When tumours in cancer patients increase the levels of an immune system molecule called interleukin-6 (IL-6), it may lead to a serious brain disorder that causes a fatal condition called ‘cachexia’ in about 50 to 80 per cent of cancer patients, a new study says.
“This is a very serious syndrome”, according to Professor Bo Li of the US-based Cold Spring Harbor Laboratory (CSHL).
“Most people with cancer die from ‘cachexia’ rather than cancer. And once a patient reaches this stage, there is no way to go back as there is virtually no cure,” he said in a study published in the journal Nature Communications.
Li and other researchers in the team found that preventing IL-6 from binding to neurons in a part of the brain called the area postrema (AP) could prevent cachexia in mice.
As a result, the mice live longer and their brains function in healthier ways.
The researchers suggested that, “In the future, drugs targeting these neurons may help make cancer cachexia a treatable disease.”
In healthy patients, ‘IL-6’ plays a key role in the natural immune response. The molecules travel throughout the body. When they encounter a potential threat, they alert the brain to coordinate a response.
According to the researchers, cancer disrupts this process, as too much IL-6 is produced, and it begins to bind to AP neurons in the brain.
“This has multiple consequences. One is that both animals and humans stop eating. The other is that this reaction causes wasting syndrome,” Lee said.
The team took a two-pronged approach to keep elevated IL-6 out of the mice’s brains. Their first strategy neutralized IL-6 with a custom antibody. The second used CRISPR to reduce the levels of IL-6 receptors in AP neurons. Both strategies produced the same results – the mice started eating again, stopped losing weight, and lived longer, the study said.
“The brain is very powerful in regulating the peripheral system. Changes in a small number of neurons in the brain have profound effects on the physiology of the entire body. I knew there was an interaction between tumors and brain function, but not to this extent,” Lee said.
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