Abstract
Pancreatic cancer is a genetic disease. Pancreatic cancers develop from one of three precursor lesions, pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasms (IPMNs), and mucinous cystic neoplasms (MCNs), and each arises in association with distinct genetic alterations. These alterations not only provide insight into the fundamental origins of pancreatic cancer but provide ample opportunity for improving early diagnosis and management of cystic precursors.
Copyright © 2012 Wiley Periodicals, Inc.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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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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Cell Transformation, Neoplastic / genetics*
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Chromogranins
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Cystadenocarcinoma, Mucinous / genetics*
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Cystadenocarcinoma, Mucinous / pathology
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DNA-Binding Proteins / metabolism
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Disease Progression
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GTP-Binding Protein alpha Subunits, Gs / metabolism
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Humans
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Mutation
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Oncogene Proteins / metabolism
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Pancreatic Neoplasms / genetics*
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Pancreatic Neoplasms / pathology
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Ubiquitin-Protein Ligases
Substances
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Chromogranins
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DNA-Binding Proteins
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Oncogene Proteins
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RNF43 protein, human
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Ubiquitin-Protein Ligases
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GNAS protein, human
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GTP-Binding Protein alpha Subunits, Gs