Publikation: Genomic landscape of diffuse glioma revealed by whole genome sequencing
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Diffuse gliomas are the commonest malignant primary brain tumour in adults. Herein, we present analysis of the genomic landscape of adult glioma, by whole genome sequencing of 403 tumours (256 glioblastoma, 89 astrocytoma, 58 oligodendroglioma; 338 primary, 65 recurrence). We identify an extended catalogue of recurrent coding and non-coding genetic mutations that represents a source for future studies and provides a high-resolution map of structural variants, copy number changes and global genome features including telomere length, mutational signatures and extrachromosomal DNA. Finally, we relate these to clinical outcome. As well as identifying drug targets for treatment of glioma our findings offer the prospect of improving treatment allocation with established targeted therapies.
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KINNERSLEY, Ben, Josephine JUNG, Alex J. CORNISH, Daniel CHUBB, Ross LAXTON, Anna FRANGOU, Andreas J. GRUBER, Amit SUD, Richard HOULSTON, Keyoumars ASHKAN, 2025. Genomic landscape of diffuse glioma revealed by whole genome sequencing. In: Nature Communications. Springer. 2025, 16(1), 4233. eISSN 2041-1723. Verfügbar unter: doi: 10.1038/s41467-025-59156-9BibTex
@article{Kinnersley2025-05-07Genom-74125,
title={Genomic landscape of diffuse glioma revealed by whole genome sequencing},
year={2025},
doi={10.1038/s41467-025-59156-9},
number={1},
volume={16},
journal={Nature Communications},
author={Kinnersley, Ben and Jung, Josephine and Cornish, Alex J. and Chubb, Daniel and Laxton, Ross and Frangou, Anna and Gruber, Andreas J. and Sud, Amit and Houlston, Richard and Ashkan, Keyoumars},
note={Article Number: 4233}
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<dcterms:abstract>Diffuse gliomas are the commonest malignant primary brain tumour in adults. Herein, we present analysis of the genomic landscape of adult glioma, by whole genome sequencing of 403 tumours (256 glioblastoma, 89 astrocytoma, 58 oligodendroglioma; 338 primary, 65 recurrence). We identify an extended catalogue of recurrent coding and non-coding genetic mutations that represents a source for future studies and provides a high-resolution map of structural variants, copy number changes and global genome features including telomere length, mutational signatures and extrachromosomal DNA. Finally, we relate these to clinical outcome. As well as identifying drug targets for treatment of glioma our findings offer the prospect of improving treatment allocation with established targeted therapies.</dcterms:abstract>
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