September 21, 2021 | Jerry Bergman

Is Cancer an Example of Evolution?

Does Everything Evolve, Even Cancer? No! Actually,
Cancer Research is Based on Intelligent Design, not Evolution

 

by Jerry Bergman, PhD

Cancer is the result of breaking genes, which happens when mutations strike. An oft-repeated claim by those who support Darwinism is that knowledge of the theory of evolution is critical to help researchers understand the cause and progression of cancer. Consequently, they argue, it is an important idea to apply when doing cancer research. Professors Sonnenschein and Soto write that “at the root of the cancer puzzle [is] … a new theory of carcinogenesis that is compatible with evolutionary theory.”[1] From my over five years doing cancer research at The Medical College of Ohio, as well as completing a Master’s thesis on the subject, it is my conclusion that, in reality, Intelligent Design is the basic assumption used in all cancer research.[2] Similarities are alleged between cancer and evolution, but attempts to link the two fail on several counts.

One fact that consistently impressed me when doing research on cancer was that many complex systems exist in the body that are designed to prevent cancer. These systems are superb examples of ingenious design. Cancer is caused by damage to this well-designed system. One example discussed below is damage to the tumor-suppressor gene called p53.

When cells become cancerous, the body’s immune system is usually able to detect and destroy the renegade cells even though the cancer cells are the body’s own cells.  Every adult has precancerous and some cancerous cells as well. It is only when the number of these cells is greater than what the immune and protection systems can handle that it becomes a problem. Cancer can also be triggered if the immune system becomes weak or is damaged from poor health habits. These include smoking, poor diet, or exposure to high levels of radiation such as radon.

Cell growth and reproduction generally involve two factors, growth factors (which initiate cell division) and growth regulation factors (which inhibit cell division when the need for more cells no longer exists). In cells, both the message to cause the cell to divide (the growth factors), and the brakes (called tumor suppressors) must be damaged before the uncontrolled cellular growth called cancer can develop.

Tumor suppressor genes regulate cell growth, and also serve to inhibit cell division if the cell or its regulatory processes are damaged. In cancer cells, the switch that tells the cell to grow and divide is jammed on like a broken motor switch causing the motor to run until it breaks. An example is the RAS gene which is commonly damaged in pancreatic and other cancers.

The Repair System

Thousands of genetic mutations occur in cells daily, and 99.99 percent of the time the damaged cells are efficiently mended by our highly effective repair systems.[3]  Only under extreme circumstances, such as when a cell is exposed to high levels of carcinogens, or when the cell has suffered significant genetic damage, can the disease of cancer gain a footing. If certain mutations damage the cell’s DNA, the tumor-suppressor gene p53 directs the cell to repair the DNA.[4]  p53 does this by promoting the expression of proteins that halt progression of the cell cycle—giving the cell time to repair its DNA before it divides. Then p53 directs the cell to repair the damage.[5] This is but one example illustrating the enormous complexity of systems designed to prevent the onset of cancer. Normally p53 is able to repair or destroy the damaged cell before it causes problems. Of the over 6.5-million people diagnosed with cancer each year, fully half of them had damaged p53 genes.[6]

When the repair mechanisms fail, cancer cells no longer perform the tasks for which they were designed, and instead rapidly proliferate. They spread their damaged cells until one or more organs can no longer perform their required functions. The result is often the death of the cancer patient, and, consequently, the death of all of the victim’s cells including the cancer cells. Although the cancer cells get a short-term “advantage” by growing and spreading, the result is not an evolutionary advantage for the organism as a whole.

The 2020 Sonnenschein and Soto Study

Sonnenschein and Soto argue that cancer is like evolution. They say their cancer-evolution rationale is based on “Darwin’s theory of evolution,” the idea that “all living organisms originated from a common ancestor that must have been endowed with the capacity to proliferate constitutively, as long as conditions for survival were met.”[7] They also believe that the current theory of carcinogenesis should be abandoned or modified, and replaced by a theory relevant to the theory of evolution.

After carefully reading their study, it appeared to me that all they were claiming was that mutations alter a cell’s internal controls. The most well-known example is heart cancer, a type of sarcoma, which is rare partly because myocardial cells very rarely divide.[8]  Epithelial cells (skin and mucus lining cells), by contrast, divide after about three days, and are among the first cells to be exposed to external carcinogens.[9] Consequently, cancer of epithelial tissue is the most common known cancer; sarcoma of the heart one of the rarest.[10] In Frontiers in Ongology this month (10 Sept 2021), Catania et al. make the case that cancer is not like evolution.

