{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T20:20:13Z","timestamp":1792182013783,"version":"4.4.0"},"reference-count":43,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6405","funder":[{"name":"SickKids Foundation"},{"DOI":"10.13039\/501100017559","name":"Garron Family Cancer Centre","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100017559","id-type":"DOI","asserted-by":"crossref"}]},{"name":"The Ewings Cancer Foundation of Canada"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2018,8,31]]},"abstract":"<jats:title>Looping together genes in cancer<\/jats:title>\n                  <jats:p>\n                    A subset of human cancers are characterized by aberrant fusion of two specific genes. In some cases, the activity of the resultant fusion protein drives tumor growth. Most fusion genes in cancer appear to arise from simple reciprocal chromosomal translocations. Anderson\n                    <jats:italic>et al.<\/jats:italic>\n                    found that the characteristic fusion gene in a bone and soft tissue tumor called Ewing sarcoma is produced by a far more complicated mechanism (see the Perspective by Imielinski and Ladanyi). In nearly half of the tumors examined, the fusion gene was created by the formation of dramatic genomic loops that disrupt multiple genes. These complex rearrangements occur in early replicating and transcriptionally active regions of the genome and are associated with poor prognosis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Science<\/jats:italic>\n                    , this issue p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" related-article-type=\"in-this-issue\" xlink:href=\"10.1126\/science.aam8419\">eaam8419<\/jats:related-article>\n                    ; see also p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" issue=\"6405\" page=\"848\" related-article-type=\"in-this-issue\" vol=\"361\" xlink:href=\"10.1126\/science.aau8231\">848<\/jats:related-article>\n                  <\/jats:p>","DOI":"10.1126\/science.aam8419","type":"journal-article","created":{"date-parts":[[2018,8,30]],"date-time":"2018-08-30T14:07:41Z","timestamp":1535638061000},"source":"Crossref","is-referenced-by-count":163,"title":["Rearrangement bursts generate canonical gene fusions in bone and soft tissue tumors"],"prefix":"10.1126","volume":"361","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4523-6327","authenticated-orcid":true,"given":"Nathaniel D.","family":"Anderson","sequence":"first","affiliation":[{"name":"Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, Ontario, Canada."},{"name":"Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8181-6348","authenticated-orcid":true,"given":"Richard","family":"de Borja","sequence":"additional","affiliation":[{"name":"Program in Genetics and Genome Biology, The 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