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Brain tumor cells killed by anti-nausea drug

New research from the University of Adelaide has shown for the first time that the growth of brain tumors can be halted by a drug currently being used to help patients recover from the side effects of chemotherapy.

The discovery has been made during a study looking at the relationship between brain tumors and a peptide associated with inflammation in the brain, called "substance P".

Substance P is commonly released throughout the body by the nervous system, and contributes to tissue swelling following injury. In the brain, levels of substance P greatly increase after traumatic brain injury and stroke.

"Researchers have known for some time that levels of substance P are also greatly increased in different tumor types around the body," says Dr Elizabeth Harford-Wright, a postdoctoral fellow in the University's Adelaide Centre for Neuroscience Research.

"We wanted to know if these elevated levels of the peptide were also present in brain tumor cells, and if so, whether or not they were affecting tumor growth. Importantly, we wanted to see if we could stop tumor growth by blocking substance P."

In laboratory studies for her PhD, Dr Harford-Wright found that levels of substance P were greatly increased in brain tumor tissue.

Knowing that substance P binds to a receptor called NK1, Dr Harford-Wright used an antagonist drug called Emend to stop substance P binding to the receptor. Emend is already used in cancer clinics to help patients with chemotherapy-induced nausea.

The results were startling.

"We were successful in blocking substance P from binding to the NK1 receptor, which resulted in a reduction in brain tumor growth and it also caused cell death in the tumor cells," Dr Harford-Wright says.

"So preventing the actions of substance P from carrying out its role in brain tumors actually halted the growth of brain cancer.

"This is a very exciting result, and it offers further opportunities to study possible brain tumor treatments over the coming years."


Contact: Dr Elizabeth Harford-Wright, University of Adelaide
University of Adelaide

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