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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.

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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.

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

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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).

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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

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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.

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Longitudinal omics data followed by preclinical treatment studies identify proteasome inhibition as potential salvage strategy for ibrutinib-resistant CLL

Project description:Chronic lymphocytic leukemia (CLL) is a malignant lymphoproliferative disorder characterized by the accumulation of small mature B cells in blood and secondary lymphoid tissues. Novel drugs, such as the Bruton tyrosine kinase (BTK) inhibitor ibrutinib, have greatly improved survival expectations of CLL patients, nevertheless acquired drug resistance represents a major challenge and the complete molecular mechanisms of which have not been elucidated yet. In order to fill this knowledge gap, we generated a mouse model of ibrutinib resistance by treating mice upon adoptive transfer of Eµ-TCL1 leukemia (TCL1-CLL) continuously with ibrutinib. After an initial response to the treatment, relapse under therapy occurs with an aggressive outgrowth of the malignant cells, resembling observations in patients. To unravel relapse mechanism, we performed transcriptome and proteome analyses of sorted TCL1-CLL cells both during treatment and after relapse. Comparative analysis of these omics layers suggested alterations in the proteasome activity as a driver of ibrutinib resistance. Accordingly, we showed that preclinical treatment with the irreversible proteasome inhibitor (PI) carfilzomib administered upon ibrutinib resistance prolonged survival of mice, thus acting as salvage therapy. Longitudinal proteomic analysis of CLL patients with ibrutinib resistance identified deregulation in protein post-translational modifications. In addition, CLL cells from ibrutinib-resistant patients effectively responded to several PIs in co-culture assays. Altogether, our results from orthogonal omics approaches identified proteasome inhibition as potentially attractive innovative salvage treatment option for CLL patients resistant or refractory to ibrutinib.

2024-10-29 | GSE215414 | GEO

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.

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

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