MYB-QKI rearrangements in Angiocentric Glioma drive tumorigenicity through a tripartite mechanism
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Ramkissoon, Lori A.
Jain, Payal
Bergthold, Guillaume
Zeid, Rhamy
Schumacher, Steven E.
Urbanski, Laura
O’Rourke, Ryan
Pelton, Kristine
Ramkissoon, Shakti H.
Han, Harry J.
Zhu, Yuankun
Choudhari, Namrata
Silva, Amanda
Boucher, Katie
Henn, Rosemary E.
Kang, Yun Jee
Knoff, David
Gladden-Young, Adrianne
Varlet, Pascale
Pages, Melanie
Horowitz, Peleg M.
Federation, Alexander
Malkin, Hayley
Tracy, Adam
Seepo, Sara
Ducar, Matthew
Hummelen, Paul Van
Santi, Mariarita
Buccoliero, Anna Maria
Scagnet, Mirko
Bowers, Daniel C.
Giannini, Caterina
Puget, Stephanie
Hawkins, Cynthia
Tabori, Uri
Klekner, Almos
Bognar, Laszlo
Burger, Peter C.
Eberhart, Charles
Rodriguez, Fausto J.
Hill, D. Ashley
Mueller, Sabine
Phillips, Joanna J.
Stiles, Charles D.
Jabado, Nada
Goren, Alon
Grill, Jacques
Waanders, Angela J.
Storm, Phillip B.
Resnick, Adam C.
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1038/ng.3500Metadata
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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.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4767685/pdf/Terms of Use
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http://nrs.harvard.edu/urn-3:HUL.InstRepos:29002633
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