| Literature DB >> 30166462 |
Nathaniel D Anderson1,2, Richard de Borja1, Matthew D Young3, Fabio Fuligni1, Andrej Rosic1, Nicola D Roberts3, Simon Hajjar1, Mehdi Layeghifard1, Ana Novokmet1, Paul E Kowalski1, Matthew Anaka1, Scott Davidson4, Mehdi Zarrei5, Badr Id Said1, L Christine Schreiner1, Remi Marchand1, Joseph Sitter1, Nalan Gokgoz6, Ledia Brunga1, Garrett T Graham7, Anthony Fullam3, Nischalan Pillay8,9, Jeffrey A Toretsky7, Akihiko Yoshida10, Tatsuhiro Shibata11,12, Markus Metzler13, Gino R Somers2,14, Stephen W Scherer1,5,15,16, Adrienne M Flanagan9,10, Peter J Campbell3,17, Joshua D Schiffman18, Mary Shago2,4, Ludmil B Alexandrov19, Jay S Wunder20,21, Irene L Andrulis6,15, David Malkin22,23,24, Sam Behjati25,26, Adam Shlien22,2,4.
Abstract
Sarcomas are cancers of the bone and soft tissue often defined by gene fusions. Ewing sarcoma involves fusions between EWSR1, a gene encoding an RNA binding protein, and E26 transformation-specific (ETS) transcription factors. We explored how and when EWSR1-ETS fusions arise by studying the whole genomes of Ewing sarcomas. In 52 of 124 (42%) of tumors, the fusion gene arises by a sudden burst of complex, loop-like rearrangements, a process called chromoplexy, rather than by simple reciprocal translocations. These loops always contained the disease-defining fusion at the center, but they disrupted multiple additional genes. The loops occurred preferentially in early replicating and transcriptionally active genomic regions. Similar loops forming canonical fusions were found in three other sarcoma types. Chromoplexy-generated fusions appear to be associated with an aggressive form of Ewing sarcoma. These loops arise early, giving rise to both primary and relapse Ewing sarcoma tumors, which can continue to evolve in parallel.Entities:
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Year: 2018 PMID: 30166462 PMCID: PMC6176908 DOI: 10.1126/science.aam8419
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728