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GNPS - Metabolomics Integration with Gene expression profiling Elucidates IL4I1 as Modulator of Ibrutinib Resistance in ABC large B cell Lymphoma

ABSTRACT: Drug resistant acute B-cell lymphoma cells were analyzed via LC-MS metabolomics to identify deregulated metabolic pathways that are associated with drug resistance.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Human

SUBMITTER: Jiangjiang Zhu Lalit Sehgal

PROVIDER: MSV000087059 | GNPS | Tue Mar 16 11:23:00 GMT 2021

REPOSITORIES: GNPS

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Integration of Metabolomics and Gene Expression Profiling Elucidates IL4I1 as Modulator of Ibrutinib Resistance in ABC-Diffuse Large B Cell Lymphoma.

Choueiry Fouad F Singh Satishkumar S Sircar Anuvrat A Laliotis Georgios G Sun Xiaowei X Chavdoula Evangelia E Zhang Shiqi S Helmig-Mason JoBeth J Hart Amber A Epperla Narendranath N Tsichlis Philip P Baiocchi Robert R Alinari Lapo L Zhu Jiangjiang J Sehgal Lalit L

Cancers 20210429 9

Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma (NHL). B-cell NHLs rely on Bruton's tyrosine kinase (BTK) mediated B-cell receptor signaling for survival and disease progression. However, they are often resistant to BTK inhibitors or soon acquire resistance after drug exposure resulting in the drug-tolerant form. The drug-tolerant clones proliferate faster, have increased metabolic activity, and shift to oxidative phosphorylation; however, how this metabolic program ...[more]

PMID: 33946867

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Metabolomics Integration with Gene expression profiling Elucidates IL4I1 as Modulator of Ibrutinib Resistance in ABC large B cell Lymphoma

Project description:Drug resistant acute B-cell lymphoma cells were analyzed via LC-MS metabolomics to identify deregulated metabolic pathways that are associated with drug resistance.

2021-03-16 | MSV000087059 | MassIVE

GENE EXPRESSION PROFILING AND MOLECULAR CHARACTERIZATION OF ANTIMONY RESISTANCE IN Leishmania amazonensis

Project description:Background: Drug resistance is a major problem in leishmaniasis chemotherapy. RNA expression profiling using DNA microarrays is a suitable approach to study simultaneous events leading to a drug-resistance phenotype. Genomic analysis has been performed primarily with Old World Leishmania species and here we investigate molecular alterations in antimony resistance in the New World species L. amazonensis. Methods/Principal Findings: We selected populations of L. amazonensis for resistance to antimony by step-wise drug pressure. Gene expression of highly resistant mutants was studied using DNA microarrays. RNA expression profiling of antimony-resistant L. amazonensis revealed the overexpression of genes involved in drug resistance including the ABC transporter MRPA and several genes related to thiol metabolism. The MRPA overexpression was validated by quantitative real-time PCR and further analysis revealed that this increased expression was correlated to gene amplification as part of extrachromosomal linear amplicons in some mutants and as part of supernumerary chromosomes in other mutants. The expression of several other genes encoding hypothetical proteins but also nucleobase and glucose transporter encoding genes were found to be modulated. Conclusions/Significance: Mechanisms classically found in Old World antimony resistant Leishmania were also highlighted in New World antimony-resistant L. amazonensis. These studies were useful to the identification of resistance molecular markers.

2011-06-11 | GSE26159 | GEO

Prediction of antibiotic resistance by large-scale phenotypic and genotypic data

Project description:The evolution of antibiotic resistance is a clear example of adaptation by natural selection. Although a number of mutations contributing to the resistance have been identified, the relationship between the mutations and the related phenotypic changes responsible for the resistance has yet to be fully elucidated. To better characterize phenotype-genotype mapping for drug resistance, we performed parallel laboratory evolution of Escherichia coli under the selection of single antibiotics and after 90 days propagation obtained resistant strains. We find that an acquisition of resistance to one drug drastically changes the resistance and susceptibility to other drugs. Based on transcriptome data of these strains, we demonstrated that the resistances could be quantitatively predicted by the expression changes of a small number of genes. Whole-genome resequencing analysis provided several candidate mutations contributing to the resistances, while phenotype-genotype mapping was suggested to be complex and included various mutations that caused similar phenotypic changes. The integration of transcriptome and genome data enables us to extract essential phenotypic changes for drug resistances. To examine the contribution of the gene expression changes to the antibiotic resistances, transcriptome of the parent strain (duplicated) and 40 resistant strains (4 parallel-evolved resistant strains for 10 antibiotics) were analyzed.

