{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T22:59:14Z","timestamp":1790809154564,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,4,16]],"date-time":"2012-04-16T00:00:00Z","timestamp":1334534400000},"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;amp; Cancer"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Adenoid cystic carcinoma (ACC) of the head and neck is a malignant tumor with poor long\u2010term prognosis. Besides the recently identified <jats:italic>MYB\u2013NFIB<\/jats:italic> fusion oncogene generated by a t(6;9) translocation, little is known about other genetic alterations in ACC. Using high\u2010resolution, array\u2010based comparative genomic hybridization, and massively paired\u2010end sequencing, we explored genomic alterations in 40 frozen ACCs. Eighty\u2010six percent of the tumors expressed <jats:italic>MYB\u2013NFIB<\/jats:italic> fusion transcripts and 97% overexpressed <jats:italic>MYB<\/jats:italic> mRNA, indicating that <jats:italic>MYB<\/jats:italic> activation is a hallmark of ACC. Thirty\u2010five recurrent copy number alterations (CNAs) were detected, including losses involving 12q, 6q, 9p, 11q, 14q, 1p, and 5q and gains involving 1q, 9p, and 22q. Grade III tumors had on average a significantly higher number of CNAs\/tumor compared to Grade I and II tumors (<jats:italic>P<\/jats:italic> = 0.007). Losses of 1p, 6q, and 15q were associated with high\u2010grade tumors, whereas losses of 14q were exclusively seen in Grade I tumors. The t(6;9) rearrangements were associated with a complex pattern of breakpoints, deletions, insertions, inversions, and for 9p also gains. Analyses of fusion\u2010negative ACCs using high\u2010resolution arrays and massively paired\u2010end sequencing revealed that <jats:italic>MYB<\/jats:italic> may also be deregulated by other mechanisms in addition to gene fusion. Our studies also identified several down\u2010regulated candidate tumor suppressor genes (<jats:italic>CTNNBIP1<\/jats:italic>, <jats:italic>CASP9<\/jats:italic>, <jats:italic>PRDM2<\/jats:italic>, and <jats:italic>SFN<\/jats:italic>) in 1p36.33\u2010p35.3 that may be of clinical significance in high\u2010grade tumors. Further, studies of these and other potential target genes may lead to the identification of novel driver genes in ACC. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/gcc.21965","type":"journal-article","created":{"date-parts":[[2012,4,16]],"date-time":"2012-04-16T09:08:04Z","timestamp":1334567284000},"page":"805-817","source":"Crossref","is-referenced-by-count":148,"title":["Clinically significant copy number alterations and complex rearrangements of <i>MYB<\/i> and <i>NFIB<\/i> in head and neck adenoid cystic carcinoma"],"prefix":"10.1002","volume":"51","author":[{"given":"Marta","family":"Persson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ywonne","family":"Andr\u00e9n","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher 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