How to Block Cancer Stem Cells
A few specific options with more to follow...
In a previous post, I wrote about cancer stem cells (CSCs) — a small population of cells within tumors believed to drive cancer growth, recurrence, and metastasis. I also briefly referenced the trophoblast theory of cancer, proposed by Dr. John Beard, which suggests that cancer behaves much like certain cells during early pregnancy (trophoblastic cells).
In this article, I would like to build on that previous post by exploring possible therapeutic pathways to inhibit cancer stem cells.
Quick Historical Primer
The idea that cancer arises from primitive, embryonic-like cells actually dates back to the late 19th century when the German scientist Julius Cohnheim suggested that misplaced embryonic cells in adult tissues — what he called “embryonic rests” — could become cancerous.
It was shortly after that when, John Beard, a Scottish embryologist, observed that the invasive behavior of the early placenta (the trophoblast) behaved like cancer.
The trophoblast is an enveloping layer that is a precursor of the placenta. The trophoblast connects the embryo to the wall of the uterus. The trophoblast forms early in pregnancy - less than a week after fertilisation. The trophoblast cells behave like cancer cells. They must invade the tissues of the mother and grow to form the placenta.
Dr. Beard observed that the trophoblast stops invading at a particular point in embryonic development, prompted by the secretion of pancreatic enzymes from the developing fetus. Beard theorised that pancreatic enzymes could control or even reverse cancer by signaling these invasive, primitive cells to stop dividing.
In the early 1900s, Beard tested his theory by injecting pancreatic enzymes into animal with tumors and observed tumor shrinkage. However, his findings were dismissed, and by the time of his death in 1924, his work had been largely forgotten.
In the 1960s, the theory was revived by Dr. William Donald Kelley, an orthodontist who claimed to heal himself from pancreatic cancer using enzyme therapy, dietary changes, and detox protocols. Kelley’s clinical work attracted the attention of Dr. Nicholas Gonzalez, who documented numerous long-term cancer survivors in Kelley's practice. Gonzalez and his colleague, Dr. Linda Isaacs, subsequently developed a formal enzyme-based cancer therapy that included large doses of pancreatic enzymes, dietary changes, coffee enemas, and other detox protocols.
Their work showed a great deal of promise in case reports and small pilot studies. Many patients lived many years beyond what would normally be expected. However, a large-scale clinical trial comparing their enzyme protocol to chemotherapy was marred by poor patient adherence, leading to inconclusive and disappointing results. Gonzalez and Isaacs attributed these failures to patient selection issues, lack of support, and the sheer difficulty of following the complex protocol.
Many patients under the direct supervision of Dr. Kelly or Dr. Gonzalez seem to have done very well. However, trying to replicate or scale-up the protocol for larger groups of patients might be difficult. Cancer patients might not have the strength to adhere to the protocol and family members may pressure them into not using an ‘unconventional approach’.
The Enzyme Hypothesis Revisited
With the discovery of protease-activated receptors (PARs) on cancer cells, interest in the enzyme hypothesis has been rekindled. (Proteases are enzymes that break down proteins).
Some studies have also shown that pancreatic proenzymes (an inactive precursor of an enzyme) may inhibit cancer growth in animals and cell cultures by impacting the behavior of CSCs.
Cohnheim, Beard, Kelley, and Gonzalez laid crucial groundwork by recognising that cancer is not merely a mass of rogue cells but a complex process involving primitive, stem-like cells that resist conventional treatments.
The legacy of pancreatic enzyme therapy is one of foresight. Potentially a stepping stone toward the next generation of cancer treatments.
It’s natural to ask, though, if there are easier ways to inhibit CSCs?
Alternative and Emerging Strategies to Target Cancer Stem Cells
The scientific community has started to formally recognise the concept of CSCs and a number of therapeutic pathways that may inhibit CSCs have been identified. This involves biochemical and physical pathways. In this article I would like to include some of the current most promising biochemical treatments. In other articles I will look at aspects related to bioelectricity and stress management - which are equally important. A ketogenic diet may also be appropriate. In a separate article I will also look at what causes the stem cells to behave in this way in the first place and what can be done to remove those causes.
The biochemical pathways are quite technical so I have entered them into a summary table as a PDF that you can access separately by clicking below. (Since most people will be interested in treatment I don’t want the technical details to unnecessarily distract).
TREATMENT
The following is a list of the current most promising biochemical treatments that have the best evidence to support their use in combating CSCs. The primary source of information for these specific treatments is Dr. Paul Marik’s Cancer Care monograph but I have also cross-referenced the information with other sources.
Just a quick note on the terminology used:
Clinical - refers to evidence gathered from studies conducted in humans.
Preclinical - refers to testing prior to testing in humans. It can be in vitro (laboratory based) or in vivo (animal testing).
1. Metformin
Mechanism: Disrupts mitochondrial function, inhibits mTOR, reduces insulin/IGF-1 signaling, impacts CSC metabolism.
