Eight medications, six supplements, one purpose: Death of cancer cells and cancer stem cells

This protocol is innovative and comprehensive. It is potent but has a low side-effect profile. When combined with important dietary and lifestyle changes (click here), the protocol not only enhances the effectiveness of conventional cancer treatment but can also serve as a standalone treatment. The therapeutic rationale for each compound below is supported by the numerous scientific references listed at the bottom. 

Repurposed medications:

1. 2-deoxy-D-glucose (2DG): Inhibits glucose metabolism in cancer cells and cancer stem cells, leading to a reduction in cellular energy, an increase of oxidative stress, impaired biosynthesis of macromolecules (cellular building blocks), and ultimately apoptosis (programmed cell death). Promotes immune destruction of cancer cells by blocking immunosuppressive tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs). This important medication is not available in any retail or compounding pharmacy. To make it available to our patients, we have it custom-synthesized by medicinal chemists and include it in the cost of treatment.
2. Acarbose: Synergizes with 2DG to further inhibit glucose metabolism to induce oxidative stress and apoptosis.
3. Aspirin: Speeds the removal of dead tumor cells by increasing resolvins to enhance macrophage phagocytosis, and inhibits platelet aggregation, thereby reducing metastasis by preventing circulating tumor cells from using platelets as a protective shield to hide from circulating immune cells.
4. Disulfiram: Inhibits numerous molecular targets related to drug resistance, DNA repair, cancer stem cells, angiogenesis, and metastasis. Reduces IL-6 and synergizes with sulfasalazine to induce cytotoxic oxidative stress in cancer cells. Promotes immune destruction of cancer cells by promoting the proliferation and infiltration of cytotoxic T-cells (CTCs) and natural killer (NK) cells, and blocking immunosuppressive tumor-associated macrophages (TAMs).
5. Metformin: Inhibits glutamine and fatty acid metabolism, downregulates oxidative phosphorylation, and inhibits mTOR signaling. This leads to a further reduction in cellular energy, an increase in metabolic stress, and ultimately the death of cancer cells and cancer stem cells.  Promotes immune destruction of cancer cells by promoting the proliferation and infiltration of cytotoxic T-cells (CTCs) and natural killer (NK) cells, and blocking immunosuppressive tumor-associated macrophages (TAMs), tumor-associated T-regulatory cells (Tregs), and myeloid-derived suppressor cells (MDSCs). Reduces the protein stability of SLC7A11 (also known as xCT), resulting in disruption of the protective antioxidant system of cancer cells by the depletion of glutathione and thioredoxin reductase.
6. Niclosamide: Inhibits hypoxia-inducible factor 1-alpha (HIF-1α) which stands at the crossroads of tumor cell metabolism and cancer-driving hypoxia, angiogenesis, inflammation, and immune evasion. Inhibits other tumor-promoting pathways such as Wnt, KRAS, STAT3, Notch, mTOR, E2F, and Myc. Activates tumor-suppressor signaling such as p53, PP2A, and AMPK; blocks DNA repair; reduces IL-6; and induces intracellular acidification. Promotes immune destruction of cancer cells by blocking immunosuppressive myeloid-derived suppressor cells (MDSCs). Induces nutrient starvation in cancer cells by blocking macropinocytosis, a process by which cancer cells engulf large volumes of extracellular fluid, aiding in nutrient uptake to support their rapid growth and survival. Niclosamide is no longer available from US pharmacies. To make it available to our patients, we obtain it from reputable overseas pharmacies and include it in the cost of treatment.
7. Sulfasalazine: Induces cysteine starvation in cancer cells by blocking the cystine transporter SLC7A11, resulting in disruption of the protective antioxidant system of cancer cells by the depletion of glutathione and thioredoxin reductase. Together with disulfiram, this induces irreversible toxicity caused by the accumulation of reactive oxygen species (ROS) and irreparable DNA damage, with subsequent cellular demise via apoptosis and ferroptosis (iron-mediated cell death). Furthermore, sulfasalazine promotes ferroptosis, reduces IL-6, and promotes the immune destruction of cancer cells by inhibiting immunosuppressive regulatory T-cells (Tregs).
8. Syrosingopine: Disables glutathione synthesis and promotes intracellular acidification and extracellular alkalinization of cancer cells by inhibiting monocarboxylate transporters 1 and 4 (MCT1 and MCT4). In combination with metformin, syrosingopine facilitates apoptosis by inhibiting essential NAD+ production pathways. These pathways allow cancer cells to convert dietary nutrients such as glucose, glutamine, and fatty acids, and high-energy fuels like lactate, pyruvate, and ketone bodies sourced from neighboring cancer-associated fibroblasts (CAFs) into much-needed energy in the form of ATP (adenosine triphosphate). This important medication is not available in any retail or compounding pharmacy. To make it available to our patients, we have it custom-synthesized by medicinal chemists and include it in the cost of treatment.

