The tumors simply didn't grow for several months
For decades, glioblastoma has followed a cruel rhythm: treatment, brief reprieve, return. Researchers at McGill University have now identified a protein called galectin1 as a key sustainer of the cancer's most resilient cells — the stem cells that quietly rebuild the tumor after every assault. By suppressing this protein in preclinical models and combining that suppression with radiation therapy, the team observed tumors halting their growth and patients living longer, offering a new way of understanding the disease not as a mass to be destroyed, but as a system to be dismantled.
- Glioblastoma kills with a pattern — surgery, radiation, and chemotherapy buy months, but the tumor almost always returns, because the root cells driving it are left untouched.
- McGill researchers pinpointed galectin1 as the protein orchestrating those root cells, working alongside HOXA5 and STAT3 to keep the cancer's stem cell machinery running.
- When galectin1 was suppressed in laboratory and animal models, tumors stopped growing for months — and pairing that suppression with radiation dramatically extended survival.
- Patient database analysis confirmed the finding: those with low expression of both galectin1 and HOXA5 showed the best clinical outcomes, bridging lab discovery and human reality.
- The path forward points toward clinical trials and CRISPR-based gene therapies targeting the galectin1-HOXA5 complex — a strategy that could finally break the disease's cycle of recurrence.
Glioblastoma is defined by a brutal pattern. Patients endure surgery, radiation, and chemotherapy, and for a few months the disease retreats — then returns. This cycle has persisted for decades because conventional treatments, however aggressive, leave intact the cancer stem cells that quietly rebuild the tumor. Kill the bulk of the growth, but leave those root cells alive, and the disease resurfaces.
A team at McGill University, led by associate professor Arezu Jahani-Asl, has identified a protein called galectin1 as a central driver of this process. Working in concert with a protein called HOXA5, galectin1 controls the genetic programs that sustain cancer stem cell behavior — the cellular seeds that keep glioblastoma alive. When the researchers suppressed galectin1 in preclinical models, tumors stopped growing for several months. More strikingly, when suppression was combined with radiation therapy, tumor response improved significantly and survival extended.
To ground the discovery in human experience, the team examined patient databases and found that those with low expression of both galectin1 and HOXA5 had the best prognoses — a clinical echo of what the lab had already shown. A third protein, STAT3, was also implicated in the network activating the cancer's most aggressive traits.
The findings are preliminary but consequential. They establish a clear target for drug development and a rationale for combining galectin1 inhibition with existing radiation protocols in future clinical trials. CRISPR gene-editing approaches are also being explored as a means of disrupting the galectin1-HOXA5 complex more precisely. If these strategies prove effective in human trials, they may offer the first meaningful shift in glioblastoma treatment in years — reframing the disease not as a tumor to be eliminated wholesale, but as a biological system sustained by specific, targetable proteins.
Glioblastoma is a relentless disease. It is the most common and most aggressive brain cancer in adults, growing fast and spreading faster. Patients undergo surgery, radiation, chemotherapy—the full arsenal of modern oncology—and for a few months, the symptoms ease. Then the tumor returns. In most cases, the cancer comes back. This pattern of temporary relief followed by recurrence has defined the disease for decades, and it happens because conventional treatments, no matter how aggressive, fail to address the root of the problem.
Researchers at McGill University have identified what that root might be. A team led by Arezu Jahani-Asl, an associate professor of medicine, discovered that a protein called galectin1 plays a central role in sustaining glioblastoma by controlling cancer stem cells—the cells that act like seeds, reproducing themselves and keeping the cancer alive. Among all the malignant cells in a tumor, some function as stem cells do in healthy tissue: they renew themselves and sustain the larger system. If you cut down weeds but leave the roots intact, the researchers note, the weeds grow back. The same principle applies to cancer. Kill the bulk of the tumor, but leave the stem cells untouched, and the disease will resurface.
The McGill team discovered that galectin1 works in tandem with another protein called HOXA5 to control the genetic programs that drive cancer stem cell behavior. When they suppressed galectin1 in preclinical models—laboratory and animal studies—something remarkable happened. The brain tumors simply stopped growing for several months. More importantly, tumors that had been treated with radiation therapy showed significantly improved response when galectin1 was also suppressed, and the animals lived longer. The finding suggested a new therapeutic strategy: target the protein, combine it with existing radiation therapy, and the results improve.
To validate their discovery, the researchers analyzed patient databases and found a striking correlation. Glioblastoma patients with low expression of both galectin1 and HOXA5 had the best prognosis. This clinical observation supported what they had seen in the lab: these two proteins, working together with a third protein called STAT3, activate the mechanisms that make glioblastoma particularly aggressive. Suppress them, and the cancer loses one of its key survival tools.
The implications are significant but still preliminary. The research provides a clear target for drug development and a rationale for combining galectin1 inhibition with radiation therapy in future clinical trials. The next phase involves comparing different approaches to suppressing the galectin1-HOXA5 complex, including newer gene therapy techniques using CRISPR technology, which allows researchers to edit genes directly. If those approaches prove effective in human trials, they could transform treatment for a disease that has resisted improvement for years. For now, the discovery represents a shift in how researchers think about glioblastoma—not as a tumor to be killed wholesale, but as a system sustained by specific proteins that can be targeted and disrupted.
Citas Notables
After we inhibited the galectin1 protein, the brain tumours simply didn't grow for several months. To improve patient response to therapy, we must exploit these newly identified vulnerabilities in cancer stem cells.— Arezu Jahani-Asl, Associate Professor of Medicine, McGill University
La Conversación del Hearth Otra perspectiva de la historia
Why does glioblastoma keep coming back after treatment?
Because the tumor has stem cells—cells that act like seeds. You can destroy most of the cancer, but if you leave those stem cells intact, they'll grow a new tumor. It's like cutting weeds without pulling the roots.
And this galectin1 protein—what does it actually do?
It's a control switch. It works with another protein called HOXA5 to tell cancer stem cells how to behave, how to reproduce, how to survive. When researchers turned off galectin1 in lab models, the tumors stopped growing.
For how long?
Several months in the preclinical studies. That's significant because glioblastoma patients usually see their tumors return within months of treatment.
Did suppressing galectin1 alone cure the cancer?
Not in the studies shown. But when they combined galectin1 suppression with radiation therapy, the results improved dramatically. The tumors responded better to the radiation, and the animals lived longer.
So this isn't a replacement for radiation—it's an enhancement?
Exactly. It's a way to make existing therapy work better by removing one of the cancer's survival mechanisms.
What's the next step?
Clinical trials in humans. But first, researchers want to test different methods of suppressing galectin1, including CRISPR gene therapy, to see which approach works best in the brain.