Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IDH status dictates oHSV mediated metabolic reprogramming affecting anti-tumor immunity

ABSTRACT: IDH status dictates oHSV mediated metabolic reprogramming affecting anti-tumor immunity

PROVIDER: PRJNA1222406 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32313990.fastq.gz	Fastqsanger.gz
	SRR32313991.fastq.gz	Fastqsanger.gz
	SRR32313992.fastq.gz	Fastqsanger.gz
	SRR32313993.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

IDH status dictates oHSV mediated metabolic reprogramming affecting anti-tumor immunity

Project description:Identification of IDH mutations has uncovered the crucial role played by metabolism in glioma-genesis. Oncolytic herpes virus (oHSV) therapy initiates direct tumor debulking by tumor lysis and also activates antitumor immunity however little is known about the role of glioma metabolism in determining oHSV efficacy. Here we identified that oHSV therapy rewired central carbon metabolism with increased glucose utilization towards oxidative phosphorylation and shuttled glutamine towards reductive carboxylation in IDH wildtype (wt) glioma. The switch in metabolism resulted in increased lipid synthesis, and cellular ROS. PKC induced ACSL4 in oHSV treated cells led to lipid peroxidation and ferroptosis. Ferroptosis was critical to launch an antitumor immune response important for efficacy. Mutant IDH (IDHR132H) gliomas are incapable of reductive carboxylation and hence ferroptosis. Pharmacological blockade of IDHR132H induced ferroptosis and antitumor immunity. This study provides a rationale to treat high grade IDHR132H glioma patients under oHSV treatment with IDHR132H inhibitor.

2025-04-02 | GSE289317 | GEO

Physiological and morphological status of cells dictates RNA biosignature of their exosomes

Project description:Physiological and morphological status of cells dictates RNA biosignature of their exosomes

| PRJNA639969 | ENA

Genotyping by array of 297 adult-type diffuse gliomas comprise IDH-mutant astrocytomas, IDH-mutant 1p/19q codeleted oligodendrogliomas, and IDH-wildtype glioblastomas

Project description:Adult-type diffuse gliomas comprise IDH-mutant astrocytomas, IDH-mutant 1p/19q codeleted oligodendrogliomas (ODG), and IDH-wildtype glioblastomas (GBM). GBM display genome instability, which may result from two genetic events leading to massive chromosome alterations: chromothripsis (CT) and whole-genome duplication (WGD). The better prognosis of the latter may be related to their genome stability compared to GBM. Pangenomic profiles of 297 adult diffuse gliomas were analyzed at initial diagnosis using SNP arrays, including 192 GBM and 105 IDH-mutant gliomas (61 astrocytomas and 44 ODG). Tumor ploidy was assessed with Genome Alteration Print and CT events with CTLPScanner and through manual screening.

2024-12-24 | E-MTAB-13542 | biostudies-arrayexpress

REST transcription factor holds the balance between the invasion and cell differentiation in IDH-mutant and IDH-wild type gliomas

Project description:Glioblastoma is the deadliest brain tumor with median survival of 15 months due to diffusive growth and lack of efficient therapy. Recurrent mutations in genes coding for isocitrate dehydrogenases (IDH) 1 or 2 cause to a change in function of the enzymes, resulting in production of 2-hydroxyglutarate, which leads to DNA hypermethylation phenotype, affecting transcription activators/repressors binding to DNA and gene expression. REST is a canonical repressor of neuronal genes in non-neuronal cells, whose levels differ between IDH wt and mut gliomas and whose expression levels correlate with the patients’ survival probability.

2022-04-15 | GSE174308 | GEO

Safety and Efficacy of NEO212 in Patients With Astrocytoma IDH-mutant, Glioblastoma IDH-wildtype or Brain Metastasis

Project description:This multi-site, Phase 1/2 clinical trial is an open-label study to identify the safety, pharmacokinetics, and efficacy of a repeated dose regimen of NEO212 for the treatment of patients with radiographically-confirmed progression of Astrocytoma IDH-mutant, Glioblastoma IDH-wildtype, and the safety, pharmacokinetics and efficacy of a repeated dose regimen of NEO212 when given with select SOC for the treatment of solid tumor patients with radiographically confirmed uncontrolled brain metastasis. The study will have three phases, Phase 1, Phase 2a and Phase 2b.

| 92735 | ecrin-mdr-crc

Expression from hemocytes misexpressing Idh-R195H vs. controls

Project description:Expression profile for hemocytes from hml-Gal4, UAS-2xEGFP larvae were compared to hemocytes from hml-Gal4, UAS-2xEGFP; UAS-Idh-R195H larvae We sought to determine which genes and pathways were upregulated or downregulated in hemocytes expressing Idh-R195H, the Drosophila homolog of the human cancer-associated IDH1-R132H mutant, in vivo. We sought to obtain homogeneous populations of hemocytes from each genotype. We compared larvae expressing Idh-R195H from the hml-Gal4 driver to larvae with the hml-Gal4 driver alone.

