A paper just published in Molecular and Cellular Endocrinology shows how precisely the sort of complex specified information and irreducible complexity that Discovery Institute fellows William A. Dembski and Michael J. Behe proclaim as evidence of intelligent design can instead combine to ensure that pancreatic cancer survives, metastasises, and ultimately kills its victims.
This, of course, is true of many diseases, which simply would not exist unless the right combination of genetic information were present and functioning correctly for the disease itself. Yet creationists routinely compartmentalise their beliefs so that harmful “designs” are excluded and blamed on something else, while only those features that appear to benefit humans are credited to a designer.
In the case of parasites, what is harmful to humans is often beneficial to the parasite, but once again the presence of harm causes the logic of creationist arguments to shift. No longer is this evidence of intelligent design, but of something called “sin”, which appears to operate as an autonomous entity capable not only of corrupting creation but of designing living organisms and manipulating their genomes. The formerly omnipotent, omnibenevolent and omniscient designer god now seems strangely impotent, indolent, or indifferent in the face of this alternative “designer”.
This theology also sits uncomfortably alongside another core fundamentalist belief: that God has a plan for everyone, and that everything that happens in a person’s life occurs as part of this divine plan. Presumably, then, that plan must include any diseases they suffer from, including cancer.
It is therefore difficult to see how creationists can escape the conclusion that their god designs and causes cancer as part of this plan, while continuing to cling to the claim that intelligent design is inherently benevolent.
Intelligent Design and Disease. A persistent problem for Intelligent Design (ID) arguments is that the very features claimed as evidence of deliberate, foresighted engineering are often central to disease, disability, and premature death.So how do complex specified genetic information and irreducible complexity together help ensure that pancreatic cancers metastasise and eventually kill their victims? This is explained for a general readership in a news release from Agência FAPESP (São Paulo Research Foundation), by Fernanda Bassette:
ID proponents such as Michael J. Behe and William A. Dembski argue that systems exhibiting irreducible complexity or complex specified information could not have evolved step-by-step and therefore must have been designed. Yet those same properties are routinely exploited by pathological processes.
Cancer is an obvious example. Tumours hijack exquisitely regulated signalling pathways, DNA repair mechanisms, and cellular migration systems — all of which are often cited by ID advocates as paradigms of intelligent design. Metastasis, in particular, depends on tightly coordinated gene regulation, cell–cell communication, and environmental sensing. These are not failures of biological systems, but their normal operation redirected by natural selection acting at the level of rogue cells.
Parasitic organisms provide another clear case. The malaria parasite (Plasmodium), for example, has a life cycle of extraordinary molecular and cellular complexity, involving multiple hosts, immune evasion strategies, and finely tuned gene expression. If complexity is evidence of design, then malaria parasites are at least as “designed” as the humans they infect.
Autoimmune diseases further undermine the design narrative. The immune system’s sophistication — often celebrated by ID proponents — is precisely what allows it to malfunction in conditions such as multiple sclerosis, lupus, and type 1 diabetes. These diseases arise not from a lack of complexity, but from too much of it, interacting in unstable and unpredictable ways.
In evolutionary biology, this presents no contradiction. Natural selection does not optimise for health, longevity, or moral outcomes; it merely preserves what works well enough to reproduce in a given environment. Intelligent Design, by contrast, selectively counts beneficial outcomes as evidence for design while treating harmful ones as exceptions requiring ad hoc theological explanations.
Disease, therefore, is not a peripheral problem for the design argument — it strikes at its core.
Study reveals protein linked to spread of pancreatic cancer through nerves
Brazilian research shows that stellate pancreatic cells produce periostin, remodeling tissue and facilitating tumor infiltration, a key mechanism of the aggressiveness and high mortality of the disease.
A new Brazilian study published in the scientific journal Molecular and Cellular Endocrinology has revealed the key role of the protein periostin and stellate pancreatic cells in allowing pancreatic cancer to infiltrate nerves and spread early, increasing the risk of metastasis. The research demonstrates how the tumor reprograms part of the surrounding healthy tissue to acquire a high capacity for invasion. This mechanism is associated with the aggressiveness of the disease and the difficulty of treatment. It also points to possible targets for more precise therapies and personalized treatments.
The most common type of pancreatic cancer is adenocarcinoma, which originates in the glandular tissue that produces pancreatic juice. It accounts for 90% of diagnosed cases. Although it is not among the most frequent types of cancer, it is considered an aggressive and highly lethal tumor, with a mortality rate almost equivalent to its incidence rate. Globally, there are approximately 510,000 new cases and nearly the same number of deaths each year.
In Brazil, the National Cancer Institute (INCA) estimates there are about 11,000 cases and 13,000 deaths every year.
It’s an aggressive cancer that’s difficult to treat. Around 10% of patients have a chance of long-term survival, such as five years after diagnosis.
The aggressiveness of this tumor is linked to perineural invasion, a process in which cancer cells infiltrate and spread along nerves. This can cause intense pain and facilitate the spread of the tumor to other regions.
Perineural invasion is a marker of cancer aggressiveness.
Pedro Luiz Serrano Uson Junior.
