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Research Indicates Molecule Sabotage May Slow Brain Cancer

Date:
March 26, 1998
Source:
Society For Neuroscience
Summary:
For the first time, researchers have found that a particularly lethal form of brain cancer tramples through healthy tissue with the help of a tumor-specific molecule. They hope that methods that can debilitate the molecule, brain-enriched hyaluronan binding protein (BEHAB), will slow the progression of the disease.
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WASHINGTON, D.C. -- For the first time, researchers have found that a particularly lethal form of brain cancer tramples through healthy tissue with the help of a tumor-specific molecule. They hope that methods that can debilitate the molecule, brain-enriched hyaluronan binding protein (BEHAB), will slow the progression of the disease.

"The experiments show that BEHAB appears to be a strong, central factor in the movement of brain cancer cells into healthy brain tissue," says neurobiology professor and lead author of the study, Susan Hockfield, PhD, of Yale University School of Medicine. "The work raises new therapeutic possibilities for the brain cancer tumors known as gliomas, which are often fatal."

Hockfield's study, funded by the National Institutes of Health, is published in the April 1 issue of The Journal of Neuroscience.

"The work is exciting because it advances our basic understanding of how glioma cells invade healthy brain tissue and provides a new animal model that can be used to evaluate future therapies," says Lois Lampson, PhD, an expert on brain tumor biology and an associate neurology professor at Brigham and Women's Hospital and Harvard Medical School. "The research opens new paths for both basic understanding and pre-clinical research."

Each year, approximately 20,000 Americans find out they have a glioma. More than half die within 18 months because the tumors often outsmart conventional treatments, such as surgery.

Gliomas arise from brain support cells called glia. The cells grow furiously until they form a mass known as a tumor. "Gliomas are exceptionally difficult to treat because their cells have an unusual ability to travel long distances through normal brain tissue and set up new tumors," says Hockfield.

"One approach to controlling the cancer would be to block the glioma cells' ability to travel, without harming healthy cells." BEHAB, also known as brevican, appears to be a prime candidate for this type of therapy because it exists in glioma tumors, but not in other kinds of brain tumors or tissue in the body, according to the scientists.

In the new study, the researchers found that BEHAB must be secreted by the tumor cells and cut in half, in order for the cancer to move and invade healthy tissue. The research was carried out on newly developed rodent brain tumor models and rodent brain tumor cell lines with genetic engineering techniques.

"Therapies that block the function of BEHAB or reduce the tumor cells' ability to make the protein, may slow tumor progression," says Hockfield. "Moreover, blocking the enzymes that cut BEHAB in half also may be an effective therapy."

In future work, the scientists plan to test the protein's value as a therapy component. They hope to find methods to block BEHAB's overall function, to reduce its production, and to inhibit its division.

Hockfield is a member of the Society for Neuroscience, an organization of more than 27,000 basic scientists and clinicians who study the brain and nervous system. The Society publishes The Journal of Neuroscience.


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Materials provided by Society For Neuroscience. Note: Content may be edited for style and length.


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Society For Neuroscience. "Research Indicates Molecule Sabotage May Slow Brain Cancer." ScienceDaily. ScienceDaily, 26 March 1998. <www.sciencedaily.com/releases/1998/03/980326081416.htm>.
Society For Neuroscience. (1998, March 26). Research Indicates Molecule Sabotage May Slow Brain Cancer. ScienceDaily. Retrieved April 18, 2024 from www.sciencedaily.com/releases/1998/03/980326081416.htm
Society For Neuroscience. "Research Indicates Molecule Sabotage May Slow Brain Cancer." ScienceDaily. www.sciencedaily.com/releases/1998/03/980326081416.htm (accessed April 18, 2024).

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