SOUTH CAROLINA: New method of targeting mutant RAS provides hope for cancer patients
Medical University of South Carolina (MUSC) Hollings Cancer Center researcher John O’Bryan and colleagues have demonstrated a new therapeutic way to block a protein that is frequently mutated in cancers. These proof-of-principle findings were published in Cell Reports. This work, which involves inhibiting the oncogenic protein RAS using small molecules, lays a strong foundation for the development of clinical anti-cancer therapies and provides a framework for other groups to target RAS in more effective ways. “The RAS protein, which was considered undruggable, is in fact able to be targeted by drugs,” said O’Bryan.
The researchers are very hopeful that this discovery can be used more comprehensively in the future. While cancers do adapt and mutate to become resistant to therapeutics, new drugs based on this concept might serve as additional tools in the arsenal to treat cancer.
O’Bryan, who is a professor in the Department of Cell and Molecular Pharmacology and Experimental Therapeutics at the MUSC, said, “RAS is one of the most central and critical regulators of cell proliferation, and it is also the most mutated in cancers. Mutated RAS drives the growth of tumors. This makes it an attractive therapeutic target.”
The RAS family of proteins are mutated in nearly 20% of human tumors; however, there has been little progress in drug development for this target. “Think of RAS as a slick ball that does not let anything bind to it. Until recently, it was thought that mutant RAS could not be targeted with drugs. Now there is one FDA-approved drug for mutant RAS in lung cancer, which demonstrates that it is possible to target mutant RAS in some cases,” said O’Bryan.