The study was conducted at the Center for Research on Inflammatory Diseases (CRID), one of FAPESP’s Research, Innovation, and Dissemination Centers (RIDCs), and its first author was researcher Carlos Alberto de Carvalho Fraga. The group sought to understand the molecular and cellular mechanisms underlying this invasion. To this end, they used technologies that allow the activity of thousands of genes in each cell to be analyzed and their exact position in the tissue to be mapped.
We were able to integrate data from dozens of samples with extremely powerful resolution.
Professor Helder Nakaya, Lead author
CRID - Centro de Pesquisa em Doenças Inflamatórias,
Ribeirão Preto, SP, Brazil.
Nakaya is also a senior researcher at Einstein Israelite Hospital and a professor at the University of São Paulo’s School of Pharmaceutical Sciences.
When analyzing this set of information in 24 pancreatic cancer samples, the researchers observed that the stroma, or the tissue that supports the tumor, plays an active role in its progression. One of the most significant findings was the behavior of pancreatic and stellate cells, which express high levels of periostin, a protein capable of remodeling the extracellular matrix – the structure that organizes and maintains healthy tissue.
The study points out that tumor cells depend on intense extracellular matrix remodeling processes to advance through tissue and reach nerves, a complex process involving specific enzymes and tissue disorganization.
Periostin participates in this remodeling, paving the way for tumor cells to invade.
Professor Helder Nakaya
The nerve, in turn, functions as a kind of “road” for this expansion.
This altered environment generates a desmoplastic reaction: intense fibrosis around the tumor formed by cells and proteins that harden and inflame the tissue. This hinders the arrival of chemotherapy and immunotherapy drugs because they have more difficulty penetrating the hardened tissue. This creates a “microenvironment” that favors the survival and spread of the tumor.
That’s why pancreatic cancer is still so difficult to treat.
Pedro Luiz Serrano Uson Junior.
The oncologist emphasizes that this ability to infiltrate is decisive for the poor prognosis of patients with pancreatic cancer.
Perineural invasion is a sign that cancer cells have gained mobility. They escape the tumor mass, travel through healthy tissue, and reach nerve and lymphatic bundles, which carry them to other regions of the body, facilitating the development of metastases.
Pedro Luiz Serrano Uson Junior.
He says that more than half of pancreatic cancer cases show perineural invasion in the early stages, which is only discovered during surgery.
Unfortunately, we discover this perineural invasion after it’s already occurred. It’s only seen in the surgical specimen when it goes for biopsy.
Pedro Luiz Serrano Uson Junior.
Promising target
Given this complex scenario, the researchers say that periostin emerges as a promising therapeutic target. Blocking its action or eliminating the stellate cells that produce it may reduce perineural invasion and limit the tumor’s metastatic capacity.
This work points to paths that may guide future approaches to treating pancreatic cancer.
Professor Helder Nakaya
Clinical trials on other tumors are already testing antibodies against periostin. According to Nakaya, this helps explore whether this pathway may also be relevant in the pancreas.
Uson points out that this strategy is part of the advance toward precision medicine.If we can develop antibodies or drugs that block these stellate cells, we’ll have tools to prevent the tumor from acquiring this invasive capacity so early.
Pedro Luiz Serrano Uson Junior.
He notes that there is currently no therapy that specifically targets perineural invasion and stresses that such a drug could be useful in treating several other cancers that share the same mechanism, including intestinal and breast cancers.
In addition to revealing new therapeutic targets, the work demonstrates the power of complex analyses performed using public databases.We were able to ask and answer new questions that the original authors hadn’t considered.
Professor Helder Nakaya
The researchers say the next step is to transform this knowledge into strategies and drugs that act predictively, before invasion occurs.Precision medicine is advancing. In the future, we’ll treat patients based on genomic and molecular changes rather than tumor type specifically. This is a significant advance in oncology.
Pedro Luiz Serrano Uson Junior.
Publication:
Once again, what the evidence shows is not a failure of biology, but its success under natural selection operating without foresight, intent, or moral constraint. The molecular machinery that enables pancreatic cancer to invade nerves, evade immune surveillance, and metastasise is not some accidental glitch, but the normal functioning of deeply conserved biological systems repurposed by selection acting at the level of malignant cells. Evolution does not “care” whether those outcomes are beneficial or catastrophic for the organism as a whole.
This creates an insoluble problem for Intelligent Design. If complexity, specificity, and tight integration are hallmarks of design, then the same criteria apply just as forcefully to cancers, parasites, and pathogens as they do to organs and metabolic pathways. Selectively counting the former as evidence against design while celebrating the latter as evidence for it is not an argument; it is special pleading.
By contrast, evolutionary biology has no difficulty accommodating these findings. It predicts that systems shaped by incremental selection, historical contingency, and trade-offs will be powerful, flexible, and efficient — but also fragile, exploitable, and prone to failure in new contexts. Disease is not an embarrassment to evolution; it is exactly what we expect from a process that optimises locally and temporarily, rather than globally and benevolently.
As with so many areas of modern biology, this research does not reveal a hidden designer at work. It reveals instead the stark indifference of natural processes — and yet another example of how the Intelligent Design narrative collapses the moment it is confronted with the full consequences of biological complexity.
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