Study: Lung Tumors May Cause Cachexia by Hacking Nervous System
A new study from NYU Langone Health reveals a pathway where lung tumors can induce cachexia, a wasting condition leading to weight and muscle loss. The findings could point to new treatment strategies.
Researchers at NYU Langone Health and its Perlmutter Cancer Center have identified a mechanism by which lung tumors can trigger cachexia, a debilitating condition characterized by progressive weight loss, muscle wasting, and a persistent feeling of sickness.
The study, published in the journal Science, determined that lung tumors lacking the LKB1 gene produce elevated levels of prostaglandin E2. This signaling molecule locally amplifies inflammation and signals via the vagus nerve to the brain, leading to reduced appetite and exacerbated cachexia, even when mice were fed a high-calorie diet.
Experiments showed that mice with LKB1-deficient lung tumors experienced worsened cachexia on a high-fat diet, linked to increased prostaglandin E2. By blocking prostaglandin E2 production or vagus nerve signaling, researchers were able to reduce weight loss and improve survival in these animal models.
The research suggests that this short-range communication between tumors and nearby neurons may be a key driver of cachexia, shifting focus from solely systemic causes. The aim is to improve patients' ability to tolerate cancer treatments.
These findings indicate that interfering with prostaglandin E2 production or signaling pathways could offer novel therapeutic approaches for managing cachexia in cancer patients, potentially improving their quality of life and treatment outcomes.