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Utilizing Omomyc to Target MYCN-Amplified Diffuse Intrinsic Pontine Gliomas

ABSTRACT: Utilizing Omomyc to Target MYCN-Amplified Diffuse Intrinsic Pontine Gliomas

PROVIDER: PRJNA833664 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19019096_1.fastq.gz	Fastqsanger.gz
	SRR19019096_2.fastq.gz	Fastqsanger.gz
	SRR19019097_1.fastq.gz	Fastqsanger.gz
	SRR19019097_2.fastq.gz	Fastqsanger.gz
	SRR19019098_1.fastq.gz	Fastqsanger.gz

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Utilizing Omomyc to Target MYCN-Amplified Diffuse Intrinsic Pontine Gliomas

Project description:Genomic studies have shown that several types of pediatric brain tumors have dysregulation of MYC family members (c-MYC and MYCN). In fact, it has been estimated that about 50% of all human cancers have increased MYC, and this is correlated with tumor aggression and poor survival. Here we focus on targeting the MYCN oncogene in diffuse intrinsic pontine glioma (DIPG). DIPG has the worst prognosis of any pediatric brain tumor and is in desperate need of viable treatment options. Here we demonstrate that using a 90-amino acid peptide, termed “Omomyc” we are able to down-regulate endogenous MYCN and inhibit growth of MYCN overexpressing DIPG cells. Furthermore, Omomyc binds to promoter regions normally occupied by MYCN to affect transcription of a subset of genes including PLK1 and LDHA, among others. In vivo expression of Omomyc in DIPG cells implanted in mice slows disease progression, suggesting that MYCN targets are important for driving rapid tumor growth and may offer insight into potential targets for treatment of MYCN driven DIPGs.

2023-12-01 | GSE201936 | GEO

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.

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

Illumina Infinium HumanMethylation450 BeadChip profiling of paediatric high grade gliomas and diffuse intrinsic pontine gliomas

Project description:We have used Illumina Infinium HumanMethylation450 BeadChip array profiling to profile paediatric high grade gliomas and diffuse intrinsic pontine gliomas. The 450K methylation array is being used to separate brain tumour samples on the basis of their methylation profiles which represent the cell of origin the time and place in which tumours arise. Methylation arrays provide data for an integrated molecular diagnosis of brain tumours and define specific molecular subgroups and subtypes of high grade gliomas carrying distinct driver mutations and patterns of somatic alterations. These data form part of an integrated meta-analysis of high grade gliomas in children combining DNA copy number, methylation and high throughput sequencing datasets.

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Pembrolizumab in Treating Younger Patients With Recurrent, Progressive, or Refractory High-Grade Gliomas, Diffuse Intrinsic Pontine Gliomas, Hypermutated Brain Tumors, Ependymoma or Medulloblastoma

Project description:This phase I trial studies the side effects and best dose of pembrolizumab and to see how well it works in treating younger patients with high-grade gliomas (brain tumors that are generally expected to be fast growing and aggressive), diffuse intrinsic pontine gliomas (brain stem tumors), brain tumors with a high number of genetic mutations, ependymoma or medulloblastoma that have come back (recurrent), progressed, or have not responded to previous treatment (refractory). Immunotherapy with monoclonal antibodies, such as pembrolizumab, may induce changes in the body’s immune system, and may interfere with the ability of tumor cells to grow and spread.

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Genome-wide Analyses of Diffuse Intrinsic Pontine Gliomas

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Circulating microRNA profiling in diffuse intrinsic pontine gliomas

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Circulating microRNA profiling in diffuse intrinsic pontine gliomas

Project description:Circulating microRNA profiling in diffuse intrinsic pontine gliomas

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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: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

Targeting SWI/SNF ATPases in H3.3K27M Diffuse Intrinsic Pontine Gliomas

Project description:Targeting SWI/SNF ATPases in H3.3K27M Diffuse Intrinsic Pontine Gliomas

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