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By using 244 K high\u2010resolution array\u2010comparative genomic hybridization (aCGH) we studied the genome alterations of 39 fine\u2010needle aspirations from pancreatic adenocarcinoma and eight human adenocarcinoma pancreatic cell lines. Using both visual inspection and GISTIC analysis, recurrent losses were observed on 1p, 3p, 4p, 6, 8p, 9, 10, 11q, 15q, 17, 18, 19p, 20p, 21, and 22 and comprised several known or suspected tumor suppressor genes such as <jats:italic>ARHGEF10, ARID1A, CDKN2A\/B, FHIT, PTEN, RB1, RUNX1\u20103, SMAD4, STK11\/LKB1, TP53,<\/jats:italic> and <jats:italic>TUSC3<\/jats:italic>. Heterozygous deletion of the 1p35\u2010p36 chromosomal region was identified in one\u2010third of the tumors and three of the cell lines. This region, commonly deleted in human cancers, contains several tumor suppressor genes including <jats:italic>ARID1A<\/jats:italic> and <jats:italic>RUNX3<\/jats:italic>. We identified frequent genetic gains on chromosome arms 1q, 3q, 5p, 6p, 7q, 8q, 12q, 15q, 18q, 19q, and 20q. Amplifications were observed in 16 tumors. <jats:italic>AKT2, CCND3, CDK4, FOXA2, GATA6, MDM2, MYC,<\/jats:italic> and <jats:italic>SMURF1<\/jats:italic> genes were gained or amplified. The most obvious amplification was located at 18q11.2 and targeted the <jats:italic>GATA6<\/jats:italic> gene, which plays a predominant role in the initial specification of the pancreas and in pancreatic cell type differentiation. In conclusion, we have identified novel biomarkers and potential therapeutic targets in pancreatic adenocarcinoma. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gcc.20870","type":"journal-article","created":{"date-parts":[[2011,3,15]],"date-time":"2011-03-15T19:45:02Z","timestamp":1300218302000},"page":"456-465","source":"Crossref","is-referenced-by-count":107,"title":["Genome profiling of pancreatic adenocarcinoma"],"prefix":"10.1002","volume":"50","author":[{"given":"David 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