Rosa Rubicondior: Malevolent Design - More Evidence Of Intelligently Designed Cancer?

Sunday, 15 February 2026

Malevolent Design - More Evidence Of Intelligently Designed Cancer?

Pancreatic cancers co-opt nerve cells to assist them to develop.

AI-generated image (ChatGPT 5.2)

Let’s get on pancreatic cancer’s nerves | Cold Spring Harbor Laboratory

Creationists seem to have pinned all their hopes of justification for their evidence-free beliefs on a false dichotomy and a classic “god of the gaps” fallacy: the claim that complex specified information and irreducible complexity are proof of design by an intelligent entity. This argument relies heavily on the parochial ignorance of its intended audience, who are expected to assume that this “designer” must be the Christian god of the Bible — or, depending on geography and cultural background, the god of the Qur’an — and that therefore those holy books must be the inerrant word of the supposed creator.

However, the problem this raises for creationists is an obvious one: who or what, within their framework, designed all the many examples of irreducible complexity and complex specified information that cause suffering, sickness, and death?

Another striking example has just been published in Cancer Discovery by Professor Jérémy Nigri and colleagues from Cold Spring Harbor Laboratory, New York, USA.

In this paper, the researchers use advanced 3D imaging to show how, even before tumours form, tumour-promoting fibroblasts — known as myCAFs — send out signals that attract nerve fibres. The myCAFs and nerve cells then work together within pancreatic lesions to create a microenvironment favourable for cancer growth. Embarrassingly for Intelligent Design advocates, this system depends entirely on the genetic capacity of myCAFs to send the correct molecular signals, and for nerve fibres to respond appropriately — a finely tuned interaction requiring precisely the sort of “irreducible complexity” they insist can only arise through intentional design.

Within the ID paradigm, these facts should be indisputable evidence of their god’s involvement — but only when the outcome is something they find beneficial, such as eyes, blood clotting, or a brain capable of abstract thought. When the very same logic points instead to cancers, parasites, and congenital diseases, it is suddenly no evidence at all, and certainly not evidence of malevolent intent on the part of the designer. The argument collapses into childish special pleading: design is invoked when convenient, but denied when morally awkward.

Background^ MyCAFs, Nerves, and the Tumour Microenvironment. Cancer is often misunderstood as simply a mass of rapidly dividing cells, but modern oncology shows it is far more than that. Tumours behave less like isolated growths and more like rogue organs, recruiting surrounding tissues and exploiting normal biological systems for their own survival.

A key concept here is the tumour microenvironment — the complex community of non-cancerous cells, blood vessels, immune cells, connective tissue, and signalling molecules that surround a tumour. Far from being passive bystanders, these cells can actively shape how a cancer develops.

What are fibroblasts and myCAFs?
Fibroblasts are ordinary connective-tissue cells found throughout the body. Their normal role is to:

produce structural scaffolding (collagen and extracellular matrix)
repair wounds
regulate inflammation and tissue maintenance

In cancers, however, fibroblasts can be hijacked and transformed into cancer-associated fibroblasts (CAFs). One particularly important subtype is the myofibroblastic CAF, or myCAF, which has features of both fibroblasts and smooth muscle cells. These myCAFs are common in aggressive cancers such as pancreatic cancer.

They can:

remodel tissue architecture
suppress immune responses
promote tumour invasion
secrete growth factors that help cancer cells thrive

Cancer and the Nervous System: Neuroplasticity in Tumours

A striking finding of recent research is that tumours can actively recruit nerve fibres, even at very early stages.

The nervous system is not simply a passive observer. Nerve cells release signalling molecules that can influence:

cell growth
inflammation
blood supply
tissue regeneration

Cancer cells — and associated stromal cells like myCAFs — can exploit these signals.

This process is sometimes described as tumour-induced neuroplasticity, meaning that the tumour environment encourages nerves to grow, reorganise, and form new connections in ways that support cancer progression.

Why is this important in pancreatic cancer?

