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Mutant IDH1 promotes glioma formation in vivo [Bisulfite-seq]

ABSTRACT: Mutant IDH1 promotes glioma formation in vivo [Bisulfite-seq]

PROVIDER: PRJNA420779 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6338710_1.fastq.gz	Fastqsanger.gz
	SRR6338710_2.fastq.gz	Fastqsanger.gz
	SRR6338711_1.fastq.gz	Fastqsanger.gz
	SRR6338711_2.fastq.gz	Fastqsanger.gz
	SRR6338712_1.fastq.gz	Fastqsanger.gz

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Mutant IDH1 promotes glioma formation in vivo

Project description:Mutant IDH1 promotes glioma formation in vivo

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Mutant IDH1 promotes glioma formation in vivo [RNA-seq]

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Mutant IDH1 promotes glioma formation in vivo [Bisulfite-seq]

Project description:Genomic DNA from IDH1 mutant and WT tumors were used to detect genome wide methylation using Agilent SureSelect XT Mouse Methyl-Seq Enrichment System capture kit following manufacturer’s recommendations.

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Mutant IDH1 promotes glioma formation in vivo [RNA-seq]

Project description:RNA was isolated from FFPE samples of IDH1 mutant, WT tumors and normal brains

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High grade glioma methylation analysis using bisulfite and oxidative bisulfite-treatment

Project description:Bisulfite and oxidative bisulfite treated sample methylation analysis of IDH1 mutant and wild-type high grade human gliomas, to profile 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). Genomic DNA isolated directly from fresh-frozen human high grade glioma specimens.

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Mutant IDH1 Promotes Glioma Formation In Vivo.

Project description:Isocitrate dehydrogenase 1 (IDH1) is the most commonly mutated gene in grade II-III glioma and secondary glioblastoma (GBM). A causal role for IDH1R132H in gliomagenesis has been proposed, but functional validation in vivo has not been demonstrated. In this study, we assessed the role of IDH1R132H in glioma development in the context of clinically relevant cooperating genetic alterations in vitro and in vivo. Immortal astrocytes expressing IDH1R132H exhibited elevated (R)-2-hydroxyglutarate levels, reduced NADPH, increased proliferation, and anchorage-independent growth. Although not sufficient on its own, IDH1R132H cooperated with PDGFA and loss of Cdkn2a, Atrx, and Pten to promote glioma development in vivo. These tumors resembled proneural human mutant IDH1 GBM genetically, histologically, and functionally. Our findings support the hypothesis that IDH1R132H promotes glioma development. This model enhances our understanding of the biology of IDH1R132H-driven gliomas and facilitates testing of therapeutic strategies designed to combat this deadly disease.

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A Brain Penetrant Mutant IDH1 Inhibitor Provides In Vivo Survival Benefit

Project description:We profiled two IDH1 mutant glioma models, grown as intracranial xenografts, treated with an IDH1 inhbitor. One model, BT424, was responsive to IDH1 inhibition by compound treatement and also displayed more transcriptional changes in response to treatment. The other model, GB10, was not responsive to IDH1 inhibition and was transcriptionally quiet after treatment with compound.

2018-02-01 | GSE105447 | GEO

Single nucleus sequencing of SOX2+ glioma stem nuclei from IDH1/TP53-mutant and wild-type glioma samples

Project description:Understanding the glioma stem cell (GSC) heterogeneity within IDH1 and TP53 mutant tumors may elucidate possible targets for astrocytoma treatment. We performed single-nucleus transcriptomics of 6 mutant and wild-type glioma samples sorted for Sox2 stem cell marker. Malignant states of different clusters were evaluated by the expression of the normal and hematopoietic markers. We found that mutant GSCs were characterized by collagen synthesis and CD44-high phenotype prone to migration, while wild-type GSCs had vulnerability points in ATP synthesis. Additionally, mutant GSCs displayed altered lipogenesis probably attributed to the low NADPH consumed by mutant IDH1. The collagen and lipid biosynthesis represent possible target pathways for prospective tackling GSCs with IDH1 R132H and TP53 point mutations, uncouplers of oxidative phosphorylation are promising to address wild-type GSC proliferation

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Gene expression profile of Idh1 wild-type and mutant glioma initiating cells

Project description:Human astrocytomas and oligodendrogliomas are defined by mutations in the metabolic enzyme isocitrate dehydrogenase (IDH) 1 or 2. Mutant IDH1 causes the production and accumulation of the metabolite 2 hydroxyglutarate, which induces genome-wide hypermethylation, and is thought to be a driver mutation of these tumours. However, there are multiple contradictory effects of mutant IDH1 in cell lines and in vivo models, prompting us to study the effect of mutant IDH1 on cell differentiation, proliferation, and apoptosis. Here we established mouse glioma initiating cells (GIC) by inactivating the tumour suppressor genes Pten and p53 in the neural stem/progenitor cell population of the forebrain, and compared these GIC with triple mutant tumours expressing in addition the Idh1 R132H mutation. We found that Idh1 mutant cells proliferate less in vitro and mice with Idh1 mutant tumour survived significantly longer than their Idh1 wild type counterparts. By comparing the RNA expression profiles of Idh wild-type and Idh mutant cells and tumours we identified endoplasmic reticulum stress pathways were significantly associated with Idh1 mutation.

2019-08-22 | GSE119741 | GEO

miRNA expression profile of Idh1 wild-type and mutant glioma initiating cells

Project description:Human astrocytomas and oligodendrogliomas are defined by mutations in the metabolic enzyme isocitrate dehydrogenase (IDH) 1 or 2. Mutant IDH1 causes the production and accumulation of the metabolite 2 hydroxyglutarate, which induces genome-wide hypermethylation, and is thought to be a driver mutation of these tumours. However, there are multiple contradictory effects of mutant IDH1 in cell lines and in vivo models, prompting us to study the effect of mutant IDH1 on cell differentiation, proliferation, and apoptosis. Here we established mouse glioma initiating cells (GIC) by inactivating the tumour suppressor genes Pten and p53 in the neural stem/progenitor cell population of the forebrain, and compared these GIC with triple mutant tumours expressing in addition the Idh1 R132H mutation. We found that Idh1 mutant cells proliferate less in vitro and mice with Idh1 mutant tumour survived significantly longer than their Idh1 wild type counterparts. By comparing the miRNA expression profiles of Idh wild-type and Idh mutant cells and tumours we identified miR-183-5p as a differentially expressed miRNA.

2019-08-22 | GSE119740 | GEO

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