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Ena-DATASET-INSTITUTE OF CANCER RESEARCH-17-12-2013-15:02:33:112-168 - samples

ABSTRACT: Whole genome sequencing of 20 tumour and normal pairs of diffuse intrinsic pontine glioma (DIPG)

PROVIDER: EGAD00001000705 | EGA |

REPOSITORIES: EGA

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Recurrent activating ACVR1 mutations in diffuse intrinsic pontine glioma.

Taylor Kathryn R KR Mackay Alan A Truffaux Nathalène N Butterfield Yaron Y Morozova Olena O Philippe Cathy C Castel David D Grasso Catherine S CS Vinci Maria M Carvalho Diana D Carcaboso Angel M AM de Torres Carmen C Cruz Ofelia O Mora Jaume J Entz-Werle Natacha N Ingram Wendy J WJ Monje Michelle M Hargrave Darren D Bullock Alex N AN Puget Stéphanie S Yip Stephen S Jones Chris C Grill Jacques J

Nature genetics 20140406 5

Diffuse intrinsic pontine gliomas (DIPGs) are highly infiltrative malignant glial neoplasms of the ventral pons that, due to their location within the brain, are unsuitable for surgical resection and consequently have a universally dismal clinical outcome. The median survival time is 9-12 months, with neither chemotherapeutic nor targeted agents showing substantial survival benefit in clinical trials in children with these tumors. We report the identification of recurrent activating mutations in ...[more]

PMID: 24705252

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Senescence induced by BMI1 inhibition is a therapeutic vulnerability in H3K27M-mutant DIPG

Project description:We studied the effect of BMI1 inhibition in diffuse intrinsic pontine glioma cells (DIPG). We reported the application of chromatin immunoprecipitation sequencing for high-thoughput profiling of BMI1 and H2AK119ub in diffuse intrinsic pontine glioma cells (DIPG) in response to BMI1 inhibition. We also performed bulk RNA sequencing of DIPG cells in response to pharmacological inhibition or knockdown of BMI1.

2020-10-22 | GSE140768 | GEO

ena-DATASET-INSTITUTE OF CANCER RESEARCH-17-12-2013-15:22:20:271-113 - samples

Project description:Whole exome sequencing of 6 tumour and normal pairs of diffuse intrinsic pontine glioma (DIPG)

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Genome-wide localization of RNA polymerase II and histone modifications in diffuse intrinsic pontine glioma cells in response to CDK9 inhibition

Project description:We report the application of chromatin immunoprecipitation for high-thoughput profiling of RNA polymerase II and histone modifications (H3K27me3 and H3K27ac) in diffuse intrinsic pontine glioma cells (DIPG) in response to CDK9 inhibition

2020-04-12 | GSE129777 | GEO

Project description:Diffuse Intrinsic Pontine Glioma

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Proteomic analysis of chemical and genetic EZH2 inhibition in diffuse intrinsic pontine glioma cell lines

Project description:Diffuse Intrinsic Pontine Glioma (DIPG) is a rare and highly aggressive pediatric tumor. The average survival time after diagnosis is less than one year. Currently, there are no effective treatments. Characteristic of DIPG is a mutation in histone H3 which leads to a substitution of Lysine 27 to Methionine (H3K27M) which deregulates Polycomb Repressive Complex 2 (PRC2), including enzymatic activity of EZH2. Previous studies have shown that inhibition of EZH2 by chemical agents decreases DIPG cell proliferation and inhibits tumor growth in vivo. My thesis project aims to confirm that EZH2 could be a therapeutic target using chemical EZH2 inhibitors, small interfering RNAs and a CRISPR/Cas9 approach in a series of DIPG tumor cell lines and to determine underlying molecular mechanisms of action.

2022-04-01 | PXD017525 | Pride

Non-inflammatory tumor microenvironment of Diffuse Intrinsic Pontine Glioma (DIPG)

Project description:Non-inflammatory tumor microenvironment of Diffuse Intrinsic Pontine Glioma (DIPG)

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Pharmacologic inhibition of histone demethylation as a therapy for pediatric brainstem glioma [ChIP-seq]

Project description:ChIP-Seq analysis of a pediatric human diffuse intrinsic pontine glioma (DIPG) cell line SF8628, harboring the K27M mutation. Goal was to obtain quantitative estimates of K27me3 immunoprecipitation change between vehicle-treated SF8628 cells [dimethyl sulfoxide, (DMSO)] and SF8628 cells incubated with 6 mM GSKJ4 at 24 hours and 72 hours. Three-condition experiment: 72 h GSKJ4-treated cells vs. 24 h GSKJ4-treated cells vs. DMSO-treated cells. Biological replicates: 1 cell line, each with 2 technical replicates per condition.

2014-07-20 | E-GEOD-59496 | biostudies-arrayexpress

Pharmacologic inhibition of histone demethylation as a therapy for pediatric brainstem glioma [ChIP-seq]

2014-07-20 | GSE59496 | 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

Functionally-defined Therapeutic Targets in DIPG

Project description:<p>Diffuse Intrinsic Pontine Glioma (DIPG) is a universally fatal childhood cancer. Here, we performed a chemical screen in patient-derived DIPG cell cultures along with RNAseq expression analysis and integrated computational modeling to identify potentially effective therapeutic strategies. Panobinostat, among the more promising agents identified, demonstrated efficacy in pontine orthotopic xenograft models of both H3K27M and histone WT DIPG. These data suggest the potential utility of specific drug combinations and provides evidence of in vivo treatment efficacy of the multi-histone deacetylase inhibitor panobinostat. We are depositing to dbGaP deep sequencing whole exome data for 22 patient tumor samples and 13 matched normals, along with RNAseq data for 12 patient tumor samples and 6 normal pediatric brain tissue samples. In addition, we are depositing 22 RNAseq samples from DIPG cell lines before and after panobinostat treatment.</p>

| phs000900 | dbGaP

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