Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer death in the United States and a major unsolved health problem worldwide with nearly all patients succumbing to their disease. Currently, there are limited effective treatment options for PDAC. K-ras oncogenic mutations are found in >90% of advanced PDAC in human patients and are thought to be initiating events in PDAC development. Moreover, K-ras mutations appear to be required for tumor maintenance, making K-ras an attractive therapeutic target. In our lab, we have developed several K-ras-induced PDAC mouse models that recapitulate the progression and histology of human PDAC. Using tumors and stable cell lines derived from these models to manipulate gene function and perform sequencing, expression profiling, and proteomic analyses, we are studying the role of K-ras in PDAC. A better understanding of the biology underlying the requirement for K-ras in pancreatic tumors may offer novel diagnostic biomarkers and more effective combination therapies against PDAC.
Immunofluorescence staining of Pancreatic ductal adenocarcinoma (PDAC) cells. Nuclear DNA (blue - DAPI), F-actin (red - phalloidin), and Paxillin (green).