| Literature DB >> 26804919 |
Marie-Claude Gingras1, Kyle R Covington2, David K Chang3, Lawrence A Donehower4, Anthony J Gill5, Michael M Ittmann6, Chad J Creighton7, Amber L Johns8, Eve Shinbrot2, Ninad Dewal2, William E Fisher9, Christian Pilarsky10, Robert Grützmann11, Michael J Overman12, Nigel B Jamieson13, George Van Buren9, Jennifer Drummond2, Kimberly Walker2, Oliver A Hampton2, Liu Xi2, Donna M Muzny2, Harsha Doddapaneni2, Sandra L Lee2, Michelle Bellair2, Jianhong Hu2, Yi Han2, Huyen H Dinh2, Mike Dahdouli2, Jaswinder S Samra14, Peter Bailey15, Nicola Waddell16, John V Pearson16, Ivon Harliwong17, Huamin Wang18, Daniela Aust19, Karin A Oien20, Ralph H Hruban21, Sally E Hodges22, Amy McElhany22, Charupong Saengboonmee23, Fraser R Duthie20, Sean M Grimmond24, Andrew V Biankin3, David A Wheeler25, Richard A Gibbs2.
Abstract
The ampulla of Vater is a complex cellular environment from which adenocarcinomas arise to form a group of histopathologically heterogenous tumors. To evaluate the molecular features of these tumors, 98 ampullary adenocarcinomas were evaluated and compared to 44 distal bile duct and 18 duodenal adenocarcinomas. Genomic analyses revealed mutations in the WNT signaling pathway among half of the patients and in all three adenocarcinomas irrespective of their origin and histological morphology. These tumors were characterized by a high frequency of inactivating mutations of ELF3, a high rate of microsatellite instability, and common focal deletions and amplifications, suggesting common attributes in the molecular pathogenesis are at play in these tumors. The high frequency of WNT pathway activating mutation, coupled with small-molecule inhibitors of β-catenin in clinical trials, suggests future treatment decisions for these patients may be guided by genomic analysis.Entities:
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Year: 2016 PMID： 26804919 PMCID： PMC4982376 DOI： 10.1016/j.celrep.2015.12.005
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423