Lung cancers can use two different mechanisms to evade KRAS-inhibiting drugs

September 30, 2026
10:42 pm

About 25% 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 to overpower 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.

The researchers found that in some cases, lung tumors undergo transformation from adenocarcinoma to squamous cell carcinoma. Both of these tumor types are commonly found in the lungs, but they are thought to arise from different cells and have different genetic profiles.

Lung cancers can use two different mechanisms to evade KRAS-inhibiting drugs

About 25% 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.

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