Scientists at McMaster University and The Hospital for Sick Children have discovered how a type of brain cell that normally supports healthy brain function can instead go rogue, helping glioblastoma grow and spread. Their findings were recently published in the Cell Press journal Neuron. The prognosis for glioblastoma remains grim, with survival often measured in months.
As putative examples of intelligent design, cells like these should be acutely embarrassing for any creationist willing to follow the evidence where it leads, because within the ID creationist paradigm the only logical conclusion is that the designer is malevolent. By contrast, as examples of how evolution produces workable but imperfect, error-prone systems, they are entirely consistent with the Theory of Evolution and yet another vindication of the science.
Glioblastoma is not simply a mass of malignant cells, but an organised ecosystem sustained by a network of interacting cells. In that sense, it is indistinguishable from the sort of irreducibly complex system that Michael J. Behe claims is evidence of intelligent design. What the researchers found is that a type of cell called an oligodendrocyte, normally responsible for supporting and insulating nerve fibres, can switch roles and actively support tumour growth. These helper cells communicate with cancer cells through a specific signalling system, creating conditions in which the tumour can flourish.
The team discovered that a crucial part of this communication system involves cell-surface receptors called CCR5. By blocking this receptor, tumour growth can be significantly slowed. CCR5 is already the target of the anti-HIV medication Maraviroc, a drug that has already been clinically tested and approved, so it offers a potentially promising treatment for glioblastoma, even if not yet a cure.
Glioblastoma worldwide: incidence at a glance. Glioblastoma is a relatively rare cancer, but it is the commonest malignant primary brain tumour in adults. Current reviews generally place its annual incidence at about 3–5 cases per 100,000 people worldwide, with rates tending to be higher in more developed regions. [1]The work of the research team, led by Professor Sheila Singh, is explained in a news release from McMaster University:
For comparison, the broader category of brain and central nervous system cancers accounted for an estimated 321,731 new cases worldwide in 2022, with a world age-standardised incidence rate of 3.5 per 100,000. Because major global cancer databases usually group these tumours together rather than listing glioblastoma separately, precise worldwide GBM totals are harder to pin down than national figures.
Geographically, incidence rates for brain and CNS cancers are highest in Europe, Australia/New Zealand, and North America, and lowest across much of Africa and parts of South and South-East Asia. Glioblastoma appears to follow the same broad pattern, with higher reported rates where cancer registration and diagnostic imaging are more complete.
Glioblastoma is also more common in men than in women. Large registry-based studies typically find a male excess of about 1.6 to 1, and English national data show an age-standardised incidence of 6.3 per 100,000 in men versus 3.8 per 100,000 in women. [2]
Age is another major factor. Glioblastoma is chiefly a disease of older adults, with a median age at diagnosis of about 64 years, and incidence rising sharply with age before peaking in the elderly. It is comparatively uncommon in children. [3]
Scientists uncover hidden cells fuelling brain cancer — and a drug that could stop them
Scientists from McMaster and the Hospital for Sick Children have uncovered a new way to slow the growth of aggressive glioblastoma, and identified an existing medication that could treat it.
A Canadian team led by scientists from McMaster and the Hospital for Sick Children has uncovered a new way to slow the growth of glioblastoma, the most aggressive and currently incurable form of brain cancer – and identified an existing medication that could treat it.
Certain brain cells — once thought to simply support healthy nerve function — actually help glioblastoma grow and spread, the research shows.
These cells send signals that strengthen the tumour, but when researchers blocked this harmful communication in lab models, they found the cancer slowed its growth significantly.
Even more promising, the study suggests an existing HIV medication could be repurposed to target this process and offer a new treatment option for patients who currently have few. The prognosis for glioblastoma is poor, with survival often measured in months.
