Abstract:
:An enormous amount of tumor sequencing data has been generated through large scale sequencing efforts. The functional consequences of the majority of mutations identified by such projects remain an open, unexplored question. This problem is particularly complicated in the case of rare mutations where frequency of occurrence alone or prediction of functional consequences are insufficient to distinguish driver from passenger or bystander mutations. We combine genome editing technology with a powerful mouse cancer model to uncover previously unsuspected rare oncogenic mutations in Burkitt's lymphoma. We identify two candidate tumor suppressors whose loss cooperate with MYC over-expression to accelerate lymphomagenesis. Our results highlight the utility of in vivo CRISPR/Cas9 screens combined with powerful mouse models to identify and validate rare oncogenic modifier events from tumor mutational data.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Katigbak A,Cencic R,Robert F,Sénécha P,Scuoppo C,Pelletier Jdoi
10.1038/srep38968subject
Has Abstractpub_date
2016-12-16 00:00:00pages
38968issn
2045-2322pii
srep38968journal_volume
6pub_type
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