Note: Single-source report; awaiting corroboration.
Researchers investigated how lung tumors contribute to cachexia, a syndrome marked by appetite loss and wasting of muscle and fat. This condition is common in advanced cancers such as lung cancer and can reduce quality of life and survival.
The study, published July 2, 2026, in Science, examined three genetic subtypes of lung cancer in mouse models. Tumors grew similarly across models, but only mice with a mutation in the Lkb1 gene showed cachexia symptoms such as reduced eating, drinking, and activity. These mice did not gain weight on a high-fat diet, which instead worsened cachexia and increased signaling in brain regions that decrease appetite.
Researchers found that mice with the Lkb1 mutation had higher levels of signaling molecules like prostaglandin E2 (PGE2) in their lungs when fed a high-fat diet. PGE2 is linked to lung inflammation and was also elevated in people with lung cancer cachexia. Further experiments showed that lowering PGE2, either with anti-inflammatory drugs or dietary omega-3 fatty acids, eased cachexia symptoms in mice.
The study also revealed that sensory fibers of the vagus nerve, which connect the lungs with the brain, may promote cachexia. When these nerve fibers were eliminated in the lungs, mice with the Lkb1 mutation ate more normally despite their condition.
These findings suggest that lung tumors may drive cachexia by sending signals via the vagus nerve to the brain, reducing appetite especially with a high-fat diet. The results may help shape future strategies to improve nutrition and outcomes for cancer patients, pending further studies.