Abstract

beta-catenin and Adenomatous poliposis coli (APC) have been implicated in non-ductal pancreatic cancers. As for many other organs, several recent publications show that beta-catenin and more largely the Wnt pathway appear to function at the level of pancreatic progenitors and endocrine cells during organogenesis. This raises the question of the cell type in which beta-catenin is mutated during tumor formation in acinar cell carcinomas, pancreatoblastomas and solid cystic papillary tumors of the pancreas.

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