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Nature Research, Nature Genetics, 3(48), p. 273-282, 2016

DOI: 10.1038/ng.3500

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

Journal article published in 2016 by Pratiti Bandopadhayay, Lori A. Ramkissoon, Payal Jain, Guillaume Bergthold, Jeremiah Wala, Rhamy Zeid, Steven E. Schumacher, Laura Urbanski, Ryan O’Rourke, William J. Gibson, Kristine Pelton, Shakti H. Ramkissoon, Harry J. Han, Yuankun Zhu, Namrata Choudhari and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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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.