2014-09-17 | E-GEOD-59408 | biostudies-arrayexpress

Glucocorticoid Resistance Gene Profiling in T-ALL Cell Lines

Project description:Baseline glucocorticoid resistance profiles were measured in a panel of 15 paediatric T-Cell acute lymphoblastic leukaemia cell lines and correlated with Affymetrix Gene expression to identify genes and pathways associated with drug resistance in T-ALL. The cell lines' resistance to Methylprednisolone (MPRED) and Dexamethasone (DEX) was then tested using the MTT assay and IC50 values (drug concentration lethal to 50% of cells) for each drug were calculated.

2012-07-09 | E-MTAB-1208 | biostudies-arrayexpress

In vitro prednisolone resistance signature in MLL-rearranged infant ALL

Project description:Acute Lymphoblastic Leukemia (ALL) in infants (<1 year of age) is characterized by a high incidence of MLL translocations which is associated with a poor prognosis. Contributing to this poor prognosis is cellular drug resistance, especially to glucocorticoids like prednisolone. Although in vitro prednisolone resistance mechanisms have been proposed in pediatric ALL, it has never been studied in MLL-rearranged infant ALL, which are highly resistant to glucocorticoids in vitro and in vivo. We analyzed primary MLL-rearranged infant ALL expression profiles, which were either in vitro prednisolone-resistant or prednisolone-sensitive, in order to study in vitro prednisolone resistance.

2011-10-12 | E-GEOD-32962 | biostudies-arrayexpress

Gene expression profiling and the effect of HDAC9 in cisplatin resistance of esophageal squamous cell carcinoma

Project description:Esophageal cancer is one of the most serious health problems globally because of its high incidence and mortality rate. Cisplatin (CDDP) is the primary treatment but limited by the drug resistance. However, the mechanism of cisplatin resistance remains unclear. Herein, the CDDP-resistant cell line TE-1/CDDP was established to compared with TE-1, the expression profiles of circRNAs mRNA and lncRNA were compared between TE-1/CDDP and TE-1 using microarray analysis, and used this as a basis for exploring possible mechanisms of drug resistance in genes such as HDAC9.

2023-09-14 | GSE242834 | GEO

Expression Proteomics of BRAF Inhibitor Resistance in Melanoma Cell Lines

Project description:To investigate mechanisms of resistance to BRAF inhibitor therapy in melanoma, BRAF mutant cell lines have been chronically exposed to BRAFi to create phenotypes with acquired drug resistance. Expression proteomics is used to examine the differences between naive and drug-resistant cells.

2016-12-13 | PXD004342 | Pride

Prediction of antibiotic resistance by large-scale phenotypic and genotypic data

2014-09-17 | GSE59408 | GEO

Gene Expression and evolution of antifungal drug resistance

Project description:We examined the gene expression changes resulting from the evolution of resistance in experimental populations of the yeast Saccharomyces cerevisiae subjected to two antifungal drugs, fluconazole (FLC) and amphotericin B (AmB). Fluconazole resistance may involve increased efflux or changes in sterol metabolism, while AmB resistance generally involves changes in sterol metabolism; for all of these types of resistance, the gene expression changes are extensive. The goal of these experiments was to test whether failure of gene expression changes all downstream of the original mutation for drug resistance would affect the ability of a mutant cell to evolve and/or to support a drug-resistant phenotype.

2008-07-28 | GSE12055 | GEO

Diffuse Large B Cell Lymphoma cell line with Acquired Resistance to PI3Kδ Inhibitor Idelalisib

Project description:RNAseq profile of TMD8 cell lines resistant to Idelalisib treatment. Idelalisib resistant TMD8 cells were generated by continuous passage in the presence of 1 μM idelalisib for 8 weeks until stable resistance to idelalisib was established. Parallel cultures were grown in the presence of 0.1% DMSO as passage-matched, drug-sensitive control lines. Sensitive and resistant TMD8 cells were clonally isolated through two rounds of single cell limiting dilution

2017-02-17 | GSE93156 | GEO

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