Journal
CANCER CELL
Volume 32, Issue 4, Pages 520-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2017.08.017
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Funding
- Cancer Research UK [C13468/A13982, C13468/A23536]
- CRIS Cancer Foundation
- Abbie's Army
- DIPG Collaborative
- Cure Starts Now Foundation
- McKenna Claire Foundation
- Lyla Nsouli Foundation
- National Institutes of Health [R01NS085336, R01NS091620]
- Dragon Master Foundation
- Kortney Rose Foundation
- Musella Foundation For Brain Tumor Research Information
- Gray Matters Foundation
- Pediatric Brain Tumor Foundation
- INSTINCT network - Brain Tumour Charity
- Great Ormond Street Children's Charity
- Children with Cancer UK
- NHS
- ICR
- Sao Paulo Research Foundation [2011/08523-7, 2012/08287-4]
- Christopher's Smile
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [11/08523-7] Funding Source: FAPESP
- Cancer Research UK [13982, 23536] Funding Source: researchfish
- Children with Cancer UK [14-175] Funding Source: researchfish
- Rosetrees Trust [M417, M200-F1] Funding Source: researchfish
- The Brain Tumour Charity [16/193] Funding Source: researchfish
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We collated data from 157 unpublished cases of pediatric high-grade glioma and diffuse intrinsic pontine glioma and 20 publicly available datasets in an integrated analysis of > 1,000 cases. We identified co-segregating mutations in histone-mutant subgroups including loss of FBXW7 in H3.3G34R/V, TOP3A rearrangements in H3.3K27M, and BCOR mutations in H3.1K27M. Histone wild-type subgroups are refined by the presence of key oncogenic events or methylation profiles more closely resembling lower-grade tumors. Genomic aberrations increase with age, highlighting the infant population as biologically and clinically distinct. Uncommon pathway dysregulation is seen in small subsets of tumors, further defining the molecular diversity of the disease, opening up avenues for biological study and providing a basis for functionally defined future treatment stratification.
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