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  • Title: The conditional expression of KRAS G12D in mouse pancreas induces disorganization of endocrine islets prior the onset of ductal pre-cancerous lesions.
    Author: Gout J, Pommier RM, Vincent DF, Ripoche D, Goddard-Léon S, Colombe A, Treilleux I, Valcourt U, Tomasini R, Dufresne M, Bertolino P, Bartholin L.
    Journal: Pancreatology; 2013; 13(3):191-5. PubMed ID: 23719586.
    Abstract:
    BACKGROUND/OBJECTIVES: Pdx1-Cre; LSL-KRAS(G12D) mice develop premalignant pancreatic ductal lesions that can possibly progress spontaneously to pancreatic ductal adenocarcinoma (PDAC). Although Pdx1-Cre is expressed in the embryonic endoderm, which gives rise to all pancreatic lineages, the possible consequences of KRAS(G12D) expression in the endocrine compartment have never been finely explored. METHODS: We examined by histology whether Pdx1-driven expression of KRAS(G12D) could induce islets of Langerhans defects. RESULTS: We observed in Pdx1-Cre; LSL-KRAS(G12D) early disorganization of the endocrine compartment including i) hyperplasia affecting all the endocrine lineages, ii) ectopic onset of Ck19-positive (ductal-like) structures within the endocrine islets, and iii) the presence of islet cells co-expressing glucagon and insulin, all occurring before the onset of ducts lesions. CONCLUSIONS: This work indicates that expression of KRAS(G12D) in Pdx1-expressing cells during embryogenesis affects the endocrine pancreas, and highlights the need to deepen possible consequences on both glucose metabolism and PDAC initiation.
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