June 2, 2020 | Jerry Bergman

Cancer Research Is Based on Intelligent Design, Not Evolution


To Understand Cancer Requires Acceptance of Irreducible Complexity

An oft-repeated claim by those who support the Darwin Party 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 understand when doing cancer research. 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 experience that Intelligent Design is the basic assumption for all cancer research.[1]

As is well documented, we have failed to reach the goal of “curing” cancer as envisioned by the 1971 War on Cancer declaration.[2] Professors Sonnenschein and Soto write in response to this problem that their aim was

ongoing critical analyses … aimed at clarifying the sources of misunderstandings at the root of the cancer puzzle while providing a plausible and comprehensive biomedical perspective as well as a new theory of carcinogenesis that is compatible with evolutionary theory.[3]

In contrast, the creationist supposition is that all living organisms originated from fully-formed archetypes which were part of the original created kinds outlined in Genesis. These organisms were endowed with the capacity to proliferate constitutively only after their kind. One fact that consistently impressed me when doing research on cancer was that the complex systems designed to prevent cancer were a superb example of ingenious design. Cancer is not caused by this system, but as we will explain, was caused by damage to this well-designed system.

Cancer Control Mechanisms in the Body

This system controls cell growth and reproduction. It consists of two parts, growth factors and growth regulation factors. Like an automobile requires an accelerator and brakes to negotiate roadways, if either system is damaged, a car can no longer function as a vehicle to transport passengers. Likewise, for the cell to function properly, it must have working accelerators and brakes. In cells, both the message to cause the cell to divide (the growth factors), and the brakes (the tumor suppressors) must be damaged before the uncontrolled cellular growth called cancer can develop.

Sonnenschein and Soto say that their 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.”[4] They further believe that the current theory of carcinogenesis should be abandoned or modified, and replaced by what they call “an organicist theory that adopts reliable principles relevant to the theories of evolution and organisms.”

After carefully reading the article, it appeared to me that all they were saying is not only mutations influence cancer development, but internal controls do as well. This is obvious. The most well-known example is heart cancer called sarcoma, which is rare partly because myocardial cells divide very rarely.[5] In contrast, epithelial cells (skin and mucus lining cells) divide after about three days, and are one of the first cells to be exposed to external carcinogens.[6] Consequently, cancer of epithelial tissue is the most common known cancer, sarcoma of the heart one of the rarest.[7]

Another article proclaimed that evolutionary theory can help to account “for the presence or absence of selective evolutionary pressure—in which conditions favor the survival of cells with certain genetic traits—and the presence or absence of physical, spatial constraints in tumors.”[8] In short, what they are saying is damage to the cell’s reproduction controls and growth brakes allows further uncontrolled cell division. In the end, the result is the death of the cancer victim and, consequently, the death of all of the victim’s cells including the cancer cells. Although a short-term advantage for the cancer cells occurs, the result is hardly an evolutionary advantage no matter how you look at it. How ‘fit’ is an organism that kills its host, and can no longer proliferate?

Built-in Protection Against Cancer

Cancer is a horrible disease but, fortunately, numerous complex systems have been built into the body to prevent it. When cells become cancerous, for example, the body’s healthy immune system is usually able to detect and destroy the renegade cells. This is true even though the cancer cells are the body’s own cells. Every adult has precancerous and some cancerous cells all the time. Cancer can develop only when the number of these cells is greater than the immune and protection systems can handle, or if the immune system becomes weak or is damaged from poor health habits.  Examples of poor health habits include smoking, a poor diet, or exposure to carcinogens, such as chemicals or high levels of radiation such as radon.

As noted, cell growth is controlled by two systems, one that causes cell growth and cell division, and another that regulates cell growth. Cancer is a result of damage to this system. Broken genes, in short, cause loss of cell growth control. Cancer cells grow unabated, causing the cells to pack tightly, resulting in hard masses called tumors. All genes that facilitate cell growth are called  proto-oncogenes; those that regulate cell growth are called tumor suppressor genes. Proto-oncogenes stimulate or cause cell division during periods of growth, such as occurs in a child. If damaged, these genes are called oncogenes, because the protein they produce continuously sends a message to the cell to divide. Normally these oncogenes only send a message to the cell nucleus to divide when they receive a message from an outside control center.

In cancer cells, the message switch which tells the cell to grow and divide is jammed on, like a broken motor switch in a car would cause the motor to run on and on until the motor breaks. An example is the RAS gene which is commonly damaged in pancreatic cancer and in many other cancers. Tumor suppressor genes regulate cell growth, and also serve to inhibit cell division if the cell or regulation control is damaged. One important tumor suppressor gene is p53 named because the p-53 protein, p-53, weighs 53 kilodaltons, equal to 53 thousand hydrogen atoms. Many proteins are named using this naming system because the name also conveys the protein size.

