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MYB-QKI rearrangements in Angiocentric Glioma drive tumorigenicity through a tripartite mechanism

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4767685.pdf (3.11 MB)

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2016

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10.1038/ng.3500

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Bandopadhayay, P., L. A. Ramkissoon, P. Jain, G. Bergthold, J. Wala, R. Zeid, S. E. Schumacher, et al. 2016. “MYB-QKI rearrangements in Angiocentric Glioma drive tumorigenicity through a tripartite mechanism.” Nature genetics 48 (3): 273-282. doi:10.1038/ng.3500. http://dx.doi.org/10.1038/ng.3500.

Abstract

Angiocentric gliomas are pediatric low-grade gliomas (PLGGs) without known recurrent genetic drivers. We performed genomic analysis of new and published data from 249 PLGGs including 19 Angiocentric Gliomas. We identified MYB-QKI fusions as a specific and single candidate driver event in Angiocentric Gliomas. In vitro and in vivo functional studies show MYB-QKI rearrangements promote tumorigenesis through three mechanisms: MYB activation by truncation, enhancer translocation driving aberrant MYB-QKI expression, and hemizygous loss of the tumor suppressor QKI. This represents the first example of a single driver rearrangement simultaneously transforming cells via three genetic and epigenetic mechanisms in a tumor.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4767685/pdf/

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http://nrs.harvard.edu/urn-3:HUL.InstRepos:29002633

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