Genome wide methylation profliling of ETMR tumours.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE52556 | GEO | 2013/11/21
SECONDARY ACCESSION(S): PRJNA229379
REPOSITORIES: GEO
Similar Datasets
Project description:Genome wide DNA methylation profiling of normal, ETMR and PNET tumours Bisulphite converted DNA from 12 ETMR, 28 PNET and 34 control samples hybridised to the Illumina 450k Human Methylation Beadchip Please note that three of the 12 EMTR samples are tumor, cell line and xenograft sample derived from a single patient. Thus, there are 10 ETMR patients, 12 samples.
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Project description:Embryonal tumours with multilayered rosettes (ETMRs) are aggressive paediatric brain tumours driven in most cases by amplification of the chromosome 19 microRNA cluster (C19MC), which upregulates the oncogene MYCN. Whether MYCN dysregulation alone is sufficient to produce ETMR-like tumours, independent of the broader C19MC machinery, has not been tested. Here, we show that sustained MYCN expression in human neuroepithelial stem (NES) cells, i.e. primitive neural progenitors resembling the proposed cell of origin of ETMR, is sufficient to generate ETMR-like brain tumours in vivo. These tumours share methylation and transcriptional signatures with ETMR and reproduce its primitive, stem-like cellular hierarchy. MYCN-expressing tumour cells are arrested at an early neural progenitor stage, and MYCN withdrawal arrests growth and engages neuronal differentiation. Our findings identify sustained MYCN as sufficient to drive an ETMR-like developmental arrest in primitive human neural cells.
2026-07-17 | GSE338545 | GEO
Project description:Embryonal tumours with multilayered rosettes (ETMRs) are aggressive paediatric brain tumours driven in most cases by amplification of the chromosome 19 microRNA cluster (C19MC), which upregulates the oncogene MYCN. Whether MYCN dysregulation alone is sufficient to produce ETMR-like tumours, independent of the broader C19MC machinery, has not been tested. Here, we show that sustained MYCN expression in human neuroepithelial stem (NES) cells, i.e. primitive neural progenitors resembling the proposed cell of origin of ETMR, is sufficient to generate ETMR-like brain tumours in vivo. These tumours share methylation and transcriptional signatures with ETMR and reproduce its primitive, stem-like cellular hierarchy. MYCN-expressing tumour cells are arrested at an early neural progenitor stage, and MYCN withdrawal arrests growth and engages neuronal differentiation. Our findings identify sustained MYCN as sufficient to drive an ETMR-like developmental arrest in primitive human neural cells.
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Project description:Primitive neuro-ectodermal tumours (PNET) of the supratentorial region are rare, highly malignant embryonal brain tumours affecting young children. Although supratentorial PNET (sPNET) are histologically similar to infratentorial PNET/medulloblastoma, sPNET have more aggressive clinical phenotypes, which suggest sPNET represents distinct biological entities. In contrast to considerable progress in understanding the signalling pathways involved in medulloblastoma, little is known about sPNET pathogenesis. We utilized the Illumina Human-6 v2 Expression BeadChip platform to define pathways dysregulated in sPNET pathogenesis. Copy number analysis was also performed on an overlapping set of PNET tumours, also available on GEO with accession code GSE14087. Keywords: gene expression, pediatric brain tumour Raw BeadStudio output files (GSE14295_normalization-none*) linked below as Supplementary files. Supplementary File GSE14295_Array2SampleTitle_associations.txt maps Array IDs (e.g., 1814647101_B) to GEO Sample Titles (e.g., PNET2).
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Project description:Embryonal tumours with multilayered rosettes (ETMRs) are aggressive paediatric brain tumours driven in most cases by amplification of the chromosome 19 microRNA cluster (C19MC), which upregulates the oncogene MYCN. Whether MYCN dysregulation alone is sufficient to produce ETMR-like tumours, independent of the broader C19MC machinery, has not been tested. Here, we show that sustained MYCN expression in human neuroepithelial stem (NES) cells, i.e. primitive neural progenitors resembling the proposed cell of origin of ETMR, is sufficient to generate ETMR-like brain tumours in vivo. NanoString nCounter miRNA profiling was used to assess microRNA expression in this MYCN-only model, which lacks C19MC amplification.
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Project description:Primitive neuro-ectodermal tumours (PNET) of the supratentorial region are rare, highly malignant embryonal brain tumours affecting young children. Although supratentorial PNET (sPNET) are histologically similar to infratentorial PNET/medulloblastoma, sPNET have more aggressive clinical phenotypes, which suggest sPNET represents distinct biological entities. In contrast to considerable progress in understanding the signalling pathways involved in medulloblastoma, little is known about sPNET pathogenesis. Prior low resolution CGH (comparative genomic hybridization) studies indicate sPNET have frequent genomic imbalances and copy number aberrations (CNAs). To define genes involved in sPNET pathogenesis, we utilized the Affymetrix 250K Nsp SNP (single nucleotide polymorphism) analysis to identify genes targeted by recurrent CNAs in primary human sPNET samples. Copy number analysis was conducted on 39 primary PNET samples. Select target genes were validated by genomic and/or RT-PCR. Our analysis revealed frequent CNA across the sPNET genome, encompassing large and focal chromosome segments, and corroborated previous reports that isochromosome 17q, an abnormality found in ~ 30% of medulloblastoma, is rare in sPNET. Keywords: single nucleotide polymorphism array, disease state analysis
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Project description:A peptidomic analysis of plasma from patients with well characterised pancreatic neuroendocrine tumours (PNET) was performed. A nano LC-MS analysis identified a number of peptides from the glucagon gene, which were idenfiried in a previous case study using multiple immunoassays. Peptides to other proteins involved in peptide secretion were also identified. Plasma from a second glucagonoma patient was analysed using a high flow approach, and this identified similar peptides to the nano analysis. In order to demonstrate the potential clinical application of LC-MS to characterising neuroendocrine tumours, a large cohort of plasma samples were analysed to demonstrate the ability of this approach to identify glucagonoma patients, and differentiate from a single insulinoma patient
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Project description:Gene expression data from this ETMR cell line was compared with gene expression data from primary ETMR tumors to search for potential drug targets in ETMR tumors.
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