The Repair System

Thousands of genetic mutations occur in cells daily, but 99.99 percent of the time the damaged cells are effectively repaired by our complex repair system.[9]  Only under extreme circumstances, such as high levels of exposure to cancer-causing agents that cause large amounts of genetic damage, can the disease called cancer occur. We know this is true because researchers of the protein molecule p-53 mentioned above, called the guardian of the genome, protects cells like an emergency brake protects a car.  If certain mutations damage the cell’s DNA, the tumor suppressor p-53 gene directs the cell to repair the DNA.[10]  P-53 does this by promoting the expression of proteins that halt progression of the cell’s division cycle—giving the cell time to repair its DNA before it divides. P-53 then directs the cell to repair the damage.


If the damage is so severe that it cannot be repaired, p-53 sends the cell into a programmed spiral of death called apoptosis [pronounced ap-o-TO-sis], which consequently prevents the cell from ever reproducing again.[11]  Apoptosis is a controlled form of cell death which employs a programmed sequence of events leading to the elimination of cells without releasing harmful substances into the surrounding area which results from necrosis. Necrosis causes inflammation and can damage other nearby tissue, resulting in gangrene.

Apoptosis plays a crucial role in maintaining body health by eliminating old worn-out cells, unhealthy cells, and cancer cells. Apoptosis is an important defense against cancer, and central to tumor development is using subterfuge to avoid apoptosis.[12] The complex apoptosis process involves blebbing (the formation of blister like protrusions along the surface of a cell), cell shrinkage, nuclear membrane fragmentation, chromosomal DNA fragmentation and, lastly, safe removal of the fragmented cell parts by phagocytes (see diagram). The average adult human loses between 50 and 70 billion cells each day due to apoptosis.[13]

Emma Farmer, a diagram of the process of apoptosis [Wiki Commons]

By these mechanisms, p-53 repairs or destroys the damaged cell before it causes problems.  Of the over 6.5-million people diagnosed with cancer each year, fully half had damaged p-53 genes.[14]  Failure of this system is usually due to cell damage caused by carcinogens in the environment, allowing cancer to develop. Conversely, apoptosis activation is a “key mechanism by which cytotoxic drugs used to treat cancer kill tumor cells.”[15]

Some of the research that has helped us understand how this cell “brake” works involved breeding a line of genetically-altered mice that produce no p-53 protein. Born looking perfectly normal, soon all of the mice had developed tumors—and by six months all were dead or dying from cancer.  This system is only one of thousands of extremely complex mechanisms built into the human body designed to insure it stays healthy.

Our Creator knew that the cell mechanism could be damaged by environmental insults such as radiation or polycyclic hydrocarbons caused by burning and, therefore, designed the complex mechanisms described above to destroy defective and damaged cells. It thereby prevents cancer successfully in the vast majority of persons. The body’s defense system can also block cancer even if the p-53 tumor suppressor system fails to destroy cancer cells. Like a double set of brakes, if the first set fails, the second set can still function to destroy cancer. Cancer develops only when both sets fail. Actually, there are several fail-safe sets in the body, and all generally have to fail in one cell before that cell becomes cancerous.

The Cell Cycle

A critical part in the understanding of cancer is to understand the cell cycle through which all cells must traverse to produce cell division. A major cause of cancer involves gene mutations that encode the components of the cell cycle checkpoints, which ensure both the orderly progression of cell development and growth, and also integrates DNA repair during the cell cycle progression.[16] One complete cell cycle, including both cell growth and cellular differentiation steps, is called a growth cycle.  The growth cycle length varies from hours to years, depending on the cell type and if the cell is normal or cancerous.

Many cells must constantly divide to replace those cells that are diseased, damaged by trauma, old age, environmental insults, or internal malfunction. The lining of the digestive tract is completely replaced in about three days, and bone marrow cells divide every two to three days to form new blood cells. At the other extreme, most neurons last the lifetime of the organism.

Cell cycle [Wiki Commons]

The length of each cell cycle, called generation time, varies enormously, but given a twenty-four hour growth cycle as a basis for comparison, an estimate of the duration of each part of the cycle is as follows:

  1. The G-1 period (G meaning gap or growth) begins with the completion of the previous cycle and the start of the DNA duplication process. This stage involves the growth of the cell and synthesis of new proteins and enzymes in order to produce cell differentiation.  To achieve this step requires about 9.5 hours in normal cells.
  2. The S period (S meaning synthesis) is the time during which synthesis of a complete new set of DNA and histones is completed. This step requires about 10.5 hours. Its length is usually determined by incorporating tritium-labeled thymidine into the newly synthesized DNA.
  3. The G-2 period, is the second gap or growth stage when the cell prepares to divide. The G-2 stage extends from the end of the completion of DNA synthesis to the beginning of the actual physical mitosis causing cell division. The total time of this period is about three hours. The G-1, S and G-2 stages are as a unit called interphase.
  4. The M period (M meaning mitosis) commences when the physical cell division occurs, resulting in two close to identical daughter cells. This stage is divided into prophase, metaphase, anaphase, and teleophase. Teleophase is culminated by cytokinesis, or the physical cell division that results in two daughter cells. The total time for this process is one hour.

