{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T03:01:25Z","timestamp":1792119685120,"version":"4.4.0"},"reference-count":38,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2017,7,1]],"date-time":"2017-07-01T00:00:00Z","timestamp":1498867200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp; Cancer"],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Gene fusions resulting from structural rearrangements are an established mechanism of tumorigenesis in pediatric cancer. In this clinical cohort, 1,350 single nucleotide polymorphism (SNP)\u2010based chromosomal microarrays from 1,211 pediatric cancer patients were evaluated for copy number alterations (CNAs) associated with gene fusions. Karyotype or fluorescence in situ hybridization studies were performed in 42% of the patients. Ten percent of the bone marrow or solid tumor specimens had SNP array\u2010associated CNAs suggestive of a gene fusion. Alterations involving\n                    <jats:italic>ETV6<\/jats:italic>\n                    ,\n                    <jats:italic>ABL1\u2010NUP214<\/jats:italic>\n                    ,\n                    <jats:italic>EBF1\u2010PDGFRB<\/jats:italic>\n                    ,\n                    <jats:italic>KMT2A(MLL), LMO2\u2010RAG<\/jats:italic>\n                    ,\n                    <jats:italic>MYH11\u2010CBFB<\/jats:italic>\n                    ,\n                    <jats:italic>NSD1\u2010NUP98<\/jats:italic>\n                    ,\n                    <jats:italic>PBX1<\/jats:italic>\n                    ,\n                    <jats:italic>STIL\u2010TAL1, ZNF384\u2010TCF3<\/jats:italic>\n                    ,\n                    <jats:italic>P2RY8\u2010CRLF2<\/jats:italic>\n                    , and\n                    <jats:italic>RUNX1T1\u2010RUNX1<\/jats:italic>\n                    fusions were detected in the bone marrow samples. The most common alteration among the low\u2010grade gliomas was a 7q34 tandem duplication resulting in a\n                    <jats:italic>KIAA1549\u2010BRAF<\/jats:italic>\n                    fusion. Additional fusions identified in the pediatric brain tumors included\n                    <jats:italic>FAM131B\u2010BRAF<\/jats:italic>\n                    and\n                    <jats:italic>RAF1\u2010QKI<\/jats:italic>\n                    .\n                    <jats:italic>COL1A1\u2010PDGFB<\/jats:italic>\n                    ,\n                    <jats:italic>CRTC1\u2010MAML2<\/jats:italic>\n                    ,\n                    <jats:italic>EWSR1<\/jats:italic>\n                    ,\n                    <jats:italic>HEY1<\/jats:italic>\n                    ,\n                    <jats:italic>PAX3<\/jats:italic>\n                    \u2010 and\n                    <jats:italic>PAX7\u2010FOXO1<\/jats:italic>\n                    , and\n                    <jats:italic>PLAG1<\/jats:italic>\n                    fusions were determined in a variety of solid tumors and a novel potential gene fusion,\n                    <jats:italic>FGFR1\u2010USP6,<\/jats:italic>\n                    was detected in an aneurysmal bone cyst. The identification of these gene fusions was instrumental in tumor diagnosis. In contrast to hematologic and solid tumors in adults that are predominantly driven by mutations, the majority of hematologic and solid tumors in children are characterized by CNAs and gene fusions. Chromosomal microarray analysis is therefore a robust platform to identify diagnostic and prognostic markers in the clinical setting.\n                  <\/jats:p>","DOI":"10.1002\/gcc.22477","type":"journal-article","created":{"date-parts":[[2017,6,9]],"date-time":"2017-06-09T05:53:36Z","timestamp":1496987616000},"page":"730-749","source":"Crossref","is-referenced-by-count":21,"title":["Copy number alterations determined by single nucleotide polymorphism array testing in the clinical laboratory are indicative of gene fusions in pediatric cancer patients"],"prefix":"10.1002","volume":"56","author":[{"given":"Tracy M.","family":"Busse","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Children's Hospital of Los Angeles Center for Personalized Medicine Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacquelyn J.","family":"Roth","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Hospital of the University of Pennsylvania Philadelphia Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donna","family":"Wilmoth","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine The Children's Hospital of Philadelphia Philadelphia Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luanne","family":"Wainwright","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine The Children's Hospital of Philadelphia Philadelphia Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Tooke","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine The Children's Hospital of Philadelphia Philadelphia Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9270-6411","authenticated-orcid":false,"given":"Jaclyn 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