Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Treatment of MEC1, EHEB and JVM2 leukemia cell lines with fludarabine, ibrutinib and idelalisib

ABSTRACT: Treatment of MEC1, EHEB and JVM2 leukemia cell lines with fludarabine, ibrutinib and idelalisib

PROVIDER: PRJNA557198 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9853980_1.fastq.gz	Fastqsanger.gz
	SRR9853980_2.fastq.gz	Fastqsanger.gz
	SRR9853990_1.fastq.gz	Fastqsanger.gz
	SRR9853990_2.fastq.gz	Fastqsanger.gz
	SRR9854000_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 72

Similar Datasets

RNA-Seq study of Cell lines rendered resistant to idelalisib and ibrutinib

Project description:BCR pathway inhibitors idelalisib and ibrutinib are the first small molecule targeted agents for B-cell malignancies. In spite of encouraging response rates in various forms of B cell diseases, patients will eventually develop relapse due to the emergence of resistant cells. To better identify the possible mechanisms of resistance we developed and characterized idelalisib- and ibrutinib-resistant variants of the human non Hodgkin’s lymphoma cell lines DoHH2 and Daudi. These resistant variants displayed a cross-resistance profile limited to PI3K inhibitors, BTK inhibitors and a SYK inhibitor but not to unrelated agents. A number of alterations were observed in the resistant lines, including a strong reduction of the Akt3 protein. Resistant lines tended to express larger amounts of CD38 and CD52 on their cell membrane and were found to display enhanced sensitivity to anti-CD38 antibodies. These results identify potential novel mechanisms of resistance to idelalisib and ibrutinib and raise the possibility that cells resistant to BCR pathway inhibitors might possess enhanced sensitivity to anti-CD38 antibodies.

2019-08-19 | GSE118707 | GEO

Treatment of MEC1, EHEB and JVM2 leukemia cell lines with fludarabine, ibrutinib and idelalisib

Project description:UGT2B17 is a recently identified molecular marker for poor prognosis and drug response in Chronic Lymphocytic Leukemia (CLL), which is the most prevalent adult leukemia subtype in the western world. The goal of this study was to investigate transcriptome changes associated with drug-induced UGT2B17 up-regulation to identify possible upstream regulators of drug response and downstream effects of UGT induction.

2020-05-28 | GSE135030 | GEO

RNA-Seq study of Cell lines rendered resistant to idelalisib and ibrutinib

Project description:RNA-Seq study of Cell lines rendered resistant to idelalisib and ibrutinib

| PRJNA486519 | ENA

Overexpression of UGT2B17 in MEC1 and JVM2 leukemia cell lines

Project description:UGT2B17 is a recently identified molecular marker for poor prognosis in Chronic Lymphocytic Leukemia (CLL), which is the most prevalent adult leukemia subtype in the western world. The goal of this study was to determine the effects of UGT2B17 expression in leukemia cells and to find molecular pathways associated with high UGT2B17 expression. We characterized the effects of UGT2B17 in two leukemia cell lines (MEC1 and JVM2) overexpressing a functional UGT2B17 enzyme. A first line of inquiries based on RNA sequencing analysis revealed a series of genes differentially expressed in UGT2B17 overexpressing cells compared to controls, with several genes related to arachidonic acid metabolism and signaling.

2019-07-29 | GSE121626 | GEO

Chronic Lymphocytic Leukemia MEC1 SF3B1 K700E and Wild Type Cell Lines' RNA-seq after Treatment with H3B-8800 Splicing Modulator.

Project description:To study the impact of SF3B1 mutations on alternative splicing and the effect of H3B-8800 splicing modulator in wild type and SF3B1-mutant chronic lymphocytic leukemia cells, we established SF3B1 K700E MEC1 CLL isogenic cell line and carried out RNA deep sequencing in SF3B1 wild type and K700E MEC1 cell lines upon H3B-8800 treatment.

2023-08-08 | GSE190087 | GEO

Activation and exhaustion of CD8 T cells in patients with chronic lymphocytic leukemia treated with ibrutinib and pembrolizumab [scRNA-seq, scTCR-seq and bulk RNA-seq]

Project description:Single-agent anti-PD-1 antibodies lack clinical efficacy in patients with chronic lymphocytic leukemia (CLL). Here, we study the peripheral blood samples from high-risk or relapsed/refractory CLL before and after combination therapy of ibrutinib, fludarabine, and pembrolizumab (IFP). We performed bulk RNA-sequencing (bulk RNA-seq) to detect the transcriptomic changes of CLL and T cells during treatment, and demonstrated the immune responses of CD8 T cells to pembrolizumab by single-cell RNA sequencing (scRNA-Seq).

2025-08-27 | GSE283397 | GEO

Overexpression of UGT2B17 in MEC1 and JVM2 leukemia cell lines

Project description:Overexpression of UGT2B17 in MEC1 and JVM2 leukemia cell lines

| PRJNA497889 | ENA

Modulation of immune system mediated by ibrutinib in chronic lymphocytic leukemia

Project description:Our project is based on the hypothesis that ibrutinib could interfere with chronic lymphocytic leukemia (CLL) microenvironment, modulating the immune response. The aim of the project is to understand if and how ibrutinib modifies the tumor microenvironment accessory cells in CLL, specifically nurse like cells (NLC).

2020-09-18 | GSE142292 | GEO

RNA-Seq of B-Cell Lines Clones, parental and resistant to Idelalisib or IMGN529

Project description:Idelalisib was the first-in-class PI3Kδ inhibitor and additional compounds are undergoing clinical investigation. To identify modalities to overcome resistance to these agents, we have developed idelalisib-resistant model derived from marginal zone lymphoma cell line (VL51). Cells were kept under idelalisib until acquisition of resistance (VL51-RER) or with no drug (parental). In this experiment we identified the modulated genes between the resistant cell line and the parental counterpart (sensitive to the drug) We invastigated the transcriptomic profiles of parental K1718 B-cell lymphoma cell lines and the same cell line made resistant to Idelalisib. in addition two B-Cells (SUDHL2 and SUDHL4) are made resistant to IMGN529 (Naratuximab emtansine) an antibody-drug conjugate (ADC) incorporating an anti-CD37 monoclonal antibody conjugated to the maytansinoid DM1 as payload.

2024-05-06 | GSE173984 | GEO

SWATH-proteomics analysis of ibrutinib mechanism of action in neutropenia and acute myeloid leukemia initiating mutated granulocyte-colony stimulating factor receptor

Project description:Neutrophil production and function are primarily determined by granulocyte colony stimulating factor receptor (G-CSFR). G-CSFRs associated mutations (mostly localized in the transmembrane and cytoplasmic domains of the receptor) have been reported with several distinct hematological abnormalities as well as malignancies, e.g. severe congenital neutropenia (SCN), acute myeloid leukemia (AML) and chronic neutrophilic leukemia (CNL). Ibrutinib, a small molecule Bruton’s tyrosine kinase (BTK) inhibitor, is FDA approved and clinically used against B-cell related leukemia. In our previous published work (Dwivedi et al., Leukemia.2019;33:75–87), we have shown ibrutinib’s efficacy in the mutated G-CSFRs based leukemia model systems (mouse and human). However, the signaling mechanism of ibrutinib’s efficacy is not explored yet. Here, we present a unique SWATH-based label free quantitative proteomics analysis of the normal and mutated G-CSFRs signaling post ibrutinib treatment, using 32D cell-line-based in vitro model system.

2020-04-27 | PXD013402 | Pride

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