Evolution Icon Evolution
Intelligent Design Icon Intelligent Design
Medicine Icon Medicine

Fighting Cancer with Intelligent Design

Casey Luskin


Antibiotic resistance is a real example of Darwinian evolution at work in nature. However, it typically entails small-scale change and a fitness cost — the breaking of useful molecular mechanisms in a cell. It is a form of evolution, but it doesn’t show significant creative evolution. So how do we fight it?

In my recent article “Does Medical Science Need Evolutionary Science?,” I discussed how we fight antibiotic resistance by using intelligent design principles, namely the fact that there are limits to how much organisms can evolve in the absence of design:

In fighting antibiotic resistance, Darwin’s theory actually provides little guidance. Indeed, quite the opposite. As SUNY Professor of Neurosurgery Michael Egnor has written here, “Darwinism tells us that … bacteria survive antibiotics that they’re not sensitive to, so non-killed bacteria will eventually outnumber killed bacteria. That’s it.”

To create drugs that outsmart evolving bacteria or cancer cells, biomedical researchers must use a process of intelligent design. They create drug cocktails that bank upon the fact that there are limits to how much living things can evolve on their own. Far from being evidence for Darwinian theory, antibiotic resistant bacteria point to what Michael Behe has called “the edge of evolution,” beyond which unguided Darwinian processes are powerless.

In simple terms, Darwinian evolution tends to work fine when only one mutation is needed to give an advantage. But when you need multiple mutations to gain an advantage, the process tends to get stuck. By throwing lots of antibiotic drugs at an organism, we force it to evolve lots of mutations — more than Darwinian evolution can produce — in order to survive. In this way, we can beat antibiotic-resistant microbes.

To explain further, let’s assume that for each antibiotic drug you throw at a disease-causing organism, it can be evaded by one single mutation in the bug. The more drugs you throw at the bug, the more mutations it must evolve in order to become resistant. By doing this, we can stack the odds in our favor: The bug has to evolve lots of mutations to survive. But only a single drug has to work to kill the organism.

For example, let’s say you throw a cocktail of five antibiotics at some pathogenic bacteria. Even if it evolves resistance to four of them (still which would be highly unlikely), if the fifth drug works to kill the organism, then you’ve beaten the bug. As you throw more antibiotic drugs at it, the likelihood of its evolving resistance decreases at an exponential rate. The odds of all the needed “resistance mutations” arising in a single organism are so low that, statistically, it’s not going to occur.

Again, if you stack the odds in your favor by creating a situation where an organism cannot evolve the needed mutations to evade your drug-cocktail, you can beat the evolution of antibiotic resistance. It only works because there are limits to how much things can evolve.

Speaking of which, here is a recent letter to the editor in the New York Times, by Dr. M. William Audeh at UCLA School of Medicine. He makes the same point with regard to fighting cancer. As the letter correctly observes, cancer is essentially a Darwinian process:

George Johnson correctly observes that immunotherapy for cancer relies on “Darwinian principles,” but the essential importance of evolutionary biology for understanding and treating cancer extends far beyond this.

Cancer entails out-of-control growth of cells. In their natural state, our cells are constrained in their reproducing by various molecular mechanisms in our genome . However, over time, mutations cause those constraints to break down. When this happens, a human cell line can begin to reproduce wildly, creating a cancerous tumor.

Now our genome has a lot of checks in place against this. That’s why cancer doesn’t typically show up early in life. It can take many years and many replications of our cells for all the requisite mutations to occur and remove all of the genomic barriers to uncontrolled cell growth.

And note that the kinds of mutations that occur to cause cancer aren’t constructive — they’re destructive, in the sense that they are breaking natural molecular mechanisms and built-in genomic checkpoints that prevent cell replication. However, once you get all the right (or rather, wrong) mutations, cancer can occur.

In a sense, then, cancer arises through a Darwinian process of mutation and replication. Cancer is a multimutation feature that involves the devolution or destruction of genomic constraints on cell proliferation.

Now that we understand how cancer works, how do we fight it? We do so in much the same way we fight antibiotic resistance: by banking on the fact that there are limits to how quickly (or how much) cells can evolve. Dr. Audeh makes this exact point:

Cancer in an individual should be thought of as an “invasive species” disrupting an ecosystem, a population of cells with extraordinary genetic diversity, possessing the ability to eventually adapt to nearly every therapy oncologists apply. The goal, in Darwinian terms, should be to reduce the genomic diversity in the cancer cell population by strategically targeting the key pathways of growth and survival which have allowed it to develop. Genomic sequencing of tumors, circulating tumor cells and cell-free DNA is providing us with the necessary information to do so. Targeting these pathways with combinations of non-cross-resistant drugs to overcome the adaptive potential of the population may produce a population “bottleneck” with low diversity — the key requirements for driving a species to extinction.

He says we kill cancer cells by using many (“combinations of”) drugs — more than they can possibly evolve resistance to.

When he says that we can “overcome the adaptive potential of the population,” he means there are limits to how much cancer cells can evolve. If we intelligently design combinations of drugs that would require more mutations than could possibly arise via Darwinian evolution, then we kill cancer cells before they evolve mutations to evade our therapy techniques.

Thus, yes, the growth of cancer in an organism, just like the proliferation of antibiotic resistant microbes, is a process of Darwinian evolution. The difference between cancer and Darwinian evolution in the real world is that in cancer, if left untreated, the cells that best survive and reproduce ultimately end up killing their host and destroying their own environment. But cancer helps us understand the sort of changes that Darwinian evolution can produce. It’s very good at breaking things, like destroying molecular barriers to cell growth. But it’s not good at creating something new, like evolving all the mutations necessary to evade anti-cancer drugs.

Darwinian principles help us understand how cancer works. At the same time, cancer points to the limits of evolutionary explanations. Darwinian thinking typically assumes that there are no constraints on how much organisms can evolve. It takes insights from intelligent design theory — that there are indeed limits or an “edge” to how much organisms can evolve — to beat antibiotic resistant microbes or cancer cells and successfully drive them into extinction.

Image: � Minerva Studio / Dollar Photo Club.


Casey Luskin

Associate Director, Center for Science and Culture
Casey Luskin is a geologist and an attorney with graduate degrees in science and law, giving him expertise in both the scientific and legal dimensions of the debate over evolution. He earned his PhD in Geology from the University of Johannesburg, and BS and MS degrees in Earth Sciences from the University of California, San Diego, where he studied evolution extensively at both the graduate and undergraduate levels. His law degree is from the University of San Diego, where he focused his studies on First Amendment law, education law, and environmental law.



cancerHealth & Wellnessscience