MD Anderson scientists have connected the dots between mutated versions of Kras, a gene that acts as a molecular on-off switch, and heightened activity of a protein complex that controls gene activation in cases of pancreatic cancer.
The study, headed by Paul Chiao, Ph.D., a professor in MD Anderson's Department of Molecular and Cellular Oncology, identified a "vicious cycle" of molecular activity and new potential target for drugs.
The research suggests interleukin-1 alpha as a potential therapeutic target, says Chiao. The study shows that mutationally activated Kras triggers a chain reaction, which activates inhibitor-blocking proteins. This in turn cycles back, pepetuating the loop.
Grants from the National Cancer Institute, including MD Anderson's Cancer Center Core Support Grant, funded the research.