Nutritional supplements:

1. Apigenin: Promotes ferroptosis and inhibits angiogenesis, cell proliferation, invasion, and metastasis. Blocks immunosuppressive tumor-associated macrophages (TAMs) and tumor-associated T-regulatory cells (Tregs). When combined with metformin, promotes reactive oxygen species (ROS)-induced apoptosis of cancer cells.
2. Copper gluconate (microdosed): Together with resveratrol (microdosed), eradicates cell-free chromatin particles.
3. Ozonated oil: Inhibits angiogenesis and metastasis by increasing oxygen availability in the tumor microenvironment, decreases inflammation, activates apoptosis of cancer cells and cancer stem cells by depleting their antioxidants, promotes immune destruction of cancer cells by inhibiting tumor-associated macrophages (TAMs), and improves quality of life of those receiving chemotherapy or radiation therapy.
4. Piperlongumine: Elevates oxidative stress of cancer cells and cancer stem cells by dually inhibiting glutathione and thioredoxin reductase synthesis; hampers critical cancer cell pathways by inhibiting NF-κB and STAT3 activation; disrupts cancer cell growth by inducing cell cycle arrest, promoting apoptosis and ferroptosis, and curbing angiogenesis; diminishes the metastatic potential of cancer cells; enhances the efficacy of conventional chemotherapy by increasing cancer cell sensitivity and inhibiting drug efflux pumps; decreases inflammation; directly binds to cysteine residues; induces autophagy; inhibits mTOR signaling; inhibits IL-6; and downregulates anti-apoptotic proteins. 
5. Resveratrol (microdosed): Together with copper gluconate (microdosed), eradicates cell-free chromatin particles.
6. Tributyrin: Suppresses cancer cell proliferation and induces apoptosis by upregulating and sequestering the p53 signaling protein in the nucleus.

The importance of eradicating cancer stem cells:

Healthy stem cells reside in the human body, and they play a crucial role in repairing damaged tissues. However, tumors also contain stem cells that contribute to the regeneration of cancerous tissue. In 1997, researchers first identified cancer stem cells, and since then, numerous studies have been conducted to better understand their biological properties.

The propor­tion of cancer stem cells in tumors is extremely low. They account for only 0.01-2% of the total tumor mass, but they are believed to constitute the origin of most tumors. Unlike the bulk tumor cells, cancer stem cells are not detectable using standard tumor biomarkers or imaging techniques. For anti-cancer therapy to be successful, both the bulk tumor cells and the cancer stem cells must be eliminated since cancer stem cells have the ability to regrow tumors repeatedly.

Cancer stem cells drive treatment failure, immune evasion, cancer progression, metastasis, and disease recurrence. Furthermore, they may be the root cause of the initial tumor formation. Although conventional cancer therapies can effectively target the bulk tumor cells, they are largely ineffective against cancer stem cells due to their highly resistant nature. In some cases, conventional treatments may even promote the proliferation of cancer stem cells. Cancer stem cells are a major obstacle to successful cancer treatment.

