In this study, we directly compared the propensity of ductal/CACs and acinar cells to form PanINs and investigated the molecular mechanisms that underlie PanIN formation.
As this final sentence of the introduction suggests, the authors hypothesized that pancreatic intraepithelial neoplasias (PanINs) and pancreatic ductal adenocarcinoma arise primarily through oncogenic KRAS-induced acinar-to-ductal reprogramming, rather than from centroacinar cells (CACs) or ductal cells, and that an inducer of ductal cell identity, SOX9, may play a role in the induction of PanINs to acinar cells.
Additionally, the authors noted that the tools needed to target CACs and ductal cells had only recently been developed, which made it possible to test this hypothesis and determine the actual origin of PanINs and PDA.