NRAS mutations are found in about 3 to 5% of colorectal cancers. A few in vitro studies using colorectal cancer cell lines expressing activated forms of N-RAS and in vivo studies using Nras mutant mouse models indicated that N-RAS activation confers resistance to stress-induced apoptosis. 



Our goal is to determine the molecular mechanisms linking mutant NRAS to resistance to apoptosis in order to find a more suitable therapeutic approach for colorectal cancer patients harboring NRAS mutations.