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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

ABSTRACT: The brain tumor immune microenvironment (TIME) continuously evolves during glioma progression, but only a limited view of a highly complex glioma associated immune contexture across isocitrate dehydrogenase mutation (IDH) classified gliomas is known. Herein, we present an unprecedentedly comprehensive view of myeloid and lymphoid cell type diversity with our m-RNA sequencing interrogation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE222518 | GEO | 2024/06/23

REPOSITORIES: GEO

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

Project description:The brain tumor immune microenvironment (TIME) continuously evolves during glioma progression, but only a limited view of a highly complex glioma associated immune contexture across isocitrate dehydrogenase mutation (IDH) classified gliomas is known. Herein, we present an unprecedentedly comprehensive view of myeloid and lymphoid cell type diversity with our single cell RNA sequencing interrogation.

2024-06-23 | GSE222520 | GEO

Gene expression profile of T cells from Isocitrate Dehydrogenase (IDH) stratified human gliomas at single cell level

Project description:The brain tumor immune microenvironment (TIME) continuously evolves during glioma progression, but only a limited view of a highly complex glioma associated immune contexture across isocitrate dehydrogenase mutation (IDH) classified gliomas is known. Herein, we present an unprecedentedly comprehensive view of T cells from brain TIME at single cell resolution, which served as part of our pan-cancer T cell atlas analysis.

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-05 | GSE222522 | GEO

Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

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Gene expression profile of T cells from Isocitrate Dehydrogenase (IDH) stratified human gliomas at single cell level

Project description:Gene expression profile of T cells from Isocitrate Dehydrogenase (IDH) stratified human gliomas at single cell level

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Zinc Finger MYND-Type Containing 8 (ZMYND8) is epigenetically regulated in mutant Isocitrate Dehydrogenase 1 (IDH1) glioma to promote radioresistance [RNA-seq]

Project description:Mutant isocitrate dehydrogenase 1 (mIDH1) alters the epigenetic regulation of chromatin, leading to a hypermethylation phenotype in adult glioma. This work focuses on identifying gene targets epigenetically dysregulated by mIDH1 to confer therapeutic resistance to ionizing radiation (IR). We evaluated changes in the transcriptome and epigenome in a radioresistant mIDH1 patient-derived glioma cell culture (GCC) following treatment with an mIDH1 specific inhibitor AGI-5198. We identified Zinc Finger MYND-Type Containing 8 (ZMYND8) as potential target of mIDH1 reprogramming. We suppressed ZMYND8 expression by shRNA knockdown and genetic knockout (KO) in mIDH1 glioma cells then assessed cellular viability to IR. We assessed the sensitivity of mIDH1 GCCS to pharmacological inhibition of ZMYND8-interacting partners: HDAC, BRD4, and PARP. Inhibition of mIDH1 lead to an upregulation of gene networks involved in replication stress. We found that the expression of ZMYND8, a regulator of DNA damage response was decreased in three patient-derived mIDH1 GCCs after treatment with AGI-5198. Knockdown of ZMYND8 expression sensitized mIDH1 GCCs to radiotherapy marked by decreased cellular viability. Following IR, mIDH1 glioma cells with ZMYND8 knockout (KO) exhibit significant phosphorylation of ATM and sustained γH2AX activation. ZMYND8 KO mIDH1 GCCs were further responsive to IR when treated with either BRD4 or HDAC inhibitors. PARP inhibition further enhanced the efficacy of radiotherapy in ZMYND8 KO mIDH1 glioma cells. These findings indicate the impact of ZMYND8 in the maintenance of genomic integrity and repair of IR-induced DNA damage in mIDH1 glioma.

2022-12-19 | GSE220716 | GEO

Zinc Finger MYND-Type Containing 8 (ZMYND8) is epigenetically regulated in mutant Isocitrate Dehydrogenase 1 (IDH1) glioma to promote radioresistance [ChIP-seq]

2022-12-19 | GSE220715 | GEO

Isocitrate protects DJ-1 null dopaminergic cells from oxidative stress through NADP+-dependent isocitrate dehydrogenase (IDH).

Project description:DJ-1 is one of the causative genes for early onset familiar Parkinson's disease (PD) and is also considered to influence the pathogenesis of sporadic PD. DJ-1 has various physiological functions which converge on controlling intracellular reactive oxygen species (ROS) levels. In RNA-sequencing analyses searching for novel anti-oxidant genes downstream of DJ-1, a gene encoding NADP+-dependent isocitrate dehydrogenase (IDH), which converts isocitrate into ?-ketoglutarate, was detected. Loss of IDH induced hyper-sensitivity to oxidative stress accompanying age-dependent mitochondrial defects and dopaminergic (DA) neuron degeneration in Drosophila, indicating its critical roles in maintaining mitochondrial integrity and DA neuron survival. Further genetic analysis suggested that DJ-1 controls IDH gene expression through nuclear factor-E2-related factor2 (Nrf2). Using Drosophila and mammalian DA models, we found that IDH suppresses intracellular and mitochondrial ROS level and subsequent DA neuron loss downstream of DJ-1. Consistently, trimethyl isocitrate (TIC), a cell permeable isocitrate, protected mammalian DJ-1 null DA cells from oxidative stress in an IDH-dependent manner. These results suggest that isocitrate and its derivatives are novel treatments for PD associated with DJ-1 dysfunction.

| S-EPMC5578699 | biostudies-literature

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