Pancreatic cancer is one of the most lethal cancers, partly because it develops within an unusually dense and complex microenvironment rich in:

fibrotic tissue
myCAFs
immune suppression
extensive nerve involvement

The interaction between fibroblasts and nerves may help explain why pancreatic cancer is so invasive and resistant to treatment.

The Evolutionary Perspective

None of this requires “design”. It is the predictable consequence of evolution producing multicellular organisms that rely on:

cell signalling
tissue repair pathways
growth mechanisms
immune modulation

Cancer arises because these systems, essential for life, can be corrupted when mutations and abnormal signalling accumulate.

What Intelligent Design advocates call “irreducible complexity” is, in reality, the vulnerability of evolved biological networks — systems that work well enough for survival and reproduction, but are not remotely “engineered” for perfection.

The background to the paper in Cancer Discovery is also the subject of a news release from Cold Spring Harbor Laboratory.

Let’s get on pancreatic cancer’s nerves

The Takeaway

CSHL postdoc Jeremy Nigri and colleagues in the Tuveson lab have discovered that the nervous system plays an active role in pancreatic cancer development—even before tumor formation. Disrupting interactions between nerves and fibroblasts could lead to new treatments or make standard procedures like chemo and immunotherapy more effective.

Pancreatic cancer has a lot of nerve. Notoriously tricky to detect, the disease also often resists traditional therapy. So, researchers are urgently looking for new ways to disrupt tumor formation. Though scientists know that the nervous system can help cancer spread, its role in the disease’s earliest stages remains unclear.

One phenomenon that is known is called perineural invasion. This means cancer cells will migrate within the nerve and use the nerve as a way to metastasize.

Professor Jeremy Nigri, lead author
Cold Spring Harbor Laboratory Cold Spring Harbor
New York, USA.

Now, Nigri and his colleagues at CSHL have discovered that the nervous system plays an active part in pancreatic cancer development, even before tumors form. Using 3D imaging, they found that tumor-promoting fibroblasts called myCAFs send out signals to attract nerve fibers. The myCAFs and nerve cells then work together within pancreatic lesions to create a favorable environment for cancer to grow. The findings are reported in Cancer Discovery, a journal of the American Association for Cancer Research.

A technique called whole-mount immunofluorescence enabled Tuveson’s team to take 3D photographs of the lesions and surrounding cells. Where standard 2D images show thin nerve fibers as scattered tiny dots, the 3D images reveal a dense network of nerves snaking through and around the myCAFs and lesions.

When we first saw this picture, I was shocked. I couldn’t even imagine the lesion like this. I’d only ever seen it in 2D.

Professor Jeremy Nigri.

3D images reveal the highly innervated microenvironment of pre-cancerous pancreatic lesions, seen here as red bubbles. Note the network of nerves in cyan and myCAFs in white.
Nigri and his colleagues ran a series of experiments on mice and human cells that uncovered a vicious cycle between myCAFs and nerves. They found myCAFs give off signals that attract nerve fibers from the sympathetic nervous system, which is responsible for our fight-or-flight response. These nerve fibers release the neurotransmitter norepinephrine, which binds to the fibroblasts and triggers a calcium spike that further activates myCAFs. This spike not only promotes pre-cancerous growth, but also pulls in even more nerve fibers, locking the system into a dangerous self-reinforcing loop.

In one experiment, we use a neurotoxin to disable the sympathetic nervous system. We show reduced fibroblast activation and a nearly 50% reduction in tumor growth.

Professor Jeremy Nigri.

Because the myCAF-nerve loop happens so early, disrupting this cycle could lead to potential new therapies. The findings suggest that clinically available drugs, including doxazosin, may be effective when combined with standard treatments like chemotherapy or immunotherapy.

The next step will be to study this more in detail and try to find a way to block the crosstalk between fibroblasts and nerves. With support from groups like the Lustgarten Foundation and Pancreatic Cancer Action Network, we hope to one day help improve patient outcomes.

Professor Jeremy Nigri.

