AI Article Synopsis
- Pdx1-Cre; LSL-KRAS(G12D) mice develop pancreatic ductal lesions that may progress to cancer, but the impact of KRAS(G12D) on endocrine pancreas has not been thoroughly studied.
- Histological analysis revealed that KRAS(G12D) expression leads to early disorganization in the endocrine compartment, including hyperplasia of endocrine lineages and unusual structures within islets.
- The findings suggest that KRAS(G12D) expression during embryonic development affects the endocrine pancreas, indicating a need to explore its implications for glucose metabolism and pancreatic cancer initiation.
Article 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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| http://dx.doi.org/10.1016/j.pan.2013.02.001 | DOI Listing |
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