Monday, 9 February 2026

Malevolent Design - How Ovarian Cancer Looks Intelligently Designed to Spread Rapidly

Creationism's intelligent designer at work
AI-generated image (ChatGPT 5.2)

Cancer cells (red) stick to mesothelial cells (green) and form hybrid spheres that cut into surrounding abdominal tissue.
Scientists now know why ovarian cancer spreads so rapidly in the abdomen | Nagoya University

If intelligent design advocates were honest enough to follow the logic of their own arguments and apply it consistently to the real world, they ought to be acutely embarrassed by the deity they are presenting to the public. Their putative designer god, judged by the evidence they themselves cite, looks less like a benevolent engineer and more like the author of suffering, disease, and death.

That uncomfortable reality is illustrated by yet another research paper showing that pain and mortality can be the direct result of the very things ID proponents celebrate as hallmarks of design: irreducible complexity and “complex specified information”.

This latest example comes from scientists at Nagoya University, Japan, who have shown how ovarian cancer forms an alliance with healthy cells that enables it to spread rapidly to other organs in the abdomen. Their paper has just been published in Science Advances.

As regular readers will be aware, a recurring theme of this blog is that ID advocates conspicuously ignore the vast number of examples from parasitology, oncology, and genetics where the very evidence they cite for an intelligent designer applies just as readily to diseases caused by parasites, pathogens, and genetic malfunctions. Applying ID’s own logic, these are not signs of benevolent craftsmanship but evidence of something far darker — a malevolent intent behind the supposed designer.

The paper in Science Advances is yet another case in point, and doubtless there will be many more soon.

The authors discovered that ovarian cancer cells gather clusters of mesothelial cells from the peritoneum and form hybrid spheres. These protect the cancer cells, help them invade other organs, and create a pathway for metastasis throughout the abdomen. Worse still, these hybrid spheres resist chemotherapy more effectively than cancer cells alone.

If something this complex resulted in something beneficial for humans, Discovery Institute fellows Michael J. Behe and William A. Dembski would doubtless have produced one or more books about it, written magazine articles, and embarked on television tours explaining how the finding devastates “Darwinism” and constitutes scientific proof of an intelligent designer — leaving their audiences in no doubt that the locally favoured god is the only entity capable of producing such complexity.

As it is, we can expect only a deafening silence from the Discovery Institute, while their hapless supporters cast about for a fundamentalist religious excuse such as “the Fall”, or perhaps invoke some other evil agent — anything, in fact, except the god of the Bible, who is apparently only credited with designing good things.

Background^ Ovarian Cancer, Metastasis, and the Dark Side of Biological Complexity. Ovarian cancer is especially deadly not simply because it grows unchecked, but because it spreads through the abdomen with frightening efficiency.

Unlike many cancers that metastasise mainly through the bloodstream, ovarian cancer often disseminates directly throughout the abdominal cavity. Tumour cells can detach from the primary growth, survive in the peritoneal fluid, and seed new tumours on the surfaces of organs such as the intestines, liver, and diaphragm. This process — known as peritoneal dissemination — is one reason ovarian cancer is so often diagnosed late, when metastasis is already widespread and difficult to treat.

The new research from Nagoya University reveals an even more disturbing layer of sophistication. The authors found that ovarian cancer cells recruit healthy mesothelial cells from the peritoneum and form hybrid spheres. These clusters protect the cancer cells, help them invade other organs, and make them more resistant to chemotherapy than cancer cells alone.

This is complexity in action — but not the kind that Intelligent Design advocates like to talk about.

ID proponents frequently argue that biological complexity is evidence of purposeful engineering. Yet the same intricate cellular machinery that supports wound healing, immune defence, and normal tissue repair can also be hijacked to produce metastasis, chemotherapy resistance, and death.

If complexity is taken as proof of design, then ovarian cancer’s metastatic toolkit is as much a product of “design” as any beneficial adaptation. The evidence does not point uniquely to benevolent craftsmanship — only to the reality that evolved biological systems are full of vulnerable pathways, exploitable mechanisms, and unintended consequences.

In nature, complexity is morally neutral. Evolution produces it freely — and cancers exploit it ruthlessly.
The work of the Japanese researchers is the subject of a news article from Nagoya University.
Scientists now know why ovarian cancer spreads so rapidly in the abdomen
Study finds floating ovarian cancer cells recruit mesothelial cells in abdominal fluid to create cancer clusters
Ovarian cancer kills more women than any other gynecological cancer. Most patients receive their diagnosis only after the disease spreads throughout the abdomen. Until now, scientists have never fully understood why this cancer advances so fast.

A new study led by Nagoya University explains why. Published in Science Advances, the study shows that cancer cells recruit help from protective mesothelial cells that normally line the abdominal cavity. Mesothelial cells lead the invasion and cancer cells follow the pathways they create. These hybrid cell clusters resist chemotherapy better than cancer alone.

Researchers examined abdominal fluid from ovarian cancer patients and found something unexpected. Cancer cells do not float alone in the abdominal cavity. Instead, they often grab onto mesothelial cells and form hybrid spheres. About 60% of all cancer spheres contain these recruited mesothelial cells. The cancer cells release a protein called TGF-β1 that transforms the mesothelial cells and causes them to develop spike-like structures that cut through tissue.