Cancer stem cells can migrate and settle in remote parts of the body, where they can lie dormant for extended periods, waiting for the right conditions to form new tumors. Though conventional treatments can shrink tumors, they cannot stop cancer relapse. In fact, even after all observable signs of cancer are gone, the existence of residual cancer stem cells increases the risk of eventually developing new and possibly more aggressive tumors.

It is not enough to solely eliminate the bulk tumor cells. To achieve long-term survival, cancer stem cells must also be eliminated. Doing so could potentially eliminate the entire cancer cell population, thereby stopping cancer metastasis and recurrence, which are the leading causes of cancer-related deaths. Components of the protocol that target cancer stem cells are 2DG, disulfiram, metformin, niclosamide, ozonated oil, piperlongumine, and sulfasalazine.

Targeting interleukin-6:

Interleukin-6 (IL-6) is a multifunctional cytokine that plays critical roles in various physiological and pathological processes. In the context of cancer, the microenvironmental IL-6 has been shown to contribute to several aspects of tumorigenesis, progression, and therapy resistance. Here’s a breakdown of the role that microenvironmental IL-6 plays in cancer:

1. Tumor growth and proliferation: IL-6 can act in an autocrine manner on cancer cells and promote their growth. For instance, in multiple myeloma, malignant plasma cells produce and respond to IL-6, which promotes their survival.
2. Inflammation: Chronic inflammation is recognized as a hallmark of cancer, and IL-6 is a key player in the inflammatory response. Elevated IL-6 levels in the tumor microenvironment can contribute to a chronic state of inflammation, which can drive the mutation rate in cells and promote tumorigenesis.
3. Angiogenesis: IL-6 has been implicated in promoting angiogenesis, the formation of new blood vessels. Tumors need an extensive blood supply to grow, and by stimulating angiogenesis, IL-6 can facilitate tumor growth and progression.
4. Invasion and metastasis: IL-6 can promote epithelial-to-mesenchymal transition (EMT), a process by which epithelial cells acquire a mesenchymal phenotype. This transition increases the invasiveness of cancer cells and their potential to metastasize to distant sites.
5. Immune evasion: IL-6 can contribute to the suppression of the anti-tumor immune response. It can influence the polarization of tumor-associated macrophages (TAMs) towards an M2 (anti-inflammatory) phenotype, which tends to promote tumor progression and suppress T-cell responses. Moreover, IL-6 can further suppress the anti-tumor immune response by leading to the expansion of myeloid-derived suppressor cells (MDSCs).
6. Treatment resistance: Elevated levels of IL-6 have been associated with resistance to various treatments, including chemotherapy and targeted therapies. For instance, in the context of breast cancer, IL-6 signaling has been shown to confer resistance to anti-HER2 therapies.

Because of the pivotal role that IL-6 plays in cancer biology, targeting the IL-6 signaling pathway is crucial. Components of the protocol that reduce IL-6 levels are disulfiram, niclosamide, piperlongumine, and sulfasalazine.

The immunology of cancer:

The immune system is intricately designed to identify and eliminate abnormal cells, including those that are cancerous. However, this natural defense mechanism can be subverted by the tumor microenvironment, which recruits and reprograms specific immune cells to create an immunosuppressive setting. Among these are tumor-associated macrophages (TAMs), T-regulatory cells (Tregs), and myeloid-derived suppressor cells (MDSCs), each of which contributes to cancer progression in unique but overlapping ways.

TAMs are often driven to differentiate from an M1 macrophage into an M2 macrophage that actively promotes immunosuppression. They accomplish this by secreting cytokines like IL-10 and TGF-β, which inhibit effector T-cell function. Additionally, TAMs are known to suppress dendritic cell maturation, making these antigen-presenting cells less effective in activating T-cells. TAMs also participate in recruiting and stimulating Tregs, which in turn amplifies the immunosuppressive signals in the tumor microenvironment. Beyond immunosuppression, TAMs play a role in angiogenesis by releasing factors such as vascular endothelial growth factor (VEGF) and facilitating tumor invasion and metastasis through the production of matrix metalloproteinases (MMPs). The components of the protocol that target TAMs are 2DG, apigenin, disulfiram, metformin, and ozonated oil.