Although neo-Darwinian (and less often Lamarckian) dynamics are regularly invoked to interpret cancer’s multifarious molecular profiles, they shine little light on how tumorigenesis unfolds and often fail to fully capture the frequency and breadth of resistance mechanisms. This uncertainty frames one of the most problematic gaps between science and practice in modern times.[11]

The authors then offer a theory of cancer which builds on a “molecular mechanism that lies outside neo-Darwinian and Lamarckian schemes.” In the neo-Darwinian model, they say, “chance plays a central role in the emergence of mutations.”[12] In their new model

the conversion of a healthy cell into a cancerous cell is neither abrupt nor accidental. Rather, it is the result of an environmentally induced process that is for one traceable and for another reversible. If this model is correct, then tracing epimutations induced by a habitual exposure to microenvironmental stress should represent a powerful strategy to anticipate the emergence of cancer. Additionally, in a world where obesity is the first cause of cancer, changes of inflammation-promoting lifestyle and dietary regimes would help reverse and reduce the induction of cancer-related mutational and adaptive events.[13]

This view puts the onus squarely on the person, not on poor design. It fits our understanding of health. If you take care of yourself properly you are more apt to be healthy, especially with the current epidemic of obesity.

Another 2021 study further challenges the Darwinian cancer theory. In the EMBO Journal 30 Aug 2021, Vendramin et al. discuss how somatic cell divisions produce cell clones but mutational changes cause a family of subclones. Being careful not to step on the feet of Darwinists, the authors cautiously wrote the following:

several lines of evidence suggest a Darwinian model alone is insufficient to fully explain cancer evolution. First, the role of macroevolutionary events in tumor initiation and progression contradicts Darwin’s central thesis of gradualism. Whole-genome doubling, chromosomal chromoplexy [a complex DNA mutational rearrangement in cancer cell genomes] and chromothripsis [mutations that cause thousands of chromosomal rearrangements in a localized genomic regions in one or a few chromosomes] represent examples of single catastrophic events which can drive tumor evolution [progression]. Second, neutral evolution can play a role in some tumors, indicating that selection is not always driving evolution. Third, increasing appreciation of the role of the ageing soma has led to recent generalized theories of age-dependent carcinogenesis. Here, we review these concepts and others, which collectively argue for a model of cancer evolution which extends beyond Darwin.[14]

They then compare cancer progression to evolution, noting that tumors often are described as a

large population of genetically diverse cells giving rise to distinct subpopulations. Subclones will compete with one another for a limited set of nutrients and metabolites and face ever-shifting selective pressures driven by both endogenous (i.e. microenvironmental pressures and geographical barriers) and exogenous (i.e. therapy) factors. The outcome of this competition is the survival of clones adapted to grow under very specific conditions, as Darwinian selection is highly contextual and blind to the future. Many clones that were dominant at one point in time may reach evolutionary dead ends and disappear, while only a minority may be able to persist. Quoting Darwin “One general law, leading to the advancement of all organic beings, namely, multiply, vary, let the strongest live and the weakest die.”

Problems with the analogy

This analogy is actually damaging to the evolutionary position. According to the comparison, natural selection in the biosphere will lead to the same end as cancer, namely “the strongest live and the weakest die.” Cancer, remember, is a killer. If cancer cells are the “more fit” in the body, they end up killing every cell, including the cancer cells. If this same process continues in the world, eventually it take down the whole ecosystem and lead to the extinction of all life.

This is especially true if, as Darwinists insist, life has been on the Earth for over two billion years. Given a wide variety of life forms and the assumption that in each generation the fittest are more likely to survive and reproduce, then the less-fit will perish, with each new generation repeating this process. This cycle will continue until eventually, in short order, only the very fittest of the fit will remain. This super-fit organism will likely also eventually become extinct due to factors such as a lack of the less-fit to exploit for food and also the accumulation of mutations. Listen to Darwin’s own definition of natural selection:

Can the principle of selection, which we have seen is so potent in the hands of man, apply in nature? I think we shall see that it can act most effectually. … Let it be borne in mind how infinitely complex and close-fitting are the mutual relations of all organic beings to each other and to their physical conditions of life. Can it, then, be thought improbable, seeing that variations useful to man have undoubtedly occurred, that other variations useful in some way to each being in the great and complex battle of life, should sometimes occur in the course of thousands of generations? If such do occur, can we doubt (remembering that many more individuals are born than can possibly survive) that individuals having any advantage, however slight, over others, would have the best chance of surviving and of procreating their kind? On the other hand, we may feel sure that any variation in the least degree injurious would be rigidly destroyed. This preservation of favourable variations and the rejection of injurious variations, I call Natural Selection. [15]

Upward progress will never occur in this scenario, partly because natural selection tends to only reduce the level of degeneration of a population by (as Darwin postulated) continually reducing even the slightly less-fit population. As a result, it could only maintain the generally fit if it selects at all.

