Critics of intelligent design (ID) sometimes argue that if the human body were designed, it would be perfect. Among other things, we would not suffer from diseases such as cancer.
Defenders of ID point out that this criticism is misplaced. Design does not imply perfection. Many things we know to be designed (such as cars) are imperfect. The “argument from imperfection” against ID is implicitly a theological argument, namely, that God is the designer and anything designed by God must be perfect. ID does not make that claim.
But cancer is now being used as an argument against ID in another sense. Writing at the BioLogos website, which presents “an evolutionary understanding of God’s creation,”1 computational biologist Joshua Swamidass has argued that “cancer regularly innovates with proteins of novel function.”2 He calls this “neo-functionalization.” According to Swamidass, this “casts serious doubt on the ID arguments from molecular biology,” namely, that proteins cannot evolve novel functions without the aid of intelligent design. He concludes that if ID were true, “then cancer as we know it would be mathematically impossible, or regularly require the direct intervention of God to initiate and be sustained.”3
Innovation or De-regulation?
But is it true that “cancer regularly innovates with proteins of novel function”? Many cancers have alterations in their DNA that are called “gain-of-function” mutations. But how novel are the functions that are gained?
Two classes of “genes” (protein-coding regions of DNA) that have been widely studied in cancer are “proto-oncogenes,” which, when mutated, lead to the uncontrolled growth that characterizes cancer cells, and “tumor suppressor genes,” which normally prevent cancer but when mutated fail to block it. The former include genes of the Ras family, while the latter include the TP53 gene.
Ras genes produce signaling proteins that induce cells to divide. In normal cells, Ras proteins (gene names are italicized, while the proteins encoded by them are not) are turned off much of the time, but when mutated, they get stuck in the “on” position (a condition called “constitutive activation”). So they induce cells to divide without stopping.4 Although this is called a “gain-of-function” mutation, the Ras protein hasn’t actually gained a new function. It has simply lost the ability to regulate its old one.5
The TP53 gene encodes a protein called p53 that has many functions. It binds to specific DNA sequences, but it also interacts with many other molecules involved in cell metabolism.6 In normal cells, the functions of p53 prevent the cell from becoming cancerous, but when TP53 mutates, this function is abolished. The mutant protein still binds to DNA, but it has lost its ability to target specific sequences, so it interacts with regions of DNA that are unaffected by normal p53. The mutant protein (designated mutp53) also accumulates at a much higher concentration than normal p53 (designated “wild-type” p53, or wtp53). Like wtp53, mutp53 continues to interact with many other molecules in the cell, but those interactions are now perverted to the point where the cell becomes cancerous and invades other tissues.7
This does not necessarily mean that mutp53 acts through mechanisms different from those of wtp53. The mutant protein binds to more regions of DNA than wtp53, not because it has gained anything, but because it has lost its sequence specificity. And the other effects of mutp53 are not as novel as they seem. According to Israeli cancer researchers Moshe Oren and Varda Rotter, “given the high concentration of mutp53 protein in tumor cells, relatively weak molecular interactions, which are marginal within the wtp53 protein, may now be amplified by mass action and reach a threshold that allows them to exert a measurable impact on biochemical processes within the cell.”8
In 2012, philosopher of biology Pierre-Luc Germain emphasized that the “new” functions in cancer cells “are not complex adaptations; in other words, they are not the result of cumulative evolution. . . . Instead, it is the pre-existing wiring of the cell which best accounts for these features.” In other words, “healthy cells—their structure, possible states, pathways, and weak spots—already contain the resources to be drawn upon and developed by cancer cells.”9
So the neo-functionalization that Swamidass attributes to cancer cells is really the de-regulation and perversion of existing functions, rather than the creation of new ones.
Swamidass goes on to argue that “evolutionary theory ‘makes sense’ of cancer.” We see “all the same genetic patterns in cancer tumors that we see in, for example, humans [and] the great apes.”10 Most DNA changes in cancer cells are not “driver” mutations that contribute to malignancy, but “passenger” mutations that simply go along for the ride. This is consistent with the modern “neutral theory of evolution,” which says that most DNA mutations have little or no effect and persist because they are not eliminated by natural selection. According to Swamidass, “this is true for cancer, and it is also true for the evolution of new species.” In other words, “cancer evolves with the same evolutionary mechanism that drives the evolution of new species.”11
But we don’t actually know what drives the evolution of new species. Except for some examples of chromosome doubling in plants (which can lead to reproductive isolation, though not to new organs or body plans), the origin of species is as much a mystery today as it was when Charles Darwin wrote his book by that name. No one has ever observed the origin of a new species by mutation and selection — certainly not by the accumulation of neutral mutations.
What we do observe is cancer.
Swamidass asks, “If evolutionary theory is wrong about the origin of species, why does it work so well for cancer?”12 Or, “if the ID proponents are right about evolution, why would we conclude anything different here?”13
Well, we conclude something different because the origin of species and the development of cancer are polar opposites. Perhaps evolutionary theory can explain the destruction of living things, but that does not mean it can explain the construction of living things.
A rough analogy would be to compare the rusting of steel with the smelting of iron ore. We see the same chemical pattern, namely, the inter-conversion of iron and iron oxide. Rusting converts iron to iron oxide, and smelting converts iron oxide to iron. The two are polar opposites. The first is explained by unguided natural processes, but the second requires intelligent design. The Iron Age would not have happened without human intelligence.
So cancer might exemplify the process of unguided evolution, but it certainly does not disprove intelligent design.
- S. Joshua Swamidass, “Cancer and Evolutionary Theory,” The BioLogos Forum (Sept. 13, 2016).
- David S. Goodsell, “The molecular perspective: The ras oncogene,” The Oncologist 4 (1999), 263–264.
- Krishnaraj Rajalingam et al., “Ras oncogenes and their downstream targets,” Biochimica et Biophysica Acta 1773 (2007), 1177–1195.
- Celia R. Berkers et al., “Metabolic regulation by p53 family members,” Cell Metabolism 18 (2013), 617–633.
- Varda Rotter, “p53, a transformation-related cellular-encoded protein, can be used as a biochemical marker for the detection of primary mouse tumor cells,” Proceedings of the National Academy of Sciences USA 80 (1983), 2613–2617.
- Moshe Oren and Varda Rotter, “Mutant p53 gain-of-function in cancer,” Cold Spring Harbor Perspectives in Biology 2 (2010).
- Pierre-Luc Germain, “Cancer cells and adaptive explanations,” Biology and Philosophy 27 (2012), 785–810.
- S. Joshua Swamidass, “Cancer and Evolutionary Theory,” The BioLogos Forum (Sept. 14, 2016).
- S. Joshua Swamidass, “Cancer and Evolution,” BioLogos (Jan. 11, 2017).
- S. Joshua Swamidass, “Cancer and Evolutionary Theory,” The BioLogos Forum (Sept 14, 2016).
Photo: Breast cancer cell, via National Cancer Institute.
Editor’s note: Dr. Wells’s latest book is Zombie Science: More Icons of Evolution. A version of this article first appeared in Salvo 42. It is published here with the permission of Jonathan Wells.