About 25 percent of lung adenocarcinomas have mutations of the gene KRAS, which drives uncontrolled cell growth. In recent years, the FDA has approved two KRAS inhibitors to treat patients with KRAS mutations. While these drugs can work well initially, tumors almost always develop resistance to them.
Usually, resistance emerges because cells reactivate KRAS activity, through mutations that prevent drug binding or by increasing KRAS expression that overpowers the effects of the inhibitor. However, in a new study, MIT researchers have modeled an alternative mechanism that cancer cells can use to become resistant to KRAS inhibition.