Journal
CELL REPORTS
Volume 14, Issue 4, Pages 907-919Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.12.005
Keywords
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Categories
Funding
- HGSC-BCM: NHGRI [U54 HG003273]
- CPRIT grant [RP101353-P7, RPI21018]
- Dan L. Duncan Cancer Center NIH P30 Cancer Center [P30 CA125123]
- Kavanagh Family Foundation
- Australian Pancreatic Cancer Genome Initiative: National Health and Medical Research Council of Australia (NHMRC) [631701, 535903, 427601]
- Queensland Government (NIRAP)
- University of Queensland
- Institute for Molecular Bioscience
- Cancer Research UK [C596/A18076, C29717/A17263]
- University of Glasgow
- Australian Government: Department of Innovation, Industry, Science and Research (DIISR)
- Australian Cancer Research Foundation (ACRF)
- Cancer Council NSW [SRP06-01, SRP11-01.ICGC]
- Cancer Institute NSW [10/ECF/2-26, 06/ECF/1-24, 09/CDF/2-40, 07/CDF/1-03, 10/CRF/1-01, 08/RSA/1-15, 07/CDF/1-28, 10/CDF/2-26, 10/FRL/2-03, 06/RSA/1-05, 09/RIG/1-02, 10/TPG/1-04, 11/REG/1-10, 11/CDF/3-26]
- Garvan Institute of Medical Research
- Avner Nahmani Pancreatic Cancer Research Foundation
- Howat Foundation
- R.T. Hall Trust
- Petre Foundation
- Philip Hemstritch Foundation
- Gastroenterological Society of Australia (GESA)
- American Association for Cancer Research (AACR) Landon Foundation - INNOVATOR Award
- Royal Australasian College of Surgeons (RACS)
- Royal Australasian College of Physicians (RACP)
- Royal College of Pathologists of Australasia (RCPA)
- Italian Ministry of Research [FIRB RBAP10AHJB]
- Associazione Italiana Ricerca Cancro [12182]
- Fondazione Italiana Malattie Pancreas - Ministero Salute [CUP_J33G13000210001]
- Wilhelm Sander Stiftung [2009.039.2]
- NIH [P50 CA62924]
- Academy of Medical Sciences (AMS) [AMS-SGCL9-Jamieson] Funding Source: researchfish
- Cancer Research UK [17263] Funding Source: researchfish
- Pancreatic Cancer UK [FLF2015_04_Glasgow] Funding Source: researchfish
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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 beta-catenin in clinical trials, suggests future treatment decisions for these patients may be guided by genomic analysis.
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