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Ampullary Cancers Harbor ELF3 Tumor Suppressor Gene Mutations and Exhibit Frequent WNT Dysregulation
Author(s) -
MarieClaude Gingras,
Kyle R. Covington,
David K. Chang,
Lawrence A. Donehower,
Anthony J. Gill,
Michael Ittmann,
Chad J. Creighton,
Amber L. Johns,
Eve Shinbrot,
Ninad Dewal,
William E. Fisher,
Christian Pilarsky,
Robert Grützmann,
Michael J. Overman,
Nigel B. Jamieson,
George Van Buren,
Jennifer Drummond,
Kimberly Walker,
Oliver Hampton,
Xi Liu,
Donna M. Muzny,
HarshaVardhan Doddapaneni,
Sandra L. Lee,
Michelle Bellair,
Taobo Hu,
Yi Han,
Huyen Dinh,
Mike Dahdouli,
Jaswinder S. Samra,
Peter J. Bailey,
Nicola Waddell,
John V. Pearson,
Ivon Harliwong,
Huamin Wang,
Daniela E. Aust,
Karin Oien,
Ralph H. Hruban,
Sally E. Hodges,
Amy L. McElhany,
Charupong Saengboonmee,
Fraser R. Duthie,
Sean M. Grimmond,
Andrew V. Biankin,
David A. Wheeler,
Richard A. Gibbs
Publication year - 2016
Publication title -
cell reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.264
H-Index - 154
eISSN - 2639-1856
pISSN - 2211-1247
DOI - 10.1016/j.celrep.2015.12.005
Subject(s) - wnt signaling pathway , biology , microsatellite instability , cancer research , adenocarcinoma , mutation , suppressor , ampulla of vater , pathogenesis , ampulla , gene , tumor suppressor gene , carcinogenesis , genetics , cancer , carcinoma , microsatellite , immunology , anatomy , allele
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.

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