Journal
CANCER CELL
Volume 37, Issue 2, Pages 243-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2020.01.004
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Funding
- National Institutes of Health (NIH): Cancer Center [P30CA16672, P30CA034196, 3P30CA016672-41S7, R01 CA190121, R01 CA120813, P0 1CA207206]
- Agilent Technologies
- Boehringer Ingelheim Fonds
- German Academic Scholarship Foundation
- Jane Coffin Childs Memorial Fund for Medical Research
- JAX Scholar program [K99 CA226387]
- American Cancer Society Fellowship [130984-PF-17-141-01-DMC]
- Intramural Program of the National Cancer Institute, NIH [Z01-BC006161]
- NATIONAL CANCER INSTITUTE [ZIABC011696] Funding Source: NIH RePORTER
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Sporadic gliomas in companion dogs provide a window on the interaction between tumorigenic mechanisms and host environment. We compared the molecular profiles of canine gliomas with those of human pediatric and adult gliomas to characterize evolutionarily conserved mammalian mutational processes in gliomagenesis. Employing whole-genome, exome, transcriptome, and methylation sequencing of 83 canine gliomas, we found alterations shared between canine and human gliomas such as the receptor tyrosine kinases, TP53 and cell-cycle pathways, and IDH1 R132. Canine gliomas showed high similarity with human pediatric gliomas per robust aneuploidy, mutational rates, relative timing of mutations, and DNA-methylation patterns. Our cross-species comparative genomic analysis provides unique insights into glioma etiology and the chronology of glioma-causing somatic alterations.
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