Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Temporal transcriptional response from primary human chronic lymphocytic leukemia (CLL)-cells after B-cell receptor stimulation.

ABSTRACT: Temporal transcriptional response from primary human chronic lymphocytic leukemia (CLL)-cells after B-cell receptor stimulation.

PROVIDER: PRJNA539961 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8979520.fastq.gz	Fastqsanger.gz
	SRR8979530.fastq.gz	Fastqsanger.gz
	SRR8979540.fastq.gz	Fastqsanger.gz
	SRR8979550.fastq.gz	Fastqsanger.gz
	SRR8979560.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 54

Similar Datasets

Temporal transcriptional response from primary human chronic lymphocytic leukemia (CLL)-cells after B-cell receptor stimulation.

Project description:The B-cell receptor (BCR) signaling is crucial for the pathophysiology of most leukemias and lymphomas originated from mature B lymphocytes and has emerged as a new therapeutic target, especially for chronic lymphocytic leukemia (CLL). However, the precise mechanisms by which BCR signaling controls neoplastic B-cell proliferation are ill characterized. This work was performed using primary leukemic cells of untreated patients at initial stage of CLL (Binet stage A / Rai 0) presenting biological characteristics of aggressive form of the disease (unmutated IGHV genes and ZAP70 protein expression). In order to mimic the primary leukemogenic step occurring in vivo, this study focused on the BCR-dependent proliferation of CLL cells induced ex vivo using anti-IgM, together with mandatory co-stimulating factors (CD40L, IL-4 and IL-21) (Schleiss, Sci Rep, 2019). Cell proliferation was objectivized by the emergence of proliferative clusters and the presence of more than 25% of CLL cells that did undergo division within the cell culture at day 6. To capture the specific actors of the proliferative response in these samples, we also included non-proliferating control CLL samples. Gene expression was analyzed by RNA-seq before stimulation (T0) and at the time points 1h, 1h30, 3h30, 6h30, 12h, 24h, 48h and 96h after cell stimulation (n=54 data points), the latest time points corresponding to the emergence of the proliferation clusters.

2021-05-12 | GSE130385 | GEO

CD40 stimulation of chronic lymphocytic leukemia (CLL) cells

Project description:CD40 stimulation of chronic lymphocytic leukemia (CLL) cells

| PRJNA830901 | ENA

CD40 stimulation + dasatinib treatment of chronic lymphocytic leukemia (CLL) cells

Project description:CD40 stimulation + dasatinib treatment of chronic lymphocytic leukemia (CLL) cells

| PRJNA1103147 | ENA

RNA-Seq of primary chronic lymphocytic leukaemia (CLL) tumours treated with anti-IgM antibodies against isotype control treated tumours

Project description:Chronic lymphocytic leukemia (CLL) is a highly heterogenous disease, with vastly diverse phenotypes that cause differing clinical courses ranging from benign disease (requiring no treatment), to a rapidly progressive disease and may require aggressive treatment therapy. Key to the B cell is the B-cell receptor (BCR); CLL utilises the BCR to evade apoptosis and promote proliferation and drug resistance through cross-talk between the TME and through BCR activation. Our experiments engage the BCR to determine downstream impact of BCR stimulation on gene expression in CLL (6 hours after stimulation).

2023-05-01 | E-MTAB-12055 | biostudies-arrayexpress

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

CD4 T cell stimulation with or without chronic lymphocytic leukemia (CLL) cells present

Project description:In this experiment we in vitro activated T cells from CLL patients either in the presence or absence of their autologous CLL cells. After 48 hours of antiCD3/antiCD28 stimulation, the CD4 cells were FACS sorted from two condition and RNA sequencing was performed on these cells.

2022-09-26 | GSE193671 | GEO

RNAseq of Chronic Lymphocytic Leukaemia with and without anti-IgM treatment at 6 hrs and 24 hrs post-stimulation

Project description:Series of Chronic Lymphocytic Leukaemia (mix of U-CLL and M-CLL) with and without anti-IgM stimulation of the B cell receptor. RNA acquired at 6hrs and 24hrs post stimulation.

2022-02-21 | E-MTAB-11195 | biostudies-arrayexpress

CD4 T cell stimulation with or without chronic lymphocytic leukemia (CLL) cells present

Project description:CD4 T cell stimulation with or without chronic lymphocytic leukemia (CLL) cells present

| PRJNA797099 | ENA

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

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data