Lung tumors hijack nervous system to drive cancer-related cachexia

According to the Cleveland Clinic, a quarter of cancer deaths can be attributed to one source: cachexia. Cachexia is a syndrome that accompanies underlying chronic illness and causes unwanted muscle and fat loss, reducing quality of life and sometimes even limiting treatment options. A new study led by Thales Papagiannakopoulos, PhD, an incoming Salk professor, points to a potential new target for preventing cachexia.

The researchers found that a common genetic subset of lung cancer is more prone to cachexia and that tumors from this subtype talk to the brain through sensory neurons in the lung. Silencing these sensory nerves to disrupt the tumor-to-brain connection reduced cachexia, as did blocking the production of the lipid signaling molecule prostaglandin E2 (PGE2) through dietary changes. The team suspects that the tumors use PGE2 to communicate with the nervous system, suggesting that blocking this communication could be a powerful therapeutic strategy to improve patient outcomes.

"These lung cancer tumors are essentially controlling human behavior by tapping into the nervous system and hijacking local lung sensory neurons," says senior author Papagiannakopoulos, who conducted the research at the New York University (NYU) Grossman School of Medicine. "This role of the peripheral nervous system in cancer cachexia is entirely novel, and I think it could point us to really exciting translational opportunities that could drastically improve cancer care."

A 2015 German study reported that cachexia affects roughly half of cancer patients and also accompanies other chronic illnesses, like Alzheimer's disease or cardiovascular disease-ultimately impacting roughly 9 million people globally.