The research was published on Jan. 21 in Neuron and led by scientists at McMaster University and the Hospital for Sick Children (SickKids). Co-first authors of the study are Kui Zhai, a research associate in the Singh Lab at McMaster, and Nick Mikolajewicz, a postdoctoral fellow in the Moffat Lab at SickKids at the time of the study.Glioblastoma isn’t just a mass of cancer cells, it’s an ecosystem. By decoding how these cells talk to each other, we’ve found a vulnerability that could be targeted with a drug that’s already on the market
.Professor Sheila K. Singh, co-senior author
Centre for Discovery in Cancer Research (CDCR)
McMaster University
Hamilton, ON, Canada.
It’s known that glioblastoma grows by forming a network of cells that communicate and support each other, and disrupting these connections can slow the cancer. This study dug deeper to uncover which brain cells are involved.
The researchers discovered that a type of cell called an oligodendrocyte, normally responsible for protecting nerve fibres, can switch roles and actually support tumour growth. These helper cells communicate with cancer cells through a specific signalling system, creating an environment that allows the tumour to thrive.
When researchers blocked this communication in lab models, the cancer slowed down significantly, showing that this interaction is critical for glioblastoma’s survival.
What makes this finding especially promising is that the signalling system involves a receptor called CCR5, which is already targeted by an existing HIV medicine called Maraviroc. This means a medication that’s already approved and widely used could potentially be repurposed to treat glioblastoma, offering hope for faster progress toward new therapies.
The cellular ecosystem within glioblastoma is far more dynamic than previously understood. In uncovering an important piece of the cancer’s biology, we also identified a potential therapeutic target that could be addressed with an existing drug. This finding opens a promising path to explore whether blocking this pathway can speed progress toward new treatment options for patients.
Jason Moffat, co-senior author.
Program in Genetics and Genome Biology
The Hospital for Sick Children
Toronto, ON, Canada.
The breakthrough builds on Singh and Moffat’s 2024 study published in Nature Medicine, which discovered that a migration path used by cells during brain development can be hijacked for cancer cell invasion. Together, these discoveries highlight a new era of glioblastoma research focused on dismantling the tumour’s complex communication networks. This research work was supported by the 2020 William Donald Nash Brain Tumour Research Fellowship administered by the Brain Tumour Foundation of Canada, and the Canadian Institutes for Health Research. Singh is a Tier 1 Canada Research Chair in Human Cancer Stem Cell Biology and Moffat is the GlaxoSmithKline Chair in Genetics & Genome Biology at The Hospital for Sick Children. Publication:
And so, once again, the evidence points not to elegant design but to the messy, makeshift outcomes of evolution. A system that normally helps maintain and protect the brain can, under the wrong conditions, be co-opted into helping one of the deadliest cancers grow and spread. That is not what anyone would expect from a competent, benevolent designer, but it is exactly the sort of imperfect, vulnerable biological arrangement that evolution produces when natural selection works only with whatever materials happen to be available.
For advocates of intelligent design, glioblastoma poses an especially awkward problem. Here we have a complex, highly organised network of interacting cells, signalling pathways and support systems which, by Michael Behe’s own standard, would qualify as “irreducibly complex”. Yet that complexity does not serve health or wellbeing; it serves a lethal tumour. If irreducible complexity is supposed to be evidence of purposeful design, then glioblastoma forces the uncomfortable conclusion that the designer deliberately produced systems capable of turning the brain into a hospitable environment for cancer.
By contrast, evolutionary biology has no such difficulty. It does not predict perfection. It predicts compromises, vulnerabilities and systems that function well enough under most circumstances, but which can fail catastrophically when regulatory controls break down. The same cells that usually support normal brain tissue can, in a different context, be recruited into a malignant process. That is tragic for patients, but scientifically it is entirely unsurprising.
And, crucially, this is where real answers come from. Not from theological excuses or attempts to redefine bad design as mysterious divine purpose or the result of some misbehaviour from Bronze Age mythology, but from scientists patiently uncovering the mechanisms involved and identifying points of intervention. In this case, their work has already highlighted a promising treatment target in CCR5 and the possible repurposing of an existing drug. That is how science advances: by confronting reality as it is, not as dogma insists it ought to be.
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