Tumour containing infiltrating neutrophils. In light grey, tumour cells. Among the infiltrating neutrophils, some do not express CCL3 (blue), while others are CCL3 positive (red). CCL3-positive neutrophils are highly conserved across tumour types and promote the growth of growing tumours.
© Mikaël Pittet – UNIGE
A recent research paper in Cancer Cell, published by a team from the Université de Genève (Unige), Switzerland, led by Professor Mikaël Pittet, describes how neutrophils — key cells of the immune system — can be reprogrammed by cancer cells and then co-opted to drive the cancer’s progression.
This process depends entirely on the presence of multiple interacting components and on specific genes being expressed in both the tumour cells and the neutrophils. Without such irreducible complexity and so-called complex specified genetic information, these cancers would fail to progress.
Regular readers of this blog will be aware that, if we accept the Intelligent Design creationists’ argument for design — namely irreducible complexity and complex specified information — then the inescapable conclusion is that this putative designer must also be the evil genius behind cancers, parasites, pathogens, genetic disorders, congenital diseases, and all the suffering they entail, along with the vast medical resources required to combat them.
Far from being the reputedly omnibenevolent and compassionate god of the Bible, creationism’s designer becomes the exact opposite: randomly mendacious and obsessively sadistic, toiling relentlessly to devise ever more ways to increase suffering in the world.
And yet creationists appear to prefer us to adopt that view of their favourite deity rather than accept the evidence that such systems have evolved — and that what we see in cancers, parasites, and pathogens is precisely what the Theory of Evolution predicts, with no supernatural malice or intent involved. For some reason, Intelligent Design creationists often seem more concerned with disproving “Darwinism” for political purposes than with promoting the god of the Bible or Qur’an.
This apparent paradox goes a long way towards explaining why they have so little hesitation in bearing false witness against scientists, misleading their followers with disinformation, and spreading blatant falsehoods. There is no pro-truth agenda in creationism. There is, however, a thinly veiled political agenda: the establishment of theocratic government — first in the USA, then elsewhere — dragging society back towards the pre-Enlightenment world of the so-called Dark Ages, when ignorance, fear, and superstition allowed unelected and unaccountable religious clerics to rule unchecked, and for most people at the lower strata of a hierarchical society, life was nasty, brutish and short.
Neutrophils — The Immune System’s First Responders Turned Accomplices. Neutrophils are the most abundant type of white blood cell in human blood and form one of the immune system’s first lines of defence. They are rapid-response cells, designed by evolution to react within minutes to infection or tissue damage.With that rant out of the way, let’s look at how the press release from Unige explains Professor Pittet’s team’s research and what it may mean for future cancer treatment.
What Neutrophils Normally Do Under healthy conditions, neutrophils play several vital roles:
- Engulfing and destroying bacteria and fungi through phagocytosis
- Releasing antimicrobial chemicals to kill invading pathogens
- Forming “neutrophil extracellular traps” (NETs) — sticky webs of DNA and proteins that immobilise microbes
- Calling in other immune cells by secreting inflammatory signalling molecules
They are, in effect, the body’s emergency paramedics: fast, aggressive, and unspecialised, meant to contain threats before the rest of the immune system mobilises.
How Cancer Hijacks Them
Cancer cells, however, are not passive targets. Tumours actively reshape their surrounding environment, releasing chemical signals that can reprogramme neutrophils into supporting the cancer rather than fighting it.
Instead of attacking the tumour, these altered neutrophils may:
- Suppress anti-tumour immune responses, disabling T cells that would otherwise kill cancer cells
- Promote tumour growth by secreting growth factors
- Encourage angiogenesis, the formation of new blood vessels to feed the tumour
- Assist metastasis, helping cancer cells invade surrounding tissue and spread to distant organs
In other words, the tumour effectively pirates the immune system, converting defenders into collaborators.
Why This Matters Evolutionarily
From an evolutionary perspective, none of this is surprising. Neutrophils evolved to respond to injury, inflammation, and infection — and tumours exploit those same pathways because cancer is fundamentally a breakdown of normal cellular regulation.
Evolution produces systems that are good enough for survival and reproduction, not systems engineered to be immune to exploitation.
A Problem for Intelligent Design
For Intelligent Design advocates, this presents an uncomfortable implication. If immune complexity is evidence of purposeful design, then what are we to make of immune cells being so easily reprogrammed into aiding lethal disease?
The immune system is not a pristine engineered defence — it is an evolved patchwork of mechanisms that can be turned against the organism under the wrong conditions.
Cancer is not a glitch in a perfect design. It is an entirely predictable consequence of biology built through evolution, not foresight.
Immune 'hijacking' predicts cancer evolution
A team from UNIGE reveals how the 'hijacking' of neutrophils, a type of immune cell, promotes cancer growth and could provide insights into disease progression.
