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To elucidate the mechanisms of malignant progression of lower-grade glioma, molecular profiling using methylation array, whole-exome sequencing, and RNA sequencing was performed for 122, 36 and 31 gliomas, respectively. This cohort included 24 matched pairs of initial lower-grade gliomas and recurrent tumors, most of which showed malignant progression. Nearly half of IDH-mutant glioblastomas that had progressed from lower-grade gliomas exhibited characteristic partial DNA demethylation in previously methylated genomic regions of their corresponding initial tumors, which had the glioma CpG island methylator phenotype (G-CIMP). In these glioblastomas, cell cycle-related genes, RB and PI3K-AKT pathway genes were frequently altered. Notably, late-replicating domain was significantly enriched in the demethylated regions that were mostly located in non-regulatory regions, suggesting that the loss of DNA methylation during malignant transformation may involve mainly passive demethylation due to a delay in maintenance of methylation during accelerated cell division. Nonetheless, a limited number of genes including IGF2BP3, which potentially drives cell proliferation, were presumed to be upregulated due to demethylation of their promoter. Our data indicated that demethylation of the G-CIMP profile found in a subset of recurrent gliomas reflects accelerated cell divisions accompanied by malignant transformation. Oncogenic genes activated by such epigenetic change represent potential therapeutic targets.
Pubmed ID: 30760837
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Bioinformatics resource system including web server and web service for functional annotation and enrichment analyses of gene lists. Consists of comprehensive knowledgebase and set of functional analysis tools. Includes gene centered database integrating heterogeneous gene annotation resources to facilitate high throughput gene functional analysis.
View all literature mentionsA service for permanent archiving and sharing of all types of personally identifiable genetic and phenotypic data resulting from biomedical research projects. The JGA contains exclusive data collected from individuals whose consent agreements authorize data release only for specific research use or to bona fide researchers. Strict protocols govern how information is managed, stored and distributed by the JGA. Once processed, all data are encrypted. The JGA accepts only de-identified data approved by JST-NBDC. The JGA implements access-granting policy whereby the decisions of who will be granted access to the data resides with the JST-NBDC. After data submission the JGA team will process the data into databases and archive the original data files. The accepted data types include manufacturer-specific raw data formats from the array-based and new sequencing platforms. The processed data such as the genotype and structural variants or any summary level statistical analyses from the original study authors are stored in databases. The JGA also accepts and distributes any phenotype data associated with the samples. For other human biological data, please contact the NBDC human data ethical committee.
View all literature mentionsCommercial vendor and service provider of laboratory reagents and antibodies. Supplier of scientific instrumentation, reagents and consumables, and software services.
View all literature mentionsSoftware tool designed for mapping short reads onto a reference genome generated from Illumina, Ion Torrent, and 454 NGS platforms. Its features include paired end alignment, methylation status analysis, automatic base quality calibration, and in built adapter trimming and base quality trimming.
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