Oncogenic Kras maintains Pancreatic Tumors through Regulation of Anabolic Glucose Metabolism

We used an inducible KrasG12D-driven PDAC mouse model to establish that advanced PDAC remains strictly dependent on KrasG12D expression. This work provides in vivo mechanistic insights into how oncogenic Kras promotes metabolic reprogramming in native tumors and illuminates potential metabolic targets that can be exploited for therapeutic benefit.

Read the Abstract

Download the PDF

Get Insights From Ron

Sign up for the latest news and updates from Ron DePinho, MD