Publication:
Jérémy Nigri, Wenjun Lan, Melanie L. Fung, Charlotte Kayser, Astrid Deschênes, Juliene Hinds, Sanjeev Kaushalya, Sara A. Pawlak, Jennifer S. Thalappillil, Sandeep Nadella, Marc Hilmi, Wungki Park, Rajya Kappagantula, Youngkyu Park, Zhen Zhao, Jonathan Preall, Christine A. Iacobuzio-Donahue, Kevin J. Tracey, Jeremy C. Borniger, David A. Tuveson;
Myofibroblasts induce neuroplasticity to promote pancreatic inflammation and cancer progression. Cancer Discov 2026; https://doi.org/10.1158/2159-8290.CD-25-1337

Abstract
Pancreatic ductal adenocarcinoma (PDAC) co-opts the peripheral nervous system through nerve hypertrophy, axonogenesis and perineural invasion, and these processes correlate with patient morbidity and mortality. Prior work has shown that autonomic nerves directly modulate neoplastic cells in PDAC, but whether cancer-associated fibroblasts (CAFs) participate in neural remodeling is unknown. Using thick tissue sections, we identified dense neo-innervation near myofibroblastic CAFs (myCAFs) in preinvasive Pancreatic Intraepithelial Neoplasms (PanINs). Mechanistically, TGF-β produced during inflammation and neoplasia triggers myofibroblast formation, and myCAFs produce axon guidance molecules that recruit sympathetic nerves. Norepinephrine released by sympathetic nerves activates myofibroblast cultures in vitro, and sympathetic nerve depletion impairs stromal activation and PDAC growth in vivo. A chemogenetic model confirmed that fibroblast-specific α1-adrenergic signaling exacerbated pancreatic inflammation and neoplasia. Therefore, beyond direct epithelial effects, sympathetic nerves promote pancreatitis and PDAC by co-opting myofibroblasts and myCAFs as disease amplifiers, highlighting CAF subtype-specific stromal interactions as putative therapeutic targets.

Jérémy Nigri, Wenjun Lan, Melanie L. Fung, Charlotte Kayser, Astrid Deschênes, Juliene Hinds, Sanjeev Kaushalya, Sara A. Pawlak, Jennifer S. Thalappillil, Sandeep Nadella, Marc Hilmi, Wungki Park, Rajya Kappagantula, Youngkyu Park, Zhen Zhao, Jonathan Preall, Christine A. Iacobuzio-Donahue, Kevin J. Tracey, Jeremy C. Borniger, David A. Tuveson;
Myofibroblasts induce neuroplasticity to promote pancreatic inflammation and cancer progression. Cancer Discov 2026; https://doi.org/10.1158/2159-8290.CD-25-1337

© 2026 by the American Association for Cancer Research.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

As always, the deeper problem for Intelligent Design advocates is that their argument cannot be applied consistently. If complex signalling networks and tightly coordinated cellular interactions are supposed to be evidence of a guiding intelligence, then they cannot selectively exclude the countless cases where those same systems produce suffering, disease, and death.

The interaction between myCAFs and nerve fibres in pancreatic cancer is not a bizarre anomaly — it is exactly what we should expect from evolved biological systems built on reused molecular pathways, tissue repair mechanisms, and cellular communication networks. Evolution does not produce perfection; it produces workable compromises, layered upon earlier compromises, all vulnerable to corruption when normal controls fail.

Cancer is not a refutation of evolutionary theory. It is one of its most tragic confirmations: a reminder that life was not engineered from scratch by an omniscient designer, but assembled through natural processes that favour survival and reproduction, not long-term health or moral outcomes.

Creationists may wish to invoke “design” when confronted with eyes or brains, but the logic does not stop there. The same complexity is present in tumours, parasites, and congenital disorders. If design is the explanation, then the designer is implicated in all of it — not just the parts that seem aesthetically pleasing.

And that is a conclusion Intelligent Design can never comfortably face.

If cancer’s exquisite complexity is not evidence for intelligent design, then neither is the blood-clotting cascade or eyes — and the entire argument evaporates.

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