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Analysis of chronic lymphocytic leukemia CLL cells and normal B cells

ABSTRACT: We have analyzed 2 normal B cells isolated from peripheral blood and 5 CLL specimens with affy 133A microarray for expression. We used microarrays to analyze gene expression in normal B cells and CLL cells. Hybridize RNA to the chip for the above mentioned total 5 samples

ORGANISM(S): Homo sapiens

SUBMITTER: Sanjai Sharma

PROVIDER: E-GEOD-18026 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Aberrant splicing of the E-cadherin transcript is a novel mechanism of gene silencing in chronic lymphocytic leukemia cells.

Sharma Sanjai S Lichtenstein Alan A

Blood 20090910 19

Premature termination codon (PTC) mutations are due to insertion or deletion of nucleotides causing a frameshift and premature termination codon in RNA. These transcripts are degraded by the nonsense-mediated decay pathway and have a very short half-life. We used a microarray technique to screen for genes that up-regulate their RNA signal upon nonsense-mediated decay pathway blockade in chronic lymphocytic leukemia (CLL) specimens and identified an E-cadherin transcript with PTC. Sequencing reve ...[more]

PMID: 19745069

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Analysis of chronic lymphocytic leukemia CLL cells and normal B cells

Project description:We have analyzed 2 normal B cells isolated from peripheral blood and 5 CLL specimens with affy 133A microarray for expression. We used microarrays to analyze gene expression in normal B cells and CLL cells.

2009-09-10 | GSE18026 | GEO

miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

Project description:miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples.

2015-06-15 | GSE62137 | GEO

The Proteome Landscape of Chronic Lymphocytic Leukemia (CLL)

Project description:Many functional consequences of mutations on tumor phenotypes in chronic lymphocytic leukemia (CLL) are only partially known. This is in part due to a scarcity of information on the proteome of CLL. We profiled the proteome of 117 CLL samples with data-independent acquisition mass spectrometry (DIA-MS) and integrated the results with genomic, transcriptomic, functional data and clinical outcome. We found trisomy 12 and IGHV to be major determinants of proteome variation in CLL (1055 and 542 differential proteins FDR of 5%). Trisomy 12 was associated with limited protein abundance buffering. Protein complex analyses detected functional units involved in BCR/PI3K/AKT signaling in CLL with trisomy 12. We associated protein expression with response to anticancer drugs, and STAT2 protein expression emerged as a biomarker for the prediction of response to kinase inhibitors including BTK and MEK inhibitors. STAT2 protein levels were determined by gene dosage (trisomy 12), stabilization in a protein complex and linked to interferon signaling in CLL. This study highlights the emerging importance of protein abundance profiling in CLL biology.

2021-09-24 | PXD022198 | Pride

miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

Project description:miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. 16 CLL patients (8 Pre samples, 15 Ctrl samples, 15 IL-4 samples), 3 NBC (3 Ctrl samples, 3 IL-4 samples)

2015-06-15 | E-GEOD-62137 | biostudies-arrayexpress

CD40 stimulation of chronic lymphocytic leukemia (CLL) cells

Project description:In this experiment we in vitro activated CLL cells on a layer of fibroblasts expressing CD40L (3T40) or nothing (3T3) for 48 hours. After the 48 hours, cells were taken off the fibroblasts and sorted for viable CD19+ cells. Then we performed RNA sequencing.

2022-05-20 | GSE201341 | GEO

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

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 | GSE92701 | GEO

Project description:Chronic lymphocytic leukemia (CLL), the most common type of leukemia in adults, is still incurable despite the development of novel therapeutic strategies. This reflects the incomplete understanding of the pathophysiology of this disease. In order to get more detailed insights into CLL development, we performed a comprehensive proteome analysis of primary human CLL cells and B cells from young and age-matched healthy individuals. For comparison, we also analyzed the chronic B cell leukemia cell line JVM-13 showing rather limited similarity to the primary cells. A principal component analysis comprising 6945 proteins separated these four groups, placing B cells of aged-matched controls between those of young donors and CLL patients. Remarkably, B cells from aged controls displayed significant regulation of proteins related to metabolic processes and stress response in mitochondria such as DLAT, FIS1 and NDUFAB1 as well as DNA repair including RAD9A, MGMT and XPA. Interestingly, these alterations apparently correlating with aging of B cells may also be essential for tumorigenesis and were observed similarly in CLL cells. In CLL cells, in addition, some remarkable unique features like the loss of tumor suppressor molecules PNN and JARID2, and high expression of CCDC88A, PIGR and ID3 otherwise associated with epithelial mesenchymal transition and stemness were determined. Furthermore, while typical hallmarks of cancer such as cell proliferation were hardly apparent for CLL cells, alterations of metabolic enzymes were another outstanding feature in comparison to normal B cells, indicating increased beta-oxidation of fatty acids and increased consumption of glutamine. Targeted metabolomics assays corroborated these results. The present findings identify previously unrecognized features of CLL cells and suggest that aging may be accompanied by proteome alterations functionally relevant for predisposing B cells to transform to CLL cells.

2017-12-06 | PXD006589 | Pride

2017-12-06 | PXD006578 | Pride

Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

Project description:Gene expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. Patient CLL01 was also treated with IL-4 plus 5 mg/ml ERK activation inhibitor peptide I, or IL-4 plus 10 µM NFkB activation inhibitor, and IL-4 plus 100 mg/ml cyclic-pifithrin-α

2014-10-06 | GSE55288 | GEO

Stromal cells support the survival of human primary chronic lymphocytic leukemia (CLL) cells

Project description:In chronic lymphocytic leukemia (CLL), the tumor cells receive survival support from stromal cells through direct cell contact, soluble factors and extracellular vesicles. The tyrosine protein kinase Lyn, is aberrantly expressed in the malignant and stromal cells in CLL tissue. We therefore studied the role of Lyn in the EV-based communication and tumor support. We compared the Lyn-dependent EV release, uptake and functionality using Lyn-proficient and deficient stromal cells and primary CLL cells. Lyn-proficient cells caused a significantly higher EV release and EV uptake as compared to Lyn-deficient ones. Also, they induced stronger support of primary CLL cells. Proteomic comparison of the EVs from Lyn-proficient and deficient stromal cell highlighted 72 significantly differentially expressed proteins, many of which belonging to the extracellular matrix organization, such as collagen, nidogen, fibronectin and endosialin (CD248). CD248, a marker of certain tumors and of cancer associated fibroblast (CAF) was significantly depleted in Lyn-deficient HS-5 cells. A knockdown of CD248 in Lyn+ HS-5 cells resulted in a diminished B-CLL cells survival feeding capacity compared to wildtype or scrambled control cells. The presented data provide preclinical evidence, that the tyrosine kinase Lyn crucially influences the EV-based communication between stromal and primary B-CLL cells by raising the EV release and their concentration of functional molecules, such as endosialin.

2023-01-12 | PXD036932 | Pride

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