Project description:In this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify gene expression profiles We analysed gene expression in paediatric brain tumours as compared to normal adult brain in order to understand the molecular profiles. Our cohort included 15 pilocytic astrocytomas, 3 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 glioblastomas, 14 ependymomas, 9 medulloblastomas, 5 atypical teratoid/rhabdoid tumours, 4 choroid plexus papillomas, 8 adult brain and 8 foetal brain controls.
Project description:In this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify gene expression profiles
Project description:In this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify microRNA profiles We analysed the microRNA profiles in paediatric brain tumours as compared to normal adult brain. Our cohort included 14 pilocytic astrocytomas, 3 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 glioblastomas, 14 ependymomas, 9 medulloblastomas, 5 atypical teratoid/rhabdoid tumours, 4 choroid plexus papillomas, 1 papillary glioneuronal, and 7 adult brain controls.
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.
Project description:DNA methylation is increasingly used for tumour classification and has expanded upon the > 100 currently known brain tumour entities. A correct diagnosis is the basis for suitable treatment for patients with brain tumours, which is the leading cause of cancer-related death in children. DNA methylation profiling is required for diagnosis of certain tumours, and used clinically for paediatric brain tumours in several countries. We therefore evaluated if the methylation-based classification is robust in different locations of the same tumour, and determined how the methylation pattern changed over time to relapse.
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.
Project description:We have used Illumina Infinium HumanMethylation450 BeadChip array profiling to profile paediatric high grade gliomas within the HERBY clinical trial. The HERBY trial was a phase-II open-label, randomised, multicentre trial evaluating bevacizumab in patients with newly-diagnosed non-brainstem HGG between the ages of 3-18yrs. The 450K methylation array was 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.