2014-10-03 | E-GEOD-62008 | biostudies-arrayexpress

Gene expression changes in IDH mutant or IDH wildtype gliomas treated with All-trans Retinoic Acid

Project description:IDH mutant cells are deficient in retinoic acid production, which impacts downstream gene expression and pathways. We looked at the effect of supplementing IDH mutant glioma cells with ATRA on gene expression and downstream pathways. We compared gene expression changes with IDH WT cells that were also treated with ATRA

2019-12-11 | GSE141789 | GEO

Insulator dysfunction and oncogene activation in IDH mutant gliomas

Project description:Gain-of-function IDH mutations define major clinical and prognostic classes of gliomas. Mutant IDH protein produces a novel onco-metabolite, 2-hydroxyglutarate (2-HG), that interferes with iron-dependent hydroxylase enzymes, including the TET family of 5'-methylcytosine hydroxylases. TET enzymes are critical for the dynamic regulation of DNA methylation. IDH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP), though the functional significance of this altered epigenetic state remains unclear. Here we show that IDH1 mutant gliomas exhibit hyper-methylation at CTCF binding sites, leading to reduced binding of this methylation-sensitive insulator protein. Loss of CTCF binding is associated with a loss of insulation between topological domains and aberrant gene activation. We specifically demonstrate that loss of CTCF at a domain boundary permits a constitutive enhancer to aberrantly interact with the receptor tyrosine kinase gene PDGFRA, a prominent glioma oncogene. Treatment of IDH mutant gliomaspheres with demethylating agent partially restores insulator function and reduces PDGFRA expression. Conversely, CRISPR-mediated disruption of the CTCF binding sequence in IDH wildtype gliomaspheres induces PDGFRA expression and increases proliferation. Our study suggests that IDH mutations promote gliomagenesis by disrupting chromosomal topology and allowing aberrant regulatory interactions that induce oncogene expression. CTCF occupancy characterization and histone H3K27 acetylation profiling in IDH1 mutant and wild-type glioma patient specimens and culture models. ChIP-seq raw data is to be made available through dbGaP (controlled access) due to patient privacy concerns.

2015-12-23 | E-GEOD-70991 | biostudies-arrayexpress

Mutant IDH modulates suppressive myeloid populations in malignant glioma

Project description:RNA-sequencing for myeloid inflammation-related genes was conducted on primary tumor samples from patients with IDH-wildtype glioblastoma (GBM) and grade 4 IDH-mutant astrocytoma (G4IMA). In addition, the IDH-wildtype murine glioma cell line GL261 and a strain of IDH-mutant GL261 were also sequenced using the murine counterpart of the RNA-sequencing myeloid innate immunity panel.

2024-05-29 | GSE268118 | GEO

Mutant IDH disables p53 tumor suppression [RNA-seq]

Project description:p53 prevents tumor initiation and progression by adapting cell fate via transcriptional regulation of target gene networks. Here, we find that cancer associated mutations in isocitrate dehydrogenase (IDH) can uncouple p53 activity from tumor suppression by perturbing chromatin states that determine target gene expression. Mutant IDH impairs tumor regressions and promotes outgrowth of cancer cells with transcriptionally active, wild type p53 in a mouse model of liver cancer where restoration of p53 activity results in tumor clearance. Mutant IDH alters p53 target gene expression through the oncometabolite 2-hydroxyglutarate (2-HG), an inhibitor of alpha-ketoglutarate (KG) dependent chromatin remodeling enzymes, without preventing p53 accumulation or global genomic binding. Rather, mutant IDH alters chromatin accessibility landscapes that dictate target gene expression. Mutant IDH interferes with the expression of pro-apoptotic p53 targets, including the death ligand receptor Fas that enables p53 dependent liver tumor regressions. Pharmacological inhibition of mutant IDH in TP53 wildtype cholangiocarcinoma cells, a tumor type where p53 and IDH mutations are mutually exclusive, potentiates p53 target gene expression and sensitizes cells to Fas ligand and chemotherapy induced apoptosis. Therefore, we implicate disruption of p53 target gene regulation as a reversable, oncogenic feature of cancer associated IDH mutations.

2025-04-30 | GSE279597 | GEO

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