Lewis Lab

Work in the Lewis lab is centered on the characterization of the roles for novel, and established, oncoproteins and tumor suppressors in the genesis and progression of pancreatic and hepatic carcinomas. The lab utilizes a variety of genetically engineered mouse models in these studies. Among other contributions, recent studies have demonstrated a critical role for the insulin-like growth factor receptor in PI3-kinase activation downstream of activated KRAS; the requirement for GLI transcription activation function during pancreatic tumorigenesis; and a novel paracrine WNT signaling mechanism that promotes the development of pancreatic mucinous cystic neoplasms. 

  • Rajurkar et al. (2012) The activity of Gli transcription factors is essential for Kras-induced pancreatic tumorigenesis. PNAS.  109(17): E1038-47.
  • Appleman et al. (2012) KRASG12D- and BRAFV600E-induced transformation of murine pancreatic epithelial cells requires MEK/ERK-stimulated IGF1R signaling. Mol Cancer Res. 10(9): 1228-39.
  • Sano et al. (2014) Activated Wnt Signaling in Stroma Contributes to Development of Pancreatic Mucinous Cystic Neoplasms. Gastroenterology.146(1): 257-67.