenuating cytokine-stimulated NF-κB-dependent gene and functional changes. However, the role of NF-κB in developing inflammatory disease is controversial, as NF-κB inhibition can promote disease progression in some contexts. NF-κB target genes play both physiological and pathophysiological roles in regulating the cellular response to cytokines. Here, using cytokine-stimulated pancreatic β-cells as an inflammatory disease model, we show that NF-κB-dependent gene products that participate in inflammation are sensitive to BET bromodomain inhibition. In contrast, gene products that maintain cellular homeostasis or protect β-cells from stressors are largely insensitive to BET bromodomain inhibition. These studies define a novel and selective role for BET bromodomain-containing proteins in regulating inflammatory gene activation.

2025-06-24 | GSE286117 | GEO

BET inhibition reforms the immune microenvironment and alleviates T-cell dysfunction in chronic lymphocytic leukemia

Project description:Redundant tumor microenvironment (TME) immunosuppressive mechanisms and epigenetic maintenance of terminal T-cell exhaustion greatly hinder functional anti-tumor T-cell responses in chronic lymphocytic leukemia (CLL). Bromodomain and extra-terminal (BET) proteins regulate key pathways contributing to CLL pathogenesis and TME interactions, including T-cell function and differentiation. Herein, we report that blocking BET protein function alleviates immunosuppressive networks in the CLL TME and repairs inherent T-cell defects. The pan-BET inhibitor OPN-51107 reduced exhaustion-associated cell signatures, fostering improved T-cell proliferation and effector function in patient samples and murine models of CLL. These findings establish the immunomodulatory action of BET-i on CLL T-cells and support the use of BET inhibitors in treatment strategies for CLL.

2024-05-21 | GSE262027 | GEO

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