How to Stop Cancer Cachexia? Start at the Top

Targeting IL-6 binding to AP neurons in brain may be effective approach

Neurons (blue) in a part of the brain called the area postrema, seen here, express a variety of genes, including receptors for the immune system molecule IL-6 (white). (Credit: Li lab/Cold Spring Harbor Laboratory).

Cancer is insidious. Throughout tumor progression, the disease hijacks otherwise healthy biological processes—like the body’s immune response—to grow and spread. When tumors elevate levels of an immune system molecule called interleukin-6 (IL-6), it can cause severe brain dysfunction. In about 50%-80% of cancer patients, this leads to a lethal wasting disease called cachexia. “It’s a very severe syndrome,” says Cold Spring Harbor Laboratory (CSHL) Professor Bo Li, PhD. “Most people with cancer die of cachexia instead of cancer. And once the patient enters this stage, there’s no way to go back because essentially there’s no treatment," he explains. Now, Li and a team of collaborators from four CSHL labs have found that blocking IL-6 from binding to neurons in a part of the brain called the area postrema (AP) prevents cachexia in mice. As a result, the mice live longer with healthier brain function. Future drugs targeting these neurons could help make cancer cachexia a treatable disease.

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