Mutations in the gene that encodes the KRAS protein are frequently encountered in various human cancers. They are found in about 30% of non-small cell lung cancers (NSCLCs), making KRAS the single most common gene mutated in this cancer. The rate of KRAS mutations in other cancers, such as pancreatic or colorectal, is even higher.
A mutant KRAS protein that is always in the “on” position activates many signaling pathways, many of which lead to unrestrained growth and proliferation of cancer cells. This makes KRAS an appealing treatment target. However, challenges abound, and researchers are exploring several different approaches to treating KRAS-mutant cancers.
Unlike mutations in proteins known as receptor tyrosine kinases, like EGFR or ALK, mutated KRAS is a very difficult protein to target with cancer drugs. (So much so that the National Institutes of Health (NIH) has undertaken a special effort to intensify the effort towards successful targeting of mutant KRAS, known as the RAS Initiative.) Continue reading…
“Cancers driven by the RAS oncogene are aggressive and difficult to treat, and thus far precision drugs haven’t been able to target the mutant RAS gene successfully.
“But in a presentation at the American Association for Cancer Research Annual Meeting on Monday, April 3, 2017 at 10:30 a.m., in Washington DC, Dana-Farber Cancer Institute scientists said a number of patients in a small study with RAS-driven lung, ovarian, and thyroid cancers got long-term clinical benefit from a combination of two drugs that targeted molecular pathways controlled by the RAS gene.
” ‘Between one-quarter and one-third of patients got long-term clinical benefit,’ said Geoffrey Shapiro, MD, PhD, director of Dana-Farber’s Early Drug Development Center. ‘Several patients were on the drugs for more than a year, and one patient has been on treatment for two and a half years. And these were heavily-treated patients without many options.’ ”