Christian Veltkamp, Benedikt Feuerecker, Constanze Mattes, Nina Schönhuber, Kathleen Schuck, Barbara Seidler, Markus Schwaiger, Roland M Schmid, Günter Schneider, Dieter Saur. (03-08-2015).

47th Annual Meeting of the European Pancreatic Club, 2015

Department: 

Research Area C

Abstract: 

Genetically engineered mouse models have dramatically improved our understanding of tumor evolution and therapeutic resistance. Recently, we showed that cell-autonomous PI3K and Pdk1 are key effectors of oncogenic Kras in the pancreas, mediating formation of pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma (PDAC). Pdk1 deletion blocked pancreatic carcinogenesis completely in a Cre/loxP-based model indicating its importance in tumor initiation. However, sequential genetic manipulation of gene expression is almost impossible using traditional Cre/loxP-based models.