Acvr1b Loss Increases Formation of Pancreatic Precancerous Lesions From Acinar and Ductal Cells of Origin.

ABSTRACT:

Background & aims

Pancreatic ductal adenocarcinoma can develop from precursor lesions, including pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasm (IPMN). Previous studies indicated that loss of Acvr1b accelerates the Kras-mediated development of papillary IPMN in the mouse pancreas; however, the cell type predominantly affected by these genetic changes remains unclear.

Methods

We investigated the contribution of cellular origin by inducing IPMN associated mutations (KRAS^G12D expression and Acvr1b loss) specifically in acinar (Ptf1a^CreER;Kras^LSL-G12D;Acvr1b^fl/fl mice) or ductal (Sox9CreER;Kras^LSL-G12D;Acvr1b^fl/fl mice) cells in mice. We then performed magnetic resonance imaging a

SUBMITTER: Saeki K 

PROVIDER: S-EPMC11404226 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature