Molecular pathways in pancreatic carcinogenesis.
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.
Pathobiology Program, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Anne M
AM
Macgregor-Das
Christine A
CA
Iacobuzio-Donahue
D002278:Carcinoma in Situ / Q000235:genetics* / Q000473:pathology; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics* / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D002864:Chromogranins; D018282:Cystadenocarcinoma, Mucinous / Q000235:genetics* / Q000473:pathology; D004268:DNA-Binding Proteins / Q000378:metabolism; D018450:Disease Progression; D019205:GTP-Binding Protein alpha Subunits, Gs / Q000378:metabolism; D006801:Humans; D009154:Mutation; D015513:Oncogene Proteins / Q000378:metabolism; D010190:Pancreatic Neoplasms / Q000235:genetics* / Q000473:pathology; D044767:Ubiquitin-Protein Ligases
D002864:Chromogranins; D004268:DNA-Binding Proteins; D015513:Oncogene Proteins; C496945:RNF43 protein, human; D044767:Ubiquitin-Protein Ligases; C406732:GNAS protein, human; D019205:GTP-Binding Protein alpha Subunits, Gs