Another major difference between cancer progression and evolutionary enhancement is most organisms are naturally born fit and already contain the required genetic variety necessary to survive. Evolution, though, is based on the belief that evolutionary progress produces increasingly more-fit organisms.

In fact the lethal problem with Darwinism is not the survival of the fittest but the arrival of the fittest. The only viable source of new genetic variation is mutations. The vast majority of mutations are either near-natural (which accumulate leading to genetic meltdown) or deleterious. Those are lethal, ending that genetic line.[16]

Summary

Cancer research requires the assumption of Intelligent Design, not evolution. To understand cancer, scientists need to understand how the highly-complex and effective genetic repair systems work. Failure of these systems is usually due to cell damage caused by carcinogens in the environment, allowing cancer to gain a foothold. Far more effective than Darwin’s theory for preventing cancer is promoting general health, especially minimizing obesity. To solve the cancer crisis, society does not need Darwin’s theory. It needs to focus more on prevention by improving health. Cancer treatments are often too late to effectively deal with emerging tumors, so earlier diagnosis is needed. The argument that evolution can help us treat cancer is not using the word evolution the way Darwin meant. Cancer kills. Darwin’s theory imagined that simple cells could evolve to become all complex life on Earth.[17] That is clearly not happening in out-of-control, broken cancer cells.


References

[1] Sonnenschein, Carlos, and Soto, Ana M. 2020. Over a century of cancer research: Inconvenient truths and promising leads, PLOS Biology 18(4):e3000670, April 1. Emphasis added.
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000670.

[2] Bergman, Jerry. 1999. Tumor Markers in Cancer Treatment. Master of Science in Biomedical Science Dissertation. Toledo, OH: Medical College of Ohio.

[3] Bergman, Jerry. 2005. The mutational repair system: A major problem for macroevolution. CRSQ 41(4):265-273, March.

[4] Bergman, Jerry. 1999. Tumor Markers in Cancer Treatment. Master of Science in Biomedical Science. Dissertation. Toledo, OH: Medical College of Ohio.

[5] Kandoth, Cyriac, et al. 2013. Mutational landscape and significance across 12 major cancer types. Nature 502(7471):333–339, October 17. doi: 10.1038/nature12634.

[6] Lakin, Nicholas D., and Jackson, Stephen P. 1999. Regulation of p53 in response to DNA damage. Oncogene 18(53):7644–7655, December 13. doi: 10.1038/sj.onc.1203015.

[7] Sonnenschein and Soto, 2020, p. 5.

[8] Al‐Rajhi, Nasser, et al., 1999. Primary pericardial synovial sarcoma: A case report and literature review. Journal of Surgical Oncology 70(3):194-198.

[9] Sonnenschein, Carlos, and Soto, Ana M. 2000. The somatic mutation theory of carcinogenesis: Why it should be dropped and replaced. Molecular Carcinogenesis 29(4):205-211, December 1. PMID: 11020241.

[10] Mullin, J.M. 2004. Epithelial barriers, compartmentation, and cancer. Science Signaling 2004(216):pe2, January 20. https://stke.sciencemag.org/content/2004/216/pe2/tab-pdf. [Link goes to your article, not Mullins’.]

[11] Catania, Francesco, et al. 2021. Bridging tumorigenesis and therapy resistance with a non-Darwinian and non-Lamarckian mechanism of adaptive evolution. Frontiers in Oncology, September 10. https://www.frontiersin.org/articles/10.3389/fonc.2021.732081/full.

[12] Catania, et al., 2021.

[13] Catania, et al., 2021. Emphasis added.

[14] Vendramin, Roberto, et al. 2021. Cancer evolution: Darwin and beyond. The EMBO Journal 40(18): e108389, August 30. https://www.embopress.org/doi/full/10.15252/embj.2021108389.

[15] Darwin, Charles. 1859. The Origin of Species.  London: Murray. P. 80-81 emphasis added.

[16] Institute of Cancer Research. 2020. Mapping how evolutionary forces affect cancer growth could help doctors choose biopsies. Phys.org, May 15. https://phys.org/news/2020-05-evolutionary-affect-cancer-growth-doctors.html

[17] Institute of Cancer Research. 2020. Mapping how evolutionary forces affect cancer growth could help doctors choose biopsies. PHYS.ORG, May 15.https://phys.org/news/2020-05-evolutionary-affect-cancer-growth-doctors.html. This paper is based on:
Chkhaidze, Ketevan, et al. 2019. Spatially constrained tumor growth affects the patterns of clonal selection and neutral drift in cancer genomic data, PLOS Computational Biology, July 29.
https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1007243.


Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.

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