Lung Cancer Research
In the late 1990s, University of Kentucky Professor Douglas Andres found that mutations in a protein known as RIT1 could initiate cancer development in laboratory models.
RIT1 works as a molecular switch. Responding to signals from outside the cell, it turns on fundamental cellular activities, and turns them off again so they don’t continue unchecked.
“Proteins like RIT1 control everything from how cells differentiate to how they grow,” Andres said. “In a disease like cancer, they often get broken in the ‘on’ position. The cells that have RIT1 mutations constantly grow, even though they don’t receive the necessary signals from the environment.”
When Andres’ initial application for funding was declined for lack of evidence, he didn’t lose hope. “I never really give up on anything,” he said.
Alice Berger, a postdoctoral researcher in Professor Matthew Meyerson’s laboratory at Broad Institute of MIT and Harvard, provided the necessary evidence. The research teams led by Andres and Meyerson showed Andres hypothesize was correct. RIT1 mutations in human lung cancers can transform non-cancerous cells into cancerous ones.
Andres has finally been awarded a two-year, $150,000 grant from the Kentucky Lung Cancer Research Program to expand upon his initial discovery.
Andres said, “With the grant we received, we will push the work forward. We hope this will lead to greater understanding of RIT1 mutations and how tumors containing them may differ from other lung tumors.”
Andres hopes to use the results to develop new tests that can diagnose RIT1-mutant lung cancers in patients. This awareness could lead to developing therapies that specifically kill cancer cells containing RIT1 mutations.
“Each time that we gain fundamental insight into a problem – that is an exhilaration,” Andres said. “Sometimes it happens in six months of work, or, in this case, it's taken 15 years between our initial discovery and our ideas actually coming to fruition.”