DNA methylation profiling of primary medulloblastoma samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE85212 | GEO | 2017/06/13
SECONDARY ACCESSION(S): PRJNA336573
REPOSITORIES: GEO
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Project description:We undertook a comprehensive clinical and biological investigation of serial medulloblastoma biopsies obtained at diagnosis and relapse. Combined MYC gene family amplifications and P53 pathway defects commonly emerged at relapse, and all patients in this molecular group died of rapidly progressive disease post-relapse. To study this genetic interaction, we investigated a transgenic model of MYCN-driven medulloblastoma and found spontaneous development of Trp53 inactivating mutations. Abrogation of Trp53 function in this model produced aggressive tumors that mimicked the characteristics of relapsed human tumors with combined P53-MYC dysfunction. Restoration of p53 activity, genetic and therapeutic suppression of MYCN all reduced tumor growth and prolonged survival. Our findings identify P53–MYC interactions which emerge at medulloblastoma relapse as biomarkers of clinically aggressive disease that may be targeted therapeutically. Using this dataset, assignation of medulloblastoma molecular subgroup by Illumina 450k microarray was performed for diagnostic and relapsed medulloblastoma samples to compare subgroup membership at diagnosis and relapse.
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Project description:Smoothened (SMO)-inhibitors recently entered clinical trials for sonic-hedgehog driven medulloblastoma (SHH-MB). Clinical response appears highly variable. To understand the mechanism(s) of primary resistance and to identify pathways co-operating with aberrant SHH-signaling, we sequenced a large cohort of SHH-MBs across all age groups by sequencing, DNA methylation and expression profiling. Our data show that most adults but only half of the pediatric patients with SHH-MB will respond to SMO inhibition as predicted by molecular analysis of the primary tumor and tested in the SHH-xenografts, demonstrating that the next generation of SMO-inhibitor trials should be based on these predictive biomarkers. To further dissect the biological differences between the different age groups within SHH medulloblastomas, we looked at the DNA methylation profiles of SHH medulloblastoma samples.
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Project description:Smoothened (SMO)-inhibitors recently entered clinical trials for sonic-hedgehog driven medulloblastoma (SHH-MB). Clinical response appears highly variable. To understand the mechanism(s) of primary resistance and to identify pathways co-operating with aberrant SHH-signaling, we sequenced a large cohort of SHH-MBs across all age groups by sequencing, DNA methylation and expression profiling. Our data show that most adults but only half of the pediatric patients with SHH-MB will respond to SMO inhibition as predicted by molecular analysis of the primary tumor and tested in the SHH-xenografts, demonstrating that the next generation of SMO-inhibitor trials should be based on these predictive biomarkers. To further dissect the biological differences between the different age groups within SHH medulloblastomas, we looked at the DNA methylation profiles of SHH medulloblastoma samples.
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Project description:Robust molecular subgrouping and copy-number profiling of medulloblastoma from small amounts of archival tumor material. Validation of patterns identified by whole-genome bisulphite sequencing in a larger cohort. DNA methylation profiles of 276 primary medulloblastoma and 8 normal cerebellum control samples were generated from fresh-frozen and formalin-fixed paraffin-embedded material using the Illumina 450k methylation array.
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Project description:Extensive high-throughput sequencing led to the characterization of four main medulloblastoma subgroups. However, to date these analyses have not attained a global comprehension of their dynamic network complexity. Wishing to get a comprehensive view of all medulloblastoma subgroups, we employed a proteomic analysis to integrate accurate protein activity. In this study we present the first analysis regrouping genomic and methylation status, whole-transcriptome sequencing and quantitative proteomics. First, our proteomic analysis clarified medulloblastoma subgroup identity. Second, analysis of proteome and phosphoproteome highlighted disregulated signalling pathways that have not been predicted by transcriptomic analysis. Altogether, combined multi-scale analyses of medulloblastoma have allowed us to identify and prioritize novel molecular drivers involved in human medulloblastoma.
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