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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE135030 | GEO | 2020/05/28

REPOSITORIES: GEO

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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

Transposon mutagenesis reveals fludarabine-resistance mechanisms in chronic lymphocytic leukemia

Project description:Purpose:To identify resistance mechanisms for the chemotherapeutic drug fludarabine in chronic lymphocytic leukemia (CLL), as innate and acquired resistance to fludarabine-based chemotherapy represents a major challenge for long-term disease control. Methods: We employed piggyBac transposon-mediated mutagenesis, combined with next-generation sequencing, to identify genes that confer resistance to fludarabine in a human CLL cell line. Results: RNA-seq profiling of fludarabine-resistant cells suggested deregulated MAPK signaling as involved in mediating drug resistance in CLL.

2016-03-31 | GSE75844 | GEO

Transposon mutagenesis reveals fludarabine-resistance mechanisms in chronic lymphocytic leukemia

2016-03-31 | E-GEOD-75844 | biostudies-arrayexpress

Nanda2013 - B cell chronic lymphocytic leukemia A model with immune response

Project description:B cell chronic lymphocytic leukemia - A model with immune response Seema Nanda 1, , Lisette dePillis 2, and Ami Radunskaya 3, 1. Tata Institute of Fundamental Research, Centre for Applicable Mathematics, Bangalore 560065, India 2. Department of Mathematics, Harvey Mudd College, Claremont, CA 91711 3. Department of Mathematics, Pomona College, Claremont, CA, 91711, United States Abstract B cell chronic lymphocytic leukemia (B-CLL) is known to have substantial clinical heterogeneity. There is no cure, but treatments allow for disease management. However, the wide range of clinical courses experienced by B-CLL patients makes prognosis and hence treatment a significant challenge. In an attempt to study disease progression across different patients via a unified yet flexible approach, we present a mathematical model of B-CLL with immune response, that can capture both rapid and slow disease progression. This model includes four different cell populations in the peripheral blood of humans: B-CLL cells, NK cells, cytotoxic T cells and helper T cells. We analyze existing data in the medical literature, determine ranges of values for parameters of the model, and compare our model outcomes to clinical patient data. The goal of this work is to provide a tool that may shed light on factors affecting the course of disease progression in patients. This modeling tool can serve as a foundation upon which future treatments can be based. Keywords: NK cell, chronic lymphocytic leukemia, mathematical model, T cell., B-CLL.

2020-01-09 | MODEL2001090002 | BioModels

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

Expression array analysis of MEC1, MEC2 and JeKo-1 cells 3h and 10h after overexpression of KLF4

Project description:In a recent study we identified the transcription factor KLF4 as deregulated by DNA methylation in chronic lymphocytic leukemia (CLL) cells in comparison to healthy B-cells. To analyze the function of KLF4 in leukemia cells and to identify downstream targets of the transcription factor we overexpressed KLF4 in 3 different cell lines: the CLL cell lines MEC1 and MEC2 and in the mantel cell lymphoma cell line JeKo-1.

2017-01-23 | GSE66514 | GEO

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

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

| PRJNA557198 | ENA

Trascriptional profiling of proliferating and resting fracntions in ibrutinib-treated CLL

Project description:Bruton’s tyrosine kinase (BTK) inhibitors such as ibrutinib represent an effective strategy for treatment of chronic lymphocytic leukemia (CLL), although ~30% of patients eventually undergo disease progression. Here we investigated the long-term modulation of the CXCR4dim/CD5bright proliferative fraction (PF) and the CXCR4bright/CD5dim resting fraction (RF) in CLL samples, and their correlation with therapeutic outcome and emergence of ibrutinib resistance. Longitudinal tracking by flow cytometry revealed that PF, initially suppressed by ibrutinib, reappeared upon early disease progression suggesting that PF evaluation could represent a sensitive and specific marker of CLL progression upon ibrutinib treatment. Transcriptomic analyses of PF at progression revealed similar proliferation signatures between pre- and post-treatment PF, demonstrating the emergence upon progression of a newly proliferating cell population.

2024-04-02 | GSE249956 | 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

CITE-Seq profiling of CLL under ibrutinib treatment reveals transcriptional evolution of leukemic and immune cells.

Project description:Ibrutinib, an irreversible Bruton Tyrosine Kinase (BTK) inhibitor, has revolutionized Chronic Lymphocytic Leukemia (CLL) treatment, but resistances to ibrutinib have emerged in relation or not to BTK mutations. Evolution patterns of CLL before and after ibrutinib therapy are often focused only on leukemic cells but must be investigated in the context of the CLL microenvironment. Single cell RNA-seq and related technologies allow a deeper characterization of cancer and normal cells. We therefore investigated whether ibrutinib treatment drives molecular changes in CLL. Here, we report the monitoring of a CLL patient under ibrutinib treatment using Cellular Indexing of Transcriptomes and Epitopes by sequencing (CITE-Seq) technology. We report that the short clinical relapse of this patient, driven by BTK mutation, is associated with intra-clonal heterogeneity and transcriptional and phenotypical modifications in both B leukemic and immune cells. These results open new therapeutic strategies for ibrutinib-refractory CLL patients.

2020-12-15 | GSE152469 | GEO

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