Treatment for pancreatic cancer had been static for decades despite the money and effort to find answers. But a significant breakthrough came this spring. A trial of a new drug called Daraxonrasib involving 500 patients with advanced pancreatic cancer lived for an extra 13 months compared with those on chemotherapy, which was half that.
While that might not seem like much, this breakthrough could have huge implications for cancers that are hard to treat, such as lung, colon, and pancreatic cancers. Some call Daraxonrasib the most important advancement in cancer treatment in 15 years.
The drug is an inhibitor of the Ras family of proteins, which are known to regulate cell growth. They turn on during cell growth and then should switch off, but in a Ras mutation, the protein is stuck in growth mode. This mutation is behind 20 percent of all human cancers, including a quarter of lung, half of colon, and 90 percent of pancreatic cancers. Even though we’ve known about these mutations, designing a drug to thwart the Ras protein has been tough. Because the mutated Ras protein is like a greaseball, a drug can’t latch on, like a climber without a ledge.
Scientists behind Daraxonrasib came up with a novel idea – by using molecular glue instead; a drug that can stick to another protein in the cell and then be large enough to wrap around the mutated protein to deactivate it. While it’s not a cure, the hope is that one day, combining the drug with other anti-cancer drugs will work against this cancer.
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Dana-Farber Cancer Institute: What is a RAS Mutation?
RAS is an oncogene, which is a gene that when mutated causes cancer. RAS — an abbreviation for rat sarcoma — is the most commonly mutated oncogene in human cancer. RAS mutations are found in 20% of all cancers and account for an estimated 260,000 cases per year in the U.S. and 3.4 million cases per year globally.