Researchers at the University of Illinois at Chicago have discovered a new way to stop the effects of genetic mutations in nearly 30% of cancer patients.
Gene mutations in the RAS family of proteins are present in nearly 90% of patients with pancreatic cancer and are also very prevalent in colon cancer, lung cancer, and melanoma (the most dangerous skin cancer).
This group of proteins includes three members: K-RAS, H-RAS, and N-RAS.
The prevalence of RAS mutations in human cancers and the dependence of tumor survival on RAS make RAS a major target for cancer research and drug discovery. Scientists and drug developers have long studied RAS oncogenes in hopes of finding a new way to treat cancer, but they have yet to find a drug that can safely inhibit oncogene activity.
A research team led by John O'Bryan, an associate professor of pharmacology at the University of Chicago School of Medicine, took a different approach to studying RAS and found a synthetic binding protein they called "NS1 monobody" (they were synthesized in the lab). Block the activity of the RAS protein.
O'Bryan, a member of the University of Illinois Cancer Center, said: "We didn't find a drug or a specific inhibitor." He held a meeting at the VA Medical Center in Jesse Brown, Chicago. “We use monoclonal antibody technology, a protein engineering technology, to identify RAS regions that are critical to its function.â€
Unlike traditional antibodies, monoclonal antibodies are not dependent on their environment and can be easily used as inhibitors of gene coding, O'Bryan said.
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