Pancreatic ductal adenocarcinoma (PDAC) has long been considered to arise from pancreatic ducts on the basis of its morphology, the occurrence of dysplasia in putative preneoplastic ductal lesions, and the absence of acinar dysplasia in the pancreas of patients with PDAC. However, evidence gathered through both in vitro studies and—more importantly—genetic mouse models of PDAC shows that ductal-type tumours can arise from acinar cells. These findings raise new important questions related to PDAC pathophysiology and call for in-depth studies of acinar cell differentiation in order to better understand PDAC biology. The authors review these issues and discuss how the novel findings should impact on future work aiming at early diagnosis and improved outcome of patients with PDAC.
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Funding This work was partially funded by grant 10/FRL/2-03 from the Cancer Institute, NSW (to IR) and grants SAF2007-60860 and ONCOBIO Consolider from Ministerio de Ciencia e Innovación (Madrid, Spain) and grant EPC-TM-NET from the EU 7th Framework Programme (to FXR).
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.
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