Researchers at the University of Alberta have discovered how glioblastoma—one of the brain's most aggressive and lethal cancers—sends out microscopic tentacles to infiltrate new regions of the brain, and they've identified a way to stop it. The findings, published in the journal Neuro-Oncology, point to a protein called FABP7 as a critical target for slowing or halting the cancer's spread.
Glioblastoma affects roughly 4 in 100,000 people, with patients facing a grim prognosis: an average survival of just 12 to 18 months. The cancer's lethality lies partly in its ability to outmaneuver conventional treatments. A team led by oncology professor Roseline Godbout investigated a recently discovered mechanism of invasion—thin, fiber-like structures called tumor microtubes that cancer cells use to rapidly penetrate new areas of the brain. These microtubes are particularly troubling because they are strongly associated with resistance to both radiotherapy and chemotherapy, making them a key obstacle to improving patient outcomes.
The research centers on FABP7, a fatty acid-binding protein normally active during brain development. In a healthy developing brain, FABP7 helps neural stem cells create fiber networks that guide young neurons to their proper positions. The University of Alberta team discovered that glioblastoma cells hijack this same developmental mechanism. The cancer cells re-express FABP7 in their tumor microtubes, essentially exploiting a natural biological highway to spread through the brain.
In laboratory experiments using human cell cultures, researchers chemically inhibited FABP7 and achieved striking results. Blocking the protein prevented tumor microtubes from forming, reduced the cancer cells' ability to migrate, and made the cells more sensitive to temozolomide, a standard chemotherapy drug. The findings weren't limited to petri dishes. When the team treated mice with glioblastoma using an FABP7 inhibitor, the animals survived significantly longer than those in a control group—a critical proof-of-concept that the approach works in living organisms.
Daniel Won-Shik Choi, who led the study as a Ph.D. student in Godbout's laboratory, emphasized the significance of the discovery: "Identifying the main players in the formation of tumor microtubes may be key to inhibiting glioblastoma cell invasion and therapy resistance." Choi, now completing postdoctoral work at McMaster University before joining the faculty at the University of Saskatchewan, sees the research as a stepping stone to better treatments.
The Godbout lab is already building on these results. The team is now testing whether inhibiting FABP7 can be even more effective when combined with standard cancer treatments—temozolomide and radiotherapy—in a larger cohort of mice. If those trials are successful, the pathway toward clinical trials in humans could be within reach.
"Our results indicate that tumor microtube formation can be mitigated by FABP7 inhibition with the potential of improving clinical outcomes in glioblastoma patients," Choi says. For patients and families facing this devastating diagnosis, the research offers a tangible glimmer of hope that the disease's most lethal mechanisms may finally be within reach.