Abstract
More information is needed about genetic factors that initiate development of pancreatic intraepithelial neoplasms-the most common precursors of pancreatic ductal adenocarcinoma. We show that more than 99% of the earliest-stage, lowest-grade, pancreatic intraepithelial neoplasm-1 lesions contain mutations in KRAS, p16/CDKN2A, GNAS, or BRAF. These findings could improve our understanding of the development and progression of these premalignant lesions.
Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Baltimore
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Carcinoma in Situ / genetics*
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Carcinoma in Situ / pathology
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Carcinoma, Pancreatic Ductal / genetics*
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Carcinoma, Pancreatic Ductal / pathology
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Chromogranins
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Cyclin-Dependent Kinase Inhibitor p16 / genetics
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DNA Mutational Analysis
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GTP-Binding Protein alpha Subunits, Gs / genetics
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Genetic Predisposition to Disease
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Humans
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Mutation*
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Neoplasm Staging
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Pancreatic Neoplasms / genetics*
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Pancreatic Neoplasms / pathology
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Phenotype
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins B-raf / genetics
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Proto-Oncogene Proteins p21(ras)
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ras Proteins / genetics
Substances
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Chromogranins
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Cyclin-Dependent Kinase Inhibitor p16
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KRAS protein, human
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Proto-Oncogene Proteins
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BRAF protein, human
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Proto-Oncogene Proteins B-raf
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GNAS protein, human
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GTP-Binding Protein alpha Subunits, Gs
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Proto-Oncogene Proteins p21(ras)
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ras Proteins