Growing cancer cells divert glucose and other nutrients away from energy-producing pathways towards those that make complex molecules that can be used as building blocks. The cancer gene Kras promotes this diversion in pancreatic cancer.
Using a mouse model of the most common type of pancreatic cancer, Alec Kimmelman at the Dana-Farber Cancer Institute in Boston, Massachusetts, Ronald DePinho, now at the MD Anderson Cancer Center in Houston, Texas, and their colleagues show that the pancreatic tumours need mutant Kras to survive. The mutant protein shunts glucose metabolism towards two pathways — one that adds sugars to proteins and another that makes precursors for DNA and RNA synthesis — by downregulating a glucose transporter and other key enzymes.
The enzymes altered by mutant Kras represent potential new drug targets, the authors conclude.