The 2010 paper in the British Journal of Cancer by M. Gerlinger and C. Swanton, “How Darwinian models inform therapeutic failure initiated by clonal heterogeneity in cancer medicine,” is presented as a clear demonstration of Darwinian evolution in action. The authors argue that the process by which tumors develop drug resistance is a microcosm of natural selection, where chemotherapy acts as a selective pressure, favoring the survival and proliferation of pre-existing resistant cancer cells. While the paper offers valuable insights into the clinical challenge of cancer therapy, its use as an analogy for the creative power of molecules-to-man evolution is profoundly misleading. A closer examination reveals that the phenomena described—natural selection acting on a population of cancer cells—do not demonstrate the origin of new biological information but rather the sorting of existing information and the net destruction of genomic integrity. This process is a textbook example of adaptive degeneration, not creative evolution.
A Fair Summary of the Research
Gerlinger and Swanton provide a compelling summary of how Darwinian principles apply to oncology. They posit that a tumor is not a uniform mass of cells but a heterogeneous population of distinct subclones, each with its own genetic variations. When a patient undergoes systemic cancer therapy, the drugs kill the susceptible cells, creating an “evolutionary bottleneck.” However, if any subclones happen to possess mutations that confer resistance, they will survive and repopulate the tumor. The paper highlights key examples, such as inactivating mutations in the MSH6 mismatch repair gene in glioblastoma, which confer resistance to temozolomide, and the T790M mutation in the EGFR gene, which confers resistance to gefitinib in lung cancer. The authors correctly note that this process is accelerated by “genomic instability,” which increases the rate of mutation and thus the genetic variation (heterogeneity) upon which selection can act. Their stated goal is to use this Darwinian framework to develop better clinical strategies, such as monitoring for resistant clones and finding ways to target the origins of this heterogeneity.
The Core Critique: A Failure to Create
The central claim of neo-Darwinism is that the tandem mechanism of random mutation and natural selection is a creative engine, capable of generating the novel specified information required to build new genes, proteins, and body plans. The evolution of cancer resistance, as described in this paper, provides zero support for this claim. Instead, it showcases the precise opposite: a process of decay, degradation, and loss of function that provides a short-term survival advantage.
First, the paper fails to document the origin of new, functional specified information. The “solutions” to the problem of chemotherapy are not novel inventions. The authors themselves note that the EGFR T790M resistance mutation was “detected in a minority population of cancer cells in some TKI-naive patients.” This means the resistance wasn’t created by the drug; it was already present in the pre-existing library of genetic variants within the tumor. Natural selection did not write a new chapter in the genetic book; it merely selected a pre-existing page. This is sorting, not creating.
Second, where mutations do arise, they are overwhelmingly degradative. The paper’s prime example is the inactivation of the MSH6 gene. This mutation confers resistance by breaking the cell’s own DNA mismatch repair machinery, which prevents the drug-induced damage from triggering cell death. This is a classic example of what biochemist Michael Behe calls “the first rule of adaptive evolution: break or blunt any functional gene whose loss would increase the number of a species’s offspring.” The cancer cell survives by crippling a sophisticated, pre-existing molecular machine. This is not forward-progressing evolution; it is adaptive degeneration. The “success” of the cancer cell comes at the cost of its own long-term genomic integrity, as the loss of MSH6 leads to a “hypermutator phenotype” that accelerates the accumulation of countless other errors.
This observation powerfully undermines the entire narrative. If the best and most rapid examples of “evolution in action” consistently involve breaking things, it fatally damages the proposition that the same mechanism can be relied upon to build the breathtakingly complex integrated systems of life. The process described is one of devolution, perfectly illustrating the principle of Genetic Entropy.
The Better Explanation: Designed Potential and Genetic Entropy
The evidence presented by Gerlinger and Swanton is far better explained by a model that incorporates principles of intelligent design, specifically the concepts of pre-loaded adaptive potential and universal genetic decay.
The fact that resistance mutations are often found pre-existing within the tumor population points to a design principle of front-loaded diversity. Just as a creator could pre-load a created “kind” with a vast library of genetic alleles to allow for rapid adaptation and speciation, a single founder cancer cell gives rise to a population with inherent variability. Natural selection acts as a powerful sorter of this pre-existing information, but it does not account for the origin of the information itself.
More profoundly, the process of gaining resistance by breaking cellular systems is a microcosm of Genetic Entropy. Dr. John Sanford’s work demonstrates that complex genomes are relentlessly accumulating mutations, the vast majority of which are slightly deleterious. Natural selection is powerless to stop this slow decay. The cancer cell’s “evolution” is a fast-motion picture of this universal principle. In its desperate struggle to survive the poison of chemotherapy, it sacrifices its own complex machinery, accumulating errors at an accelerated rate. It gains short-term survival at the price of long-term, irreversible genetic decay. This is not the engine of creation that supposedly built life from a simple cell to a human being; it is an engine of destruction, a confirmation that information-rich systems inevitably degrade over time, as predicted by the Second Law of Thermodynamics and a biblical worldview that posits a “very good” creation now subject to a universal curse of decay.
Conclusion
Gerlinger and Swanton’s paper is an important contribution to cancer medicine, correctly identifying natural selection as a key factor in drug resistance. However, to extrapolate this process to the grand narrative of molecules-to-man evolution is an unjustifiable leap of faith. The “evolution” observed in cancer is not a creative process of building new functions, but a degenerative process of sorting pre-existing information and breaking existing systems for short-term survival. It demonstrates not the power of mutation and selection to generate novelty, but its tendency to produce adaptive decay. The evidence, when viewed without the philosophical lens of materialism, points away from a blind, unguided process and toward a model of designed systems that are now, like all of creation, in a state of inexorable decline.
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