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Homo sapiens

ABSTRACT: Identification of NOTCH1 bound genes in chronic lymphocytic leukaemia (CLL) cells

PROVIDER: PRJNA358396 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5123580.fastq.gz	Fastqsanger.gz
	SRR5123590.fastq.gz	Fastqsanger.gz
	SRR5123600.fastq.gz	Fastqsanger.gz
	SRR5123581.fastq.gz	Fastqsanger.gz
	SRR5123591.fastq.gz	Fastqsanger.gz

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Identification of genes induced by NOTCH1 in a chronic lymphocytic leukaemia (CLL) cell line and tracking of these genes in primary CLL patients

Project description:NOTCH1 is mutationally activated in ~15% of cases of chronic lymphocytic leukaemia (CLL), but its role in B-cell development and leukemogenesis is not known. Here, we report that the active intracellular portion of NOTCH1 (ICN1) is detectable in ~50% of peripheral blood CLL cases lacking gene mutations. We identify a ‘NOTCH1 CLL gene expression signature’ in CLL cells, and show that this signature is significantly enriched in primary CLL cases expressing ICN1, independent of NOTCH1 mutation. NOTCH1 target genes include key regulators of B-cell proliferation, survival and signal transduction physiology. In particular, we show that MYC is a direct target of NOTCH1 via B-cell specific distal regulatory elements, thus implicating this oncogene in the pathogenesis of the disease.

2017-03-24 | GSE92626 | GEO

Identification of NOTCH1 bound genes in chronic lymphocytic leukaemia (CLL) cells

2017-03-24 | GSE92701 | GEO

Homo sapiens

Project description:Identification of genes induced by NOTCH1 in a chronic lymphocytic leukaemia (CLL) cell line and tracking of these genes in primary CLL patients

| PRJNA358194 | ENA

Characterisation of gene expression changes in T cells from patients presenting with AML compared with healthy T cells

Project description:Work previously published by our group has demonstrated that T cells from patients with chronic lymphocytic leukaemia (CLL) show differentially regulated genes compared with healthy T cells. This study was initiated to examine if these gene expression changes were unique to CLL T cells or common to an alternative leukaemia, acute myeloid leukaemia (AML). Keywords: Comparison of immune cells in health and disease

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RNA-seq of NOTCH1 mutation in chronic lymphocytic leukemia cell BaF3.

Project description:The hotspot c.7541_7542delCT NOTCH1 mutation has been proven to have a unfavorable clinical impact in chronic lymphocytic leukemia (CLL). The aim of our study was to investigate the influence of NOTCH1 mutation(c.7541_7542delCT) on NOTCH1 signaling in CLL cells using Gene Expression Profiling.

2021-03-23 | GSE115728 | GEO

Active AKT Signaling triggers CLL towards Richter's transformation via over-activation of Notch1

Project description:Richter's syndrome (RS) is an aggressive transformation of Chronic Lymphocytic Leukaemia (CLL) frequently due to TP53, CDKN2, MYC or NOTCH1 mutations. whereas a significant proportion displays no specifically acquired driver mutation. We observe constitutive AKT phosphorylation not only in high-risk CLL patients harbouring p53 and NOTCH mutations but also in numerous RS patients. Consistently, genetic over-activation of AKT within the Eµ-TCL1 CLL mouse model results in a high-grade lymphoma phenotype of Richters syndrome. Multiomics assessment of our novel mouse model revealed a S100 defined subcluster of highly proliferative lymphoma cells developing from indolent CLL-like B-cells as a consequence of sudden NOTCH activation being fueled by enhanced NOTCH ligand exposure from T-cells in the microenvironment. Our data link AKT and NOTCH signaling in patient samples, genomic alterations, phosphoproteome and single-cell transcriptome profiles. Collectively, we have identified active AKT as a causative transforming pathway of indolent CLL towards aggressive RS thus providing novel mechanistic insights into the molecular understanding of RS.

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miRNAseq CLL38

Project description:miRNAseq of chronic lymphocytic leukaemia (CLL) subsets comprising of Unmutated CLL and Mutated CLL. Mutated CLL cases were further subdivided based on B cell receptor signalling capacity.

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Project description:RNAseq of chronic lymphocytic leukaemia (CLL) subsets comprising of Unmutated CLL and Mutated CLL. Mutated CLL cases were further subdivided based on B cell receptor signalling capacity.

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DNA methylation arrays of thirty-eight basal tumour samples from CLL patients

Project description:DNA methylation arrays of chronic lymphocytic leukaemia (CLL) subsets comprising of Unmutated CLL and Mutated CLL. Mutated CLL cases were further subdivided based on B cell receptor signalling capacity.

2023-05-11 | E-MTAB-12018 | biostudies-arrayexpress

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Project description:Functional studies to investigate gene mutations recurrent in B cell lymphoma have been hampered by the inability to genetically manipulate primary cells, attributed to low transduction efficacy and procedure-associated toxicity. Alternative approaches utilize cell lines and mouse models, which often only poorly represent the genomic complexity and biology of the primary malignancy. To overcome these limitations, we have developed a method to retrovirally transfer genes into primary malignant B cells with high transduction efficacy and minimal toxicity. Using this method, we investigated the functions of NOTCH1, the most commonly mutated gene in CLL, by generating isogenic primary tumor cells from patients with Chronic Lymphocytic Leukemia (CLL) and Mantle Cell Lymphoma (MCL), differing only in their expression of NOTCH1. Our data demonstrate that NOTCH1 facilitates immune escape of malignant B cells by up-regulating PD-L1, partly dependent on autocrine interferon-g signaling. In addition, NOTCH1 causes silencing of the entire HLA-class II locus via suppression of the transcriptional co-activator CIITA. These NOTCH1-mediated immune escape mechanisms are associated with the expansion of CD4+ T cells in vivo, further contributing to the poor clinical outcome of NOTCH1-mutated CLL and MCL

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