Sept. 21 (UPI) -- Researchers at Stanford University report in a new study this week that the growth of specific aggressive brain tumors was stopped by cutting off access to a signaling molecule.
The tumors, called high-grade gliomas, are a group of deadly brain cancers that include adult glioblastoma, anaplastic oligodendroglioma, pediatric glioblastoma and pediatric diffuse intrinsic pontine glioma, or DIPG.
New treatments are vital since five-year survival rates the tumors are 60 percent for anaplastic oligodendroglioma, roughly 10 percent for adult and pediatric glioblastoma, and nonexistant for DIPG.
The study, published Wednesday in Nature, shows that high-grade gliomas stopped growing in mice when a signaling molecule, neurogligin-3, was absent or the molecule's activity was blocked by drugs.
"We thought that when we put glioma cells into a mouse brain that was neuroligin-3 deficient, that might decrease tumor growth to some measurable extent. What we found was really startling to us: For several months, these brain tumors simply didn't grow," Dr. Michelle Monje, an assistant professor of neurology, said in a press release.
"The findings suggest that interrupting the neuroligin-3 signal could be a helpful strategy for controlling high-grade gliomas in human patients."
Researchers examined mice that were genetically engineered to lack neuroligin-3 and had nearly normal brain function. Once the mice were implanted with any of the forms of human high-grade glioma, the cancer cells could not proliferate and the tumor growth was halted for several months.
"Lack of neuroligin-3 doesn't kill the cancer cells; the cells that are there remain there, but they do not grow," Monje said. "However, four and a half months after implantation, tumors in some mice circumvented their dependency on neuroligin-3 and began to grow again."
Researchers conducted follow-up testing to examine the cell signals involved in neuroligin-3's role in the division of glioma cells. They found that neuroligin-3 activates multiple cancer promoting signaling pathways and increases the expression of genes involved in cell proliferation, promotion of malignancy, function of potassium channels and synapse function.
"We have a really clear path forward for therapy; we are in the process of working with the company that owns the clinically characterized compound in an effort to bring it to a clinical trial for brain tumor patients," Monje said. "We will have to attack these tumors from many different angles to cure them. Any measurable extension of life and improvement of quality of life is a real win for these patients."