Not all brain tumors behave alike. Some are much deadlier than others.

High-grade gliomas, or HGGs, rank among the deadliest brain tumors.

HGGs cause more brain tumor deaths than any other type in children and adults.

Despite major advances in cancer research, survival rates for HGG patients have not improved.

However, Stanford University researchers may have discovered a way to improve those outcomes.

Their study, published in Cell, identified one factor that drives HGG growth.

The brain’s neural activity, especially activity in the cerebral cortex, can stimulate these tumors.

Michelle Monje, the study’s senior author, found the result surprising. CIRM partly funded the research through two grants.

Most tumors do not grow in response to normal organ activity.

“We do not think that bile production promotes liver cancer growth,” Monje said.

“Nor do we think that breathing promotes lung cancer growth. However, brain function drives these brain cancers.”

The researchers analyzed tumor cells from HGG patients and implanted them in laboratory mice.

They then identified how the brain’s activity stimulated tumor growth.

A protein called neuroligin-3 appeared to drive this process.

Four distinct types of HGG affect the brain. Each type has different molecular and genetic characteristics.

However, neuroligin-3 played the same role in all four types.

The researchers found this result especially concerning because neuroligin-3 supports normal brain development.

The protein also helps maintain and repair healthy brain tissue.

HGG tumors hijack neuroligin-3 to support their own growth.

The researchers reached this conclusion after studying the molecular processes behind brain activity and tumor development.

First, they used a technique called optogenetics.

This technique uses genetic manipulation to add light-sensitive proteins to specific neurons.

Researchers can then activate or deactivate those neurons with light.

The team applied optogenetics to mice with implanted tumors.

The tumors grew significantly faster when researchers activated the neurons.

The researchers then investigated why this occurred.

Additional biochemical analyses and mouse experiments confirmed that the tumors hijacked neuroligin-3 to promote growth.

The team also examined data from the Cancer Genome Atlas, a public database of human cancer genetics.

They found that HGG patients with higher brain levels of neuroligin-3 had shorter survival times.

These findings highlight HGG’s aggressive nature but also offer researchers a promising opportunity.

Monje hopes researchers can block or eliminate neuroligin-3 around tumors.

This strategy could create a barrier that limits tumor growth.