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SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE225029 | GEO | 2025/02/08

REPOSITORIES: GEO

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SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [CUT&RUN]

Project description:To identify potential direct targets of SUV39H1, we performed Cut&Run-seq for H3K9me3 and SUV39H1 genomic occupancy

2025-02-08 | GSE225028 | GEO

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [RNA-seq]

Project description:To investigate Chaetocin impact on Diffuse intrinsic pontine gliomas treatment We then performed gene expression profiling analysis using data obtained from RNA-seq of Chaetocin treatment and SUV39H1 knockdown in SU-DIPG36 cells

2025-02-08 | GSE225027 | GEO

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas

Project description:SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas

| PRJNA933586 | ENA

SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [CUT&RUN]

Project description:SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [CUT&RUN]

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SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [RNA-seq]

Project description:SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas [RNA-seq]

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Diffuse intrinsic pontine gliomas: new waves.

Project description: Not available

| S-EPMC3280815 | biostudies-literature

Genome-wide Analyses of Diffuse Intrinsic Pontine Gliomas

Project description:Purpose: More than 90% of children with diffuse intrinsic pontine glioma (DIPG) die within 2 years of diagnosis. There is a dire need to identify therapeutic targets, however lack of patient material for research has limited progress. We evaluated a large cohort of diffuse intrinsic pontine gliomas (DIPGs) to identify recurrent genomic abnormalities and gene expression signatures underlying DIPG. Patients and Methods: We used single nucleotide polymorphism arrays to evaluate genomic copy number imbalances in 43 DIPGs from 40 patients and in 8 low-grade exophytic brainstem gliomas. Gene expression arrays were used to evaluate expression signatures from 27 DIPGs, 6 low-grade exophytic brainstem gliomas and 66 low-grade gliomas arising outside the brainstem. Results: Frequencies of specific large-scale and focal imbalances varied significantly between DIPGs and pediatric glioblastomas outside the brainstem. Focal amplifications of genes within the receptor tyrosine kinase-Ras-PI3-kinase signaling pathway were found in 47% of DIPG, with PDGFRA and MET showing the highest frequency. 30% of DIPG contained focal amplifications of cell-cycle regulatory genes controlling RB phosphorylation, and 21% had concurrent amplification of genes from both pathways. Some tumors showed heterogeneity in amplification patterns. DIPGs showed distinct gene expression signatures relating to developmental processes compared to pediatric glioblastomas arising outside the brainstem, while expression signatures of low-grade exophytic brainstem gliomas were similar to low-grade gliomas outside the brainstem. Copy number analaysis: 43 DIPG samples, 8 Low Grade Gliomas using SNP6.0. Available matched normals are also profiled with SNP6.0. Expression analysis: 29 DIPG samples, 6 Low grade samples Please contact Suzanne Baker at Suzanne.Baker@stjude.org for CEL files and genotype calls.

| S-ECPF-GEOD-26576 | biostudies-other

Genome-wide Analyses of Diffuse Intrinsic Pontine Gliomas

2011-09-20 | E-GEOD-26576 | biostudies-arrayexpress

Mesenchymal transition and PDGFRA amplification/mutation are key distinct oncogenic events in pediatric diffuse intrinsic pontine gliomas.

Project description:Diffuse intrinsic pontine glioma (DIPG) is one of the most frequent malignant pediatric brain tumor and its prognosis is universaly fatal. No significant improvement has been made in last thirty years over the standard treatment with radiotherapy. To address the paucity of understanding of DIPGs, we have carried out integrated molecular profiling of a large series of samples obtained with stereotactic biopsy at diagnosis. While chromosomal imbalances did not distinguish DIPG and supratentorial tumors on CGHarrays, gene expression profiling revealed clear differences between them, with brainstem gliomas resembling midline/thalamic tumours, indicating a closely-related origin. Two distinct subgroups of DIPG were identified. The first subgroup displayed mesenchymal and pro-angiogenic characteristics, with stem cell markers enrichment consistent with the possibility to grow tumor stem cells from these biopsies. The other subgroup displayed oligodendroglial features, and appeared largely driven by PDGFRA, in particular through amplification and/or novel missense mutations in the extracellular domain. Patients in this later group had a significantly worse outcome with an hazard ratio for early deaths, ie before 10 months, 8 fold greater that the ones in the other subgroup (p = 0.041, Cox regression model). The worse outcome of patients with the oligodendroglial type of tumors was confirmed on a series of 55 paraffin-embedded biopsy samples at diagnosis (median OS of 7.73 versus 12.37 months, p = 0.045, log-rank test). Two distinct transcriptional subclasses of DIPG with specific genomic alterations can be defined at diagnosis by oligodendroglial differentiation or mesenchymal transition, respectively. Classifying these tumors by signal transduction pathway activation and by mutation in pathway member genes may be particularily valuable for the development of targeted therapies.

| S-EPMC3289615 | biostudies-literature

Targeting SWI/SNF ATPases in H3.3K27M diffuse intrinsic pontine gliomas.

Project description:Diffuse midline gliomas (DMGs) including diffuse intrinsic pontine gliomas (DIPGs) bearing lysine-to-methionine mutations in histone H3 at lysine 27 (H3K27M) are lethal childhood brain cancers. These tumors harbor a global reduction in the transcriptional repressive mark H3K27me3 accompanied by an increase in the transcriptional activation mark H3K27ac. We postulated that H3K27M mutations, in addition to altering H3K27 modifications, reprogram the master chromatin remodeling switch/sucrose nonfermentable (SWI/SNF) complex. The SWI/SNF complex can exist in two main forms termed BAF and PBAF that play central roles in neurodevelopment and cancer. Moreover, BAF antagonizes PRC2, the main enzyme catalyzing H3K27me3. We demonstrate that H3K27M gliomas show increased protein levels of the SWI/SNF complex ATPase subunits SMARCA4 and SMARCA2, and the PBAF component PBRM1. Additionally, knockdown of mutant H3K27M lowered SMARCA4 protein levels. The proteolysis targeting chimera (PROTAC) AU-15330 that simultaneously targets SMARCA4, SMARCA2, and PBRM1 for degradation exhibits cytotoxicity in H3.3K27M but not H3 wild-type cells. AU-15330 lowered chromatin accessibility measured by ATAC-Seq at nonpromoter regions and reduced global H3K27ac levels. Integrated analysis of gene expression, proteomics, and chromatin accessibility in AU-15330-treated cells demonstrated reduction in the levels of FOXO1, a key member of the forkhead family of transcription factors. Moreover, genetic or pharmacologic targeting of FOXO1 resulted in cell death in H3K27M cells. Overall, our results suggest that H3K27M up-regulates SMARCA4 levels and combined targeting of SWI/SNF ATPases in H3.3K27M can serve as a potent therapeutic strategy for these deadly childhood brain tumors.

| S-EPMC10161095 | biostudies-literature

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