Tregs further complement this immunosuppressive landscape. They are proficient in inhibiting effector T-cell activation by releasing their own set of immunosuppressive cytokines, such as IL-10 and TGF-β. Tregs can also exert their suppressive effects through direct cell-to-cell interactions with other immune entities like CD8+ T cells and dendritic cells. Additionally, Tregs engage in metabolic competition by consuming IL-2, a growth factor that is essential for the functioning of effector T cells. Some evidence even suggests a role for Tregs in supporting the immunosuppressive functions of TAMs. The components of the protocol that target Tregs are apigenin, metformin, and sulfasalazine.

MDSCs are another major player in this scenario. They have broad immunosuppressive capabilities, often producing high levels of arginase and reactive oxygen species (ROS) that impair T-cell receptor signaling and thus inhibit T-cell function. MDSCs also secrete cytokines such as IL-10 and TGF-β; and can induce the formation and activation of Tregs, contributing to a multi-layered suppression of anti-tumor immunity. Moreover, MDSCs are known to inhibit the activities of natural killer (NK) cells, adding another layer of complexity to the immunosuppressive environment. The components of the protocol that target MDSCs are 2DG, metformin, and niclosamide.

Iron dependency in cancer and the therapeutic potential of ferroptosis:

Cancer cells often exhibit profound iron uptake and retention due to their heightened metabolic demands for proliferation. This iron dependency accentuates the production of reactive oxygen species and lipid peroxides, especially in the presence of excess iron. As a result, these cells become more vulnerable to ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation. By exploiting this increased susceptibility, therapies that induce or amplify ferroptosis can selectively target and eliminate iron-addicted cancer cells. Here’s why targeting ferroptosis is considered crucial in cancer treatment:

1. Treatment-resistant tumors: Some tumors are resistant to conventional therapies that aim to induce apoptosis. Ferroptosis offers an alternative mechanism to induce cell death in these resistant cancer cells.
2. Cancer specificity: Normal cells have robust antioxidant defenses to prevent lipid peroxidation, making them relatively resistant to ferroptosis. In contrast, certain cancer cells, due to their metabolic profiles, are more susceptible to ferroptotic cell death. Therefore, targeting ferroptosis can be more selective for cancer cells.
3. Tumor microenvironment: The tumor microenvironment, especially in solid tumors, is often deprived of nutrients and oxygen, making it susceptible to oxidative stress. By targeting ferroptosis, one can exploit this vulnerability of the tumor microenvironment.
4. Synergistic effects: Combining ferroptosis-inducing agents with other treatments, such as chemotherapy, radiation, or immunotherapy, might result in synergistic anti-tumor effects. This can potentially lower the doses of conventional therapies, reducing side effects.
5. Inhibition of cancer stem cells: Preliminary studies have suggested that inducing ferroptosis can target cancer stem cells, which are believed to be the root cause of tumor initiation, metastasis, and therapeutic resistance.
6. Targeting specific mutations: Some tumors with specific genetic mutations (e.g., tumors with mutations in p53) have shown increased sensitivity to ferroptosis. Targeting ferroptosis can be a strategy to exploit these genetic vulnerabilities.
7. Metastasis prevention: There’s evidence to suggest that inducing ferroptosis can prevent cancer metastasis, which is a significant cause of cancer-related deaths.
8. Overcoming drug resistance: Inducing ferroptosis can potentially overcome resistance to targeted therapies. For instance, certain tumors that develop resistance to EGFR inhibitors may still be susceptible to ferroptosis inducers.

The components of the protocol that promote ferroptosis are apigenin, piperlongumine, and sulfasalazine.