Evidence:
Strong clinical and preclinical evidence.
Associated with improved outcomes in cancer patients (both diabetic and non-diabetic).
Multiple studies show inhibition of CSC proliferation and tumor recurrence.
Evidence Level: ⭐⭐⭐⭐⭐ (Tier One, repurposed pharmaceutical)
2. Curcumin
Mechanism: Inhibits multiple CSC pathways (NF-κB, STAT3, Hedgehog, WNT/β-catenin), reduces self-renewal and chemoresistance.
Evidence:
Extensive preclinical evidence, numerous in vitro/in vivo studies.
Human data are mostly observational, but promising.
Evidence Level: ⭐⭐⭐⭐ (Tier One, widely researched natural compound)
3. Disulfiram (Antabuse)
Mechanism: Inhibits aldehyde dehydrogenase (ALDH), an enzyme overexpressed in CSCs; induces oxidative stress and apoptosis.
Evidence:
Strong preclinical evidence and growing human observational data.
Shown to enhance chemotherapy efficacy by targeting CSC populations.
Evidence Level: ⭐⭐⭐⭐ (Tier One, repurposed pharmaceutical)
4. Ivermectin
Mechanism: Modulates WNT/β-catenin and Hippo pathways; reduces proliferation and survival of CSCs.
Evidence:
Emerging but rapidly growing evidence base (in vitro, and in vivo).
Early clinical observations.
Evidence Level: ⭐⭐⭐⭐ (Tier One, repurposed pharmaceutical)
5. Green Tea Extract (EGCG)
Mechanism: Inhibits CSC self-renewal, blocks CSC niche signaling (WNT, Hedgehog, and Notch pathways).
Evidence:
Multiple in vitro and in vivo studies.
Epidemiological studies suggest protective effects in populations with high green tea consumption.
Evidence Level: ⭐⭐⭐⭐ (Tier One, supported by both mechanistic and epidemiological data, natural compound)
6. Berberine
Mechanism: Inhibits cancer-promoting pathways (AMPK, mTOR, PI3K); suppresses CSC proliferation and survival.
Evidence:
Strong mechanistic and preclinical data.
Limited clinical data but growing support.
Evidence Level: ⭐⭐⭐⭐ (Tier One)
7. Mebendazole / Albendazole / Fenbendazole
Mechanism: Disrupts microtubules, inhibits cell division, may impair CSC replication.
Evidence:
Preclinical animal studies with strong support.
Human data mostly anecdotal and observational but emerging.
Evidence Level: ⭐⭐⭐ (Tier One, though less human data to date than the top agents)
✅ Conclusion: Strongest Evidence to Date
Based on cumulative mechanistic, preclinical, and clinical evidence from the Cancer Care monograph and other sources, the most robust biochemical CSC-targeting agents to date are:
Metformin, Curcumin, Disulfiram, Ivermectin, Green Tea Extract (EGCG), and Berberine.
However, we should also consider the safety profile of these agents. My understanding is that disulfiram can have significant and severe side effects. The other treatments, especially curcumin and ivermectin, are safe. Some sources suggest that curcumin is not easily absorbed and should be combined with piperine (black pepper extract).
**We should also always check for possible interactions with any other medications or supplementation we are using.
Enzyme therapy, for those who can follow the protocol, may still be able to compete in terms of efficacy. However, I think the main point from this information is that an integrative approach to cancer is essential and far superior to conventional treatments that involve only surgery. chemotherapy and radiation.
1 in 2 of us are currently on a path to a cancer diagnosis at some point.
This is something that affects us all. It is important that information is immediately available to people to enable them to make informed choices and not simply follow the profit-driven approach.
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All these proposed cancer treatments are hypothetical and speculative, but they can’t be any worse than presently prevailing toxic chemicals that seek to eradicate deranged “cancer cells” based on the unproven notion that cancer is caused by “mutations” that are induced by environmental stresses. Delbruck and Luria refuted that hypothesis even before the discovery of DNA. They proved that mutations occur at random, regardless of environmental stress. So, the conventional treatments (toxic chemicals, harmful radiation, and mutilating surgery) fly in the very face of science. Not only is their rationale refuted, but all of these so-called “treatments” are known causes of cancer. Furthermore, nearly seventy years of experience has demonstrated that they reduce life span compared to no treatment at all, and have yet to demonstrate reliable cure of anything.
Stress theory, which hypothesizes that all forms of disease, including cancer, are caused by unrelenting environmental stresses that induce harmful stress mechanism hyperactivity, has always offered the most promising prospect for an effective “unified theory of medicine” that would confer a set of simple, safe, reliable treatments that would cure all forms of disease by restoring normal stress mechanism activity and effective organ function. Basically, this would entail synergistic combinations of anesthesia, analgesia, hypercarbia, and thrombin inhibition. www.stressmechanism.com
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