Predicting tumour progression is one of the major challenges in oncology. Scientists at the University of Geneva (UNIGE) and the Ludwig Institute for Cancer Research have discovered that neutrophils, a type of immune cell, undergo reprogramming when they come into contact with the tumour ecosystem and contribute to its progression. They then produce a molecule — the chemokine CCL3 — which promotes cancer growth rather than fighting it. This mechanism appears to be a major variable in tumour biology and could serve as an indicator of disease progression. These findings are published in the journal Cancer Cell.
A tumour is not just a cluster of cancer cells but develops within a complex ecosystem where different cell populations interact.
One of the difficulties lies in identifying, in an environment we are only now beginning to understand, the elements that truly influence the tumour's ability to grow. In 2023, we showed that the expression of two genes in macrophages is strongly linked to disease progression. This constitutes a simple but informative variable for understanding tumours and anticipating their trajectory. Our new study highlights a second variable, this time involving another population of immune cells: neutrophils.
Professor Mikaël Pittet, Senior author
Department of Pathology and Immunology
Faculty of Medicine
University of Geneva
Geneva, Switzerland.
A deleterious reprogramming
Neutrophils represent one of the most abundant populations in the immune system. They typically constitute the first line of defence against infections and injuries. In the context of cancer, however, their presence is generally a bad omen.
We discovered that neutrophils recruited by the tumour undergo a reprogramming of their activity: they begin producing a molecule locally—the chemokine CCL3—which promotes tumour growth.
Professor Mikaël Pittet.
An experimental and bioinformatics challenge
Neutrophils are particularly difficult to study and to manipulate genetically. We combined different approaches to control the expression of the CCL3 gene specifically in neutrophils, without inhibiting it in other cells. A delicate exercise!
Dr. Evangelia Bolli, co-lead author
Department of Pathology and Immunology
Faculty of Medicine
University of Geneva
Geneva, Switzerland.
The result? Without CCL3, neutrophils lose their pro-tumour action. They retain their physiological functions in the blood and can even accumulate in tumours, but no longer adopt the deleterious reprogramming previously observed.
To complete their analysis, the research team re-examined data from numerous independent studies.
We had to innovate to detect neutrophils more accurately. Their low genetic activity often makes them invisible using standard analysis tools. By developing a new method, we have been able to show that, in many cancers, these cells share a common trajectory: they produce large amounts of CCL3, which is associated with pro-tumour activity.
Pratyaksha Wirapati, co-first author
Department of Pathology and Immunology
Faculty of Medicine
University of Geneva
Geneva, Switzerland.
Towards a potential prognostic marker
With CCL3, Mikaël Pittet's team has now identified a new variable likely to provide information on tumour progression.
We are deciphering the 'identity card' of tumours, by identifying, one by one, the key variables that determine the evolution of the disease. Our work suggests that there is a limited number of these variables. Once they are properly identified, they could help better tailor the management of each patient and, ultimately, offer more effective and personalised care.
Professor Mikaël Pittet.
Publication:
What this research highlights, once again, is that the biological world does not resemble the product of foresightful, benevolent engineering. Instead, it looks exactly like what evolution predicts: a patchwork of systems shaped by selection for short-term survival, vulnerable to exploitation, and capable of being hijacked in ways that are catastrophic for the organism.
Neutrophils did not “evolve for cancer”, of course. They evolved as rapid-response immune cells, effective enough against infection and injury to be favoured over countless generations. But tumours, themselves the result of mutational breakdown and runaway cellular replication, exploit the very signalling pathways that normally serve the body. There is no intent here, no malice, no supernatural plot — merely the cold, indifferent logic of evolutionary processes acting on imperfect biological machinery.
For Intelligent Design advocates, however, this presents an intractable dilemma. If immune complexity is supposed to be evidence of purposeful design, then what are we to conclude when that same complexity can be reprogrammed into aiding lethal disease? The only honest answer is that design arguments collapse the moment biology fails to conform to comforting theology. Complexity is not a hallmark of benevolence — cancers, parasites and pathogens are every bit as complex as anything creationists like to praise.
In reality, the evolutionary explanation is not only vastly more coherent, but also morally cleaner. Evolution does not pretend that suffering is part of a perfect plan. It predicts, unflinchingly, that organisms will be vulnerable, that systems will have trade-offs, and that natural selection produces what works well enough — not what is optimal, nor what is compassionate.
And it is precisely because cancer is an evolved consequence of multicellular life, rather than a deliberately inflicted punishment or “design feature”, that science can investigate it, understand it, and ultimately find ways to disrupt it.
Creationism offers only excuses for suffering. Evolution offers explanations — and with them, the tools to fight back.
The evidence stubbornly refuses to glorify a designer. It simply tells the true story of life as it really is: evolved, imperfect, and entirely natural.
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