Targeting cell-free chromatin particles: A new frontier in cancer therapy:

In a tumor, even without treatment, a substantial number of cancer cells spontaneously die each day. This is due to the high rate of cell proliferation and the unstable nature of cancer cells, which often have defects in their DNA repair mechanisms and can be more prone to apoptosis (programmed cell death) or necrosis (cell death due to injury or disease). Scientists discovered that when cancer cells die, either spontaneously or from treatment such as chemotherapy, cell-free chromatin particles are released into the tumor microenvironment where they are readily internalized by surviving cancer cells and inflict DNA damage, inflammation, immune suppression, increased toxicity from chemotherapy, and ultimately, more cancer.

Our DNA is stored on our chromosomes as densely packed units called chromatin which contains DNA and proteins called histones. This configuration prevents the long strands of DNA from becoming tangled and plays an important role in stabilizing the DNA during cell division, preventing DNA damage, and maintaining normal gene expression. Cell-free chromatin particles are composed of tiny fragments of DNA and histones without other cellular components. These particles are released from cancer cells undergoing apoptosis—the mechanism a cell undertakes for self-destruction, activated when the cell senses significant self-damage.

Scientists also found that cell-free chromatin particles are released into the bloodstream from the billions of normal cells that die each day as we age. These particles readily enter healthy cells and integrate into their DNA. This leads to DNA damage, mitochondrial dysfunction, activation of apoptotic and inflammatory pathways, and impairment of mitochondrial function. This process triggers a vicious cycle and ongoing chain reaction that perpetuates the aging process and increases the risk of cancer.

Some scientists believe that the lifelong assault on healthy cells by internalized cell-free chromatin particles may not only be the chief underlying cause of the aging process and cancer, but also may act as a global instigator of other age-associated disorders, including cardiovascular disease, diabetes, sepsis, and Alzheimer’s disease.

Fortunately, scientists found a way to safely neutralize cell-free chromatin particles by using minute and specific oral doses of resveratrol and copper to generate oxygen radicals in the stomach. These radicals are readily absorbed into the circulation and permeate the extracellular spaces of the tumor microenvironment and deactivate cell-free chromatin particles. In an animal model, this was found to downregulate several biological hallmarks of aging and neurodegeneration. In a human model using patients with advanced oral cancer, it was found that deactivating cell-free chromatin particles downregulated the hallmarks of cancer, as well as five immune checkpoint (suppressor) proteins. 

Pill burden:

Taking too many pills can compromise quality of life, incur extra expenses, and potentially harm kidney, liver, or heart function. With this in mind, we begin our approach with these six carefully selected compounds, which are designed to comprehensively target the twelve key pathways essential for both cancer cells and cancer stem cells, as outlined above:

1. Aspirin
2. Copper gluconate (microdosed)
3. Metformin
4. Ozonated oil
5. Piperlongumine
6. Resveratrol (microdosed)
7. Syrosingopine

Treatment cost:

The average oncologist manages between 250 and 500 patients. Dr. Thomas limits his caseload to fewer than 50. This allows him to provide highly attentive care and to dedicate time to vital research that directly benefits his patients. The treatment protocol necessitates close medical supervision, management, and ongoing support by Dr. Thomas. After an initial in-office physical examination, treatment begins. Follow-up visits are conducted via telemedicine and yearly physical exams are performed. While under his care, patients have unlimited email access to Dr. Thomas.

The cost for our services is a flat rate of $2850 per month. This is less expensive than alternative cancer treatment in Mexico or Europe. Clinics there typically charge $7,000 to $20,000 per week (click here and scroll down to FAQs and click “What are the costs of stage 4 cancer treatments at a clinic?”). Despite their high costs, many of these clinics lack a more comprehensive understanding of tumor biology, which could pose a threat if they fail to target key vulnerabilities of cancer.

Our monthly fee includes the 2DG, niclosamide, and syrosingopine. Other costs are for the medications available at the local pharmacy (acarbose, aspirin, disulfiram, metformin, sulfasalazine); and supplements available online (apigenin, copper gluconate, ozonated oil, piperlongumine, resveratol, tributyrin). These total between $300 and $400 per month. Treatment is maintained until remission or disease stabilization is achieved. This usually takes 6-18 months. Afterward, we employ a simpler and less expensive protocol. For more information, click here.

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