Invadopodia, spike structures that do the digging for cancer

When ovarian cancer develops, cancer cells break off from the tumor. These cells enter the abdominal fluid and float freely. The fluid moves around as you breathe and move your body. This movement carries the cancer cells to different spots in the abdomen.

Most other cancers spread differently. Breast cancer or lung cancer cells enter blood vessels. They travel through the bloodstream to reach distant organs. Doctors can sometimes track these cancers through blood tests because blood moves in predictable paths through vessels.

Ovarian cancer cells avoid blood vessels entirely. They float in fluid that has no fixed path. This floating stage happens before the cancer cells attach to new organs. Scientists did not fully understand what happened during the floating period or how cells worked together to spread cancer so quickly.

The research team discovered that cancer cells recruit protective mesothelial cells that have shed from the abdominal cavity lining during this floating stage. The two cell types stick together and form hybrid spheres. The mesothelial cells then grow invadopodia, spike-like structures that drill into surrounding tissue. The hybrid spheres resist chemotherapy drugs more effectively and invade tissues faster when they land on organs.

Outsourcing the hard work of cell invasion

The researchers examined abdominal fluid from ovarian cancer patients using advanced microscopy to watch this process in real time. They confirmed their findings with mouse models and single-cell genetic analysis.

Lead author Dr. Kaname Uno, a former PhD student and current Visiting Researcher at Nagoya University’s Graduate School of Medicine, explained that the cancer cells do not need to become more invasive themselves.

They manipulate mesothelial cells to do the tissue invasion work. They undergo minimal genetic and molecular changes and just migrate through the openings that mesothelial cells create.

Dr Kaname Uno, lead author.
Department of Obstetrics and Gynecology
Nagoya University Graduate School of Medicine
Nagoya, Japan.

Dr. Uno worked as a gynecologist for eight years before he pursued research. One of his patients changed his career path. She had clear screening results just three months before doctors found advanced ovarian cancer. Current medical tools failed to detect the cancer early enough to save her life. This motivated Dr. Uno to investigate why ovarian cancer spreads so rapidly.

This discovery opens new treatment possibilities. Current chemotherapy targets cancer cells but ignores the mesothelial accomplices. Future drugs could block the TGF-β1 signal or prevent the formation of these dangerous partnerships. The research also suggests that doctors could monitor these cell clusters in abdominal fluid to predict disease progression and treatment response.

Publication:


Abstract
Patients with epithelial ovarian cancer (EOC) are often diagnosed with peritoneal metastasis and ascites, the accumulation of intraperitoneal fluid containing nonmalignant cells. However, the interactions between EOC and nonmalignant cells before peritoneal metastasis remain unclear. To investigate this, whole EOC spheroids were observed using a multiphoton microscope, and their invasion ability was assessed. Mesothelial cells were identified as notable components of ascites through morphological assessment, immunohistochemical/immunofluorescence staining, and single-cell RNA sequencing analyses. Almost all EOC cells were spheroids, with 60% containing mesothelial cells. EOC cells quickly generate aggregated spheroids with mesothelial cells, and these aggregated cancer-mesothelial spheroids (ACMSs) invade collagen or mesothelial layers. Mesothelial cells forming ACMSs initiated the invasion. RNA sequencing analysis revealed marked RNA expression changes in mesothelial cells, whereas the changes in EOC cells were minor. Transforming growth factor–β1–stimulated mesothelial cells showed increased invadopodium formation along with fascin-1 up-regulation. These findings suggest that EOC cells alter mesothelial cells through ACMSs, thereby elucidating the rapid spread of EOC in the abdominal cavity.


Once again, the real lesson of this research is not merely medical — important though it is for understanding and ultimately treating a devastating disease — but philosophical. It exposes the selective blindness at the heart of Intelligent Design advocacy. The Discovery Institute and its supporters are eager to point to complexity in biology as evidence of a guiding intelligence, but they become strangely mute when that same complexity produces parasites, cancers, congenital disorders, and the countless other afflictions that fill hospitals and graveyards.

The uncomfortable truth is that the biochemical sophistication of metastatic ovarian cancer is every bit as “irreducibly complex” and “information-rich” as anything Behe or Dembski have ever waved about as supposed proof of divine craftsmanship. If their logic were applied consistently, then the designer responsible for such systems would have to be credited not only with eyes and wings, but with tumours, chemotherapy resistance, and the ruthless exploitation of healthy tissue for malignant ends.

Predictably, creationist excuses will be produced on cue: the Fall, original sin, corruption of a once-perfect creation, or perhaps some shadowy secondary evil agent. But none of these ad hoc theological patches alter the central point. The complexity is real, the suffering is real, and the mechanisms are exactly what evolutionary theory predicts — not the products of foresightful engineering, but of natural processes that tinker, compromise, and leave organisms vulnerable to breakdown and exploitation.

Far from being evidence for design, ovarian cancer is yet another reminder that biology is not the work of an omnibenevolent architect. It is the outcome of evolution: powerful, creative, indifferent — and sometimes lethal.

And the evidence, as always, stubbornly refuses to support creationism.




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