Cells that are caused to stop at one stage in the cell cycle, such as those cells lacking peptide growth factors, do not progress beyond mitosis and are said to be in the resting or G-0 stage. These G-0 cells can be stimulated to re-enter the cycle by growth factors that are diffused to the inside from the outside of the cell membrane. Many factors can cause cell growth to be halted, including a large family of growth inhibitory agents and contact inhibition, when a cell butts up close to other cells, causing growth to cease.[17]

If certain damage exists in the genes, p-53 works by blocking the cell cycle progression at the G1/S checkpoint, as shown in the diagram. If damage exists, p-53 facilitates the cascade of the steps required for repair.[18] And if repair cannot be completed, p53 initiates apoptosis, the complex that causes cell suicide mentioned above. The products of some tumor suppressor genes and oncogenes interact with each other in various ways, complicating the picture. Another concept that is obvious is irreducible complexity. Damage to a part of each of the systems discussed above causes the entire system to fail. All of the parts must be present and working for the system to function.

How Radiation Cancer Therapy Functions

Most normal cells eventually divide, and when cell division is complete, the cell goes into a G-0 rest cycle until another signal causes another cell division. During this intermission, the cell repairs any damage sustained earlier. As just noted, if the damage cannot be repaired, apoptosis is triggered, which kills the cells and recycles the parts. In cancer cells, though, cell cycle control is normally damaged and, when entering the G-0 rest stage, it immediately begins cell division again. Methods doctors use to kill cancer exploit this fact. For example, radiation treatment involves damaging a large number of both normal and cancerous cells. Normal cells have time to repair the damage caused by radiation in the G-0 cell cycle stage. Cancer cells, by contrast, either die, or divide without repairing the damage. Consequently, each radiation treatment increases the level of damage to cancer cells until the damage is so great that the cell dies. Radiation can also cause cancer in rare cases, called secondary cancer.


This review has barely breached the subject of how the body is well-designed to fight cancer. Generally, cancer occurs only due to genetically inherited mutations and mutations that occur in cells as adults. The major contributors to cancer, besides inherited mutations, are high-level exposure to mutagens, poor diet, and age. Cancer is a disease of aging because the 99.99 percent successful repair rate eventually with age results in a set of damages to the system which causes cancer. Thus, claims that evolution can help us to treat cancer are using the word evolution in ways contrary to Darwin’s theory, which imagined simple cells evolving to become all complex life on Earth.*

*One can see the fallacy in this news article: “Mapping how evolutionary forces affect cancer growth could help doctors choose biopsies.” The authors mistakenly call it a case of “evolution” when cancer progresses, caused by increasing damage to cells. That is clearly not what Darwin had in mind.[19]


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

[2]  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.

[3] Sonnenschein and Soto, 2020, p. 1. Emphasis added.

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

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

[6] 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.

[7] Mullin, J. M. 2004. Epithelial Barriers, Compartmentation, and Cancer. Science Signaling. 2004(216). January 20. https://stke.sciencemag.org/content/2004/216/pe2/tab-pdf.

[8] 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

[9] Bergman, Jerry. 2005. The Mutational Repair System: A Major Problem for Macroevolution. CRSQ 41(4):265-273, March.

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

[11] Bergman, Jerry. 2008. “Origins of Apoptosis: Selfish Genes or Intelligent Design?” CRSQ 44(3):204-212, Winter.

[12] Debatin, Klaus-Michael. 2004. Apoptosis pathways in cancer and cancer therapy. Cancer Immunology, Immunotherapy 53:153-159, p. 153, January 29.

[13] Chen, George G., and Lai, Paul B.S. (Eds.). 2009. Apoptosis in Carcinogenesis and Chemotherapy: Apoptosis in cancer. Netherlands: Springer.

[14] Lakin, Nicholas D. and Jackson, Stephen P. 1999. Regulation of p53 in response to DNA damage. Oncogene 18(53):7644–7655, December 13.

[15] Plati, Jessica; Bucur, Octavian, and Khosravi-Far, Roya. 2011. Apoptotic cell signaling in cancer progression and therapy. Integrative Biology (Cambridge) 3(4):279-296, April.

[16] Hartwell, Leland H., and Weinert, Ted A. 1989. Checkpoints: Controls that ensure the order of cell cycle events. Science 246(4930):629-633, November 3.

[17] Weinberg, Robert A. 1995. The retinoblastoma protein and cell cycle control. Cell 81(3):323-330, May 5.

[18] Malkin, David, et al. 1990. Germ Line p53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms. Science 250(4985):1233-1238, November 30.

[19] Institute of Cancer Research. 2020. Mapping how evolutionary forces affect cancer growth could help doctors choose biopsies. Phys.org, May 15. Paper this 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.

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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