GLIOBLASTOMA BREAKTHROUGH: NEW DISCOVERY REVEALS HIDDEN DRIVER OF DEADLY BRAIN CANCER

Australian scientists have uncovered a new mechanism behind glioblastoma, offering fresh hope for more targeted and effective treatments.

A new glioblastoma breakthrough from Australian researchers has revealed a hidden driver behind one of the deadliest forms of brain cancer, potentially opening the door to more effective treatments.

The study, led by scientists at the Centre for Cancer Biology in Adelaide, found that a protein known as CD47 does far more than previously understood.

While it has long been linked to helping cancer evade the immune system, researchers now say it actively drives tumour growth and spread.

That shift in understanding could prove significant.

Glioblastoma is one of the most aggressive cancers, with most patients surviving less than 18 months after diagnosis.

Even with surgery, radiation and chemotherapy, the disease almost always returns, making new treatment pathways critical.

What the glioblastoma discovery reveals

The glioblastoma research, published in the journal PNAS, shows that CD47 plays a direct role inside tumour cells, helping them grow, move and invade surrounding brain tissue.

“We’ve known for some time that CD47 acts as a kind of ‘don’t eat me’ signal that helps cancer cells hide from the immune system,” said Dr Nirmal Robinson, senior author of the study.

“What we’ve discovered is that CD47 is doing much more than that; it’s actually driving the cancer’s ability to spread and grow.”

Researchers found that CD47 is most abundant at the edges of tumours, the areas responsible for the spread of cancer into healthy brain tissue.

Patients with higher protein levels were also found to have poorer survival outcomes.

Why CD47 could change glioblastoma treatment

In laboratory and animal model testing, blocking or removing CD47 had a striking effect.

Tumour cells grew more slowly, spread less, and in some cases, survival time nearly doubled. Notably, these results were observed even in the absence of immune cells, confirming that CD47 plays a direct role in tumour behaviour.

The team also identified another protein, ROBO2, which works alongside CD47 to promote tumour growth.

“Essentially, CD47 is shielding ROBO2, allowing it to accumulate and drive tumour progression,” said Dr Ruhi Polara, who co-led the research.

“When we remove CD47, ROBO2 is degraded, and the cancer cells lose their ability to grow and invade effectively.”

This newly identified pathway, involving CD47, ITCH and ROBO2, gives researchers a clearer picture of how glioblastoma spreads.

What this means for future glioblastoma therapies

While therapies targeting CD47 are already being explored in clinical trials for other cancers, results in glioblastoma have so far been limited.

This research suggests a more targeted approach, focusing on the CD47-ROBO2 pathway, could be more effective.

“By understanding this mechanism, we now have new targets to explore,” Dr Polara said.

“This could lead to the development of therapies that specifically block the tumour’s ability to spread.”

Researchers say the findings also highlight the need to look beyond the immune system when developing cancer treatments.

“This work changes how we think about CD47,” Dr Robinson said. “It’s not just an immune checkpoint; it’s a central regulator of tumour biology in its own right.”

Further research is needed before these findings translate into clinical treatments, but the discovery marks a significant step forward in understanding and potentially treating glioblastoma.