Tina Kaczor, ND, FABNO
Few topics in modern science have stirred deeper emotions or ignited more controversy than the use of human stem cells in medicine. Our understanding of these pluripotent cells has increased exponentially through rapidly advancing technologies and an intense desire to unlock the healing potential of these seemingly malleable cells. In the shadow of the media’s attention on the therapeutic use of stem cells lies an under-reported hypothesis into the genesis of the No. 2 cause of death in America: cancer.
The Role of Stem Cells
To understand how stem cells are implicated in carcinogenesis, let us step back to understand the putative role of adult stem cells in healthy cellular processes. This is not a discussion of embryonic stem cells, but adult stem cells, the kind that you and I are currently producing and utilizing in our daily cellular repair processes. Adult stem cells have the capacity to differentiate into various types of mature cells. Differentiation depends on their location and the molecular signals of the given cellular environment. Adult stem cells are not only present in the basal layer of various tissues, but they also travel through the bloodstream. They are thought to be recruited to sites of injury for the express purpose of providing the cellular foundation for repair. This mobility is a revolutionary concept, and even more intriguing is that hematopoietic stem cells can be recruited to distant tissues and triggered to differentiate into virtually any cell in the body.
Carcinogenesis and Stem Cells
Carcinogenesis is the result of repeated attacks on a cell’s DNA that result in multiple mutations, culminating in disruption of normal cellular processes. In a simplified version, a cell’s DNA is essentially battered and bruised by free radicals (particularly in the absence of antioxidants), whether they are derived from chemicals, radiation or the cell’s own metabolic processes. Implicit in this model is the idea that mature cells of a given tissue are going backwards, or reverting to a more primitive state. Indeed, the aggressiveness of any given cancer does correspond to a less differentiated, or more primitive, appearance.
There are, however, two ways to achieve this primitive appearance. Perhaps, instead of going backwards, a cell is prevented from going forward in its normal differentiation pathways. Perhaps, at a site of cellular injury, the maturation process is thwarted. This scenario would require the presence of immature cells in the process of differentiation.
Enter the stem cell.
Even before molecular techniques verified the presence of stem cells in cancers, there were several reasons to suspect their existence. First, tumors are heterogeneous collections of cells, not clonal populations, reflecting various stages of maturation, much like the well-defined hematopoietic hierarchy. Second, if cells are taken from this heterogeneous tumor and transplanted into an animal, only a few of the cells are capable of giving rise to a new tumorous growth, indicating that only a small subpopulation is even capable of continued proliferation. Moreover, the newly formed tumor is not a clonal proliferation but is heterogeneous itself, with cells at various stages of differentiation; again, a phenomenon that is analogous to the progeny of hematopoietic stem cells. Finally, the presence of a subset of self-renewing (and treatment-resistant) stem cells would allow for the accumulation of learned mutations throughout the course of treatment and progression, a phenomenon that has been the bane of conventional cancer therapies.
We had expected the existence of stem cells, and now there is evidence of their presence in various cancers, including leukemias, lymphomas, brain, prostate and colon cancers. While this is interesting in its own right, the relevant question for us as practitioners is, “How does this affect patient care?”
Cancer Initiation
First, let us recap this new theory of cancer initiation at a cellular level: Tissue is injured either due to physical trauma, viral/ bacterial infection, repeated radiation exposures or chemical exposures. Stem cells are drawn to the site of injury to provide the foundation for cellular repair. If all goes well, the stem cells differentiate into the needed cell type and repair the damaged tissue. This normal, healthy process requires a limited use of inflammatory mediators. If for some reason inflammatory mediators become a chronic presence, the normal molecular maturation process breaks down, essentially preventing full differentiation of the cells.
This hypothesis was elegantly demonstrated in a mouse model of gastric cancer, in which chronic gastric inflammation was ensured by giving immunosuppressed mice an infection akin to Helicobacter pylori in humans. These mice also received hematopoietic stem cells with radiolabeled DNA. When the mice were sacrificed, the gastric carcinoma cells that developed contained the radiolabeled DNA isotopes from the stem cells, indicating that the stem cells likely gave rise to the cancer.
Back to the question of patient care. To be honest, the theory of stem cell carcinogenesis does not revolutionize naturopathic oncology treatments. It does, however, give us a new framework in which to understand many of the naturopathic therapies we currently use for cancer patients. It reinforces our use of anti-inflammatory therapies, such as curcumin, quercetin, enzymes, fish oil and antioxidants; as well as prodifferentiation nutrients such as vitamins D and A. It can be reasoned that removing the source of irritation through immune enhancement or detoxification is of greater value, with an understanding that this is an ongoing process of continued lack of differentiation of cells. We must remember that the stem cells in any given tumor are continually evolving, and sometimes preventing the cells from becoming more aggressive is a more readily achievable goal than cytotoxicity with natural agents. Our goal with natural agents then becomes stability of disease, not necessarily eradication.
The stem cell carcinogenesis theory is another scenario of molecular science delineating the mechanism of a long-held tenet of naturopathic medicine: namely, an irritant giving rise to inflammation, and chronic inflammation giving rise to chronic degenerative diseases, including cancer.
References for this article were not available as of press time. For more information, contact Dr. Kaczor as listed in her bio below.
Tina Kaczor, ND graduated from NCNM and completed a two-year clinical residency in integrative oncology at Cancer Treatment Centers of America. She is well trained in the language and protocols of conventional cancer care; with this she is able to expertly define integrative treatments for all types of cancer. Currently, her professional focus is on nutrient involvement in the biochemistry and molecular basis of disease. Dr. Kaczor specializes in chronic degenerative diseases, such as cancer, diabetes, cardiovascular disease, Parkinson’s disease and heavy-metal toxicity. She currently practices at the Clinic of Natural Medicine in Eugene, Ore.
