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Publication : MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism.

First Author  Bandopadhayay P Year  2016
Journal  Nat Genet Volume  48
Issue  3 Pages  273-82
PubMed ID  26829751 Mgi Jnum  J:231978
Mgi Id  MGI:5775686 Doi  10.1038/ng.3500
Citation  Bandopadhayay P, et al. (2016) MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism. Nat Genet 48(3):273-82
abstractText  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 that 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. To our knowledge, 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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