Blocking brain-liver communication may prevent deadly weight loss in cancer

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Nearly a third of cancer-related deaths are caused by cachexia, a currently incurable metabolic syndrome that involves substantial weight loss, including depletion of muscle mass and body fat.

Researchers from the Weizmann Institute of Science and the University of Texas MD Anderson Cancer Centre have discovered that one of the reasons for this loss is disrupted communication between the brain and the liver.

When the activity of the vagus nerve, a major axis of brain-liver communication, is dysregulated by cancer-triggered inflammation, the result is damage to liver metabolism and the development of a life-threatening syndrome.

Since the method is based on technologies approved for clinical use, it is likely to reach patients relatively soon.

In a study published in Cell, a research team led by Dr. Naama Darzi from Prof. Ayelet Erez’s lab at Weizmann and Dr. Aliesha Garrett from Prof. Xiling Shen’s lab at MD Andreson showed that targeted blocking of the right vagus nerve – even when performed by noninvasive means – prevented cachexia’s development in mice, enhanced their response to chemotherapy and improved their overall health and survival.

The method, already being tested in clinical trials, offers a new therapeutic approach that may lead to improved quality of life and even survival for cancer patients.

Since the method is based on technologies approved for clinical use, it is likely to reach patients relatively soon.

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The prevalence of cachexia in cancer patients is as high as 85% in some cancers; it is among the highest in pancreatic and lung tumours.

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Beyond opening new treatment options for cancer patients, this research demonstrates that the brain-body communication plays a critical role in our health and disease.


Source: Weizmann Institute of Science

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The ONA Editor curates oncology news, views and reviews from Australia and around the world for our readers. In aggregated content, original sources will be acknowledged in the article footer.

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