Sick of the Oxygen Theory of the Cambrian Explosion? Here’s the Cancer Theory
You thought you’d heard it all? All the desperate materialist theories seeking to explain the burst of biological novelty some 530 million years ago that Meyer writes about in Darwin’s Doubt? You were wrong. Along comes Lund University in Sweden with a “Novel hypothesis on why animals diversified on Earth.” Get ready for the cancer theory of the Cambrian explosion.
Can tumors teach us about animal evolution on Earth? Researchers believe so and now present a novel hypothesis of why animal diversity increased dramatically on Earth about half a billion years ago. A biological innovation may have been key. [Emphasis added.]
Not many of us who have seen friends suffer or die from cancer would sanctify tumors as “biological innovations” leading to anything good.
The new hypothesis holds that the dramatic diversification of animals resulted from a revolution within the animals’ own biology, rather than in the surrounding chemistry on Earth’s surface.
This will be a hard sell, but charitably, let’s give them their slot on the Cambrian Gong Show and try to understand their act. It’s good to see they toss out the oxygen theory, the runner-up for worst explanation. Agreed, “a causal relationship between the Cambrian explosion and increasing atmospheric oxygen lacks convincing evidence.” With itching ears we await their convincing evidence for the new hypothesis.
The leader figure behind the cancer theory is geobiologist Emma Hammarlund. She got in touch with a tumor biologist, Sven Påhlman, to consider how cancer acts like a multicellular organism.
“I wanted to learn what tumor scientists observe on a daily basis, in terms of tissue growth and how it relates to oxygen. Tumours are after all, and unfortunately, successful versions of multicellularity”, explains Emma Hammarlund.
OK, so we have multicellularity. Tumors don’t seem to automatically grow eyes and articulated limbs, though. As far as we can tell, tumors only seem to be good at killing their hosts. What’s up with this new hypothesis?
The team, including also tumor biologist Dr. Kristoffer von Stedingk at Lund University’s Paediatrics division, tackled the historic question of why animals developed so late and dramatically with novel clues from the field of tumour biology.
Basically, they looked at stem cells to see how they respond to oxygen. Generally, low oxygen (hypoxia) is a threat to a cell, and stem cells are particularly sensitive to hypoxia (are you still following?). Stem cells, therefore, have various mechanisms to deal with fluctuating oxygen levels. Well lo and behold, tumor cells do, too!
These systems involve a protein that can ‘fool’ cells [to] act as if the setting was hypoxic. This can also fool cells to get stem cell-like properties.
Tumor cells, they say, are able to maintain their stem-cell-like traits in spite of low oxygen. This gives them the freedom to evolve, just like microbes found a way to use sunlight. (What?) You may have to read this news several times to see how they get from point A, an uncontrolled tumor cell, to point B, a trilobite.
The new hypothesis that gives credit to a biological innovation to have triggered animal diversification is similar to how we think of biological innovations changing life in the past. Just the presence of free oxygen is the result of some microbes finding a way of using sunlight to get energy. This was also a biological event.
Dr. Hammarlund is a little clearer about what she means in her article at The Conversation, “Cancer tumours could help unravel the mystery of the Cambrian explosion.”
Could tumours help us explain the explosion of life of Earth? Scientists have typically explained the period of history when large animal species became much more diverse very quickly as the result of the planet’s rising oxygen levels. But my colleagues and I have developed a new idea that the change might have started within animals’ own biology, based on evidence from proteins found in tumours. It wasn’t until animals developed these proteins that they could take advantage of the oxygen and start diversifying.
This new hypothesis appears partly motivated by the failure of the oxygen theory to account for the Cambrian explosion. Here’s how it goes. In short, proteins “developed” out of nowhere. By chance, they gave cells the opportunity to “take advantage” of oxygen. This set them free to diversify. And there you go: trilobites.
Does she explain exactly how they diversified into animals with multi-system, hierarchical body plans with complex systems and behaviors? Not at all. Take a look at this newly discovered Cambrian bristle worm from Marble Canyon in Canada and see if it looks like the product of a tumor set free to diversify (Live Science).
Maybe the original paper in Nature Ecology & Evolution can clarify things. The title is, “Refined control of cell stemness allowed animal evolution in the oxic realm.” The peer-reviewed explanation follows:
Animal diversification on Earth has long been presumed to be associated with the increasing extent of oxic niches. Here, we challenge that view. We start with the fact that hypoxia (<1–3% O2) maintains cellular immaturity (stemness), whereas adult stem cells continuously — and paradoxically — regenerate animal tissue in oxygenated settings. Novel insights from tumour biology illuminate how cell stemness nevertheless can be achieved through the action of oxygen-sensing transcription factors in oxygenated, regenerating tissue. We suggest that these hypoxia-inducible transcription factors provided animals with unprecedented control over cell stemness that allowed them to cope with fluctuating oxygen concentrations. Thus, a refinement of the cellular hypoxia-response machinery enabled cell stemness at oxic conditions and, then, animals to evolve into the oxic realm. This view on the onset of animal diversification is consistent with geological evidence and provides a new perspective on the challenges and evolution of multicellular life.
From this, you see that all they are really doing is “enabling” microbes to evolve into animals, no matter how much oxygen is present. The authors endow microbes with new transcription factors that don’t restrict the action of their stem-cell properties as oxygen levels rise. Microbes can now become “successful versions of multicellularity” like cancerous tumors, and thus evolve into the Cambrian animals. Are we missing something? Do the judges want to gong this show yet?
In his recent book, Zombie Science, Jonathan Wells already gonged the cancer act when it played in a different venue. Evolutionists feel depressed at the lack of enthusiasm for Darwinism in medical science. A recent paper in PLOS ONE admits this:
Evolutionary biology currently has a marginal place within medicine. There is even a significant tendency to avoid the ‘e-word’ in the biomedical literature when referring to antimicrobial resistance.
In his chapter on antimicrobial existence as an icon of evolution (Chapter 8), Wells discusses the cancer hypothesis as another proposed example of “speciation” of sorts. This claim goes back to Julian Huxley in 1958, and continues today. Most recently, Joshua Swamidass used cancer not as an example of speciation, but of evolution by mutation and selection of the “fittest variants” (not fittest for the host, obviously). Swamidass and others try to view tumor cells as innovators. Wells looks into the examples provided by evolutionists and finds them lacking true novelty. They only rewire existing complex functions, but already have existing complex resources to draw on (p. 166). This is not innovation. It’s more like theft.
Evolutionary theory, furthermore, does little to guide medical science into new treatment options for cancer patients. Its value is “questionable, at best,” Wells concludes (p. 167). It certainly fails as evidence for evolution.
But some people argue that cancer is at least of value in providing evidence for evolutionary theory. Something doesn’t seem right here. According to evolutionary theory, the human body originated by mutation and selection, though the evidence shows that those processes cannot produce anything like a human body. Now we have evidence that mutation and selection can produce cancer, which destroys the human body. How does that support evolutionary theory? (pp. 167-168).
Applying this reasoning to Hammarlund’s cancer hypothesis for the Cambrian explosion, one finds no evidence that tumors can innovate the body plans of Cambrian animals. Jonathan Wells’s last paragraph applies here as well:
Darwinian evolution needs examples of biological processes that build new forms and functions. Cancer destroys these things. Saying cancer is evidence for biological evolution is like saying that I have a theory that explains the rise of modern civilization, and the evidence for my theory is the night of the living dead. (p. 168).
So to the cancer theory for the Cambrian explosion, the most desperate yet, we hit the gong and await the next act.
Photo credit: Emma Hammarlund and Sofie Mohlin, via Lund University.