Cancer Treatment

To eradicate cancer, one must attack the cancer cells AND the environment. This requires multiple modalities, aimed at the cells, the environment, and the cell to cell communication mechanisms. The following is a synopsis of some of the treatment modalities we use at RICTRI:


  1. Immunotherapy; to stimulate the innate immune system;

    1. Coley's toxins - consists of heat-killed bacteria that stimulate the innate immune system to attack abnormal cells, including cancer.

    2. GcMAF is a macrophage activating factor that is normally inhibited by cancer cells. GcMAF activates macrophages to kill cancer cells.

    3. Interleukin-2 (Proleukin) is a substance produced by the body that stimulates production of cytotoxic T cells, which can kill cancer cells.

    4. GM-CSF (Leukine) stimulates the bone marrow to produce more granulocytes and macrophages. This recombinant drug has shown to be helpful in inhibiting cancer progression especially when given in conjunction with a vaccine.

    5. Whole body hyperthermia is a process where the patient is warmed to a temperature of up to 104 degrees Fahrenheit. Increased temperature stimulates increased innate immune function.

  2. Glycolytic inhibitors; DCA, or dichloroacetate inhibits the cancer cells' ability to utilize sugar, while promoting normal mitochondrial oxidative phosphorylation (cancer cells that use oxidative phosphorylation are more susceptible to being destroyed).

  3. Matrix metalloproteinase inhibitor (MMPI); cancer cells "dig in" to normal tissue by secreting an enzyme that breaks down this tissue. Doxycycline (a commonly used antibiotic), in higher doses than typically used for infection, inhibits release of this enzyme.

  4. 5-alpha reductase inhibitors; Dutasteride (Avodart) is a 5-alpha reductase-1 and 2 inhibitor used in high doses for "hormone refractory prostate cancer."

  5. Cox-2 inhibitor; cox-2 inhibitors (Celebrex) promote apoptosis, or programmed cell death in cancer cells. Synergy has been seen when combined with doxycycline, the MMPI.

  6. Angiogenesis inhibitors

    1. Ammonium tetrathiomolybdate; tumors can not grow without sprouting new vessels. Vessel formation is dependent on adequate amounts of copper; if copper is depleted, tumors can not develop more blood vessels. Ammonium tetrathiomolybdate chelates copper, thereby inhibiting angiogenesis.

    2. Low molecular weight heparins (normally used when patients develop blood clots) inhibit metastases by interfering with the binding of cancer cells to platelets (cancer cells often attach themselves to platelets for transport to another location).

  7. Cancer cell cytotoxic agents; vitamin C, at high doses intravenously, when used with vitamin K3 at a ratio of 100:1, is preferentially cytotoxic to cancer cells, while leaving normal cells unharmed. Oncologists will often tell patients not to take vitamin C because it is an anti-oxidant and it will interfere with the effectiveness of chemotherapy. These oncologists are unaware that at high doses, vitamin C acts as a pro-oxidant in cancer cells, leading to cancer cell death.

  8. Mitosis inhibitors; cancer cells divide rapidly through a process called mitosis. Mitosis occurs through a process known as spindle formation. During spindle formation, spindles pull the chromosomes to opposite sides of the cell, in preparation for cell division. Noscapine, an opioid agonist binds to the spindles, inhibiting mitosis.

  9. Aromatase inhibitors; research has shown that several cancers, including breast, cervical, uterine, lung, prostate, and colorectal, often fuel their growth through the production of estrogen. Aromatase inhibitors block production of estrogen.

  10. IGF-1; IGF-1, or insulin-like growth factor-1 is a growth factor that often fuels cancer growth. Octreotide inhibits the production of IGF-1.

  11. GnRh agonists; GnRh agonists, or gonadotropin releasing hormone agonists may inhibit cancer in 2 ways. GnRh inhibits production of the sex steroids; if the cancer is dependent on sex steroids, GnRh will slow cancer growth. In addition, many cancers have receptors for GnRh, which when stimulated, inhibit cancer growth.

  12. Vitamin D2 analogues; vitamin D, as is mentioned below under the heading, "Vitamins and Supplements," inhibits cancer growth through multiple mechanisms, in a dose-dependent fashion. The higher the dose of vitamin D, the greater the cancer suppression. The problem with giving high dose intravenous vitamin D3 (this is the type of vitamin D that we normally consume), is that it can cause dangerously elevated vitamin D levels. Vitamin D2 analogues, such as paricalcitol and hectorol, inhibit cancer as effectively as vitamin D3 without increasing calcium levels.

Vitamins and Supplements

  1. Vitamin D3; vitamin D inhibits cancer growth through multiple mechanisms; it inhibits the release of proteinases from cancer cells, such as matrix metalloproteinase and cathepsin; it inhibits IGF-1 stimulated growth; it arrests the cancer cell growth cycle. Also, many cancer cells have vitamin D receptors, which inhibit cell growth when bound to vitamin D.

  2. Avemar; fermented wheat germ extract that has shown to inhibit cancer growth through multiple mechanisms; it inhibits DNA synthesis, improves natural killer cell activity, and promotes apoptosis (programmed cell death) in almost every cancer cell line studied.

  3. Melatonin; inhibits cancer growth through multiple mechanisms; interferes with activation of the estrogen receptor; inhibits telomerase activity in cancer cells (telomerase keeps the cancer cells immortal); promotes apoptosis (programmed cell death); stimulates cytotoxic activity of macrophages.

  4. Curcumin; inhibits cancer growth through multiple mechanisms; interferes with activation of the estrogen receptor; inhibits nuclear factor kappa beta; inhibits cyclooxygenase and lipooxygenase pathways; promotes apoptosis in cancer cells.

  5. Lycopene; inhibits cancer growth through multiple mechanisms. Most of the research has been done with prostate cancer, but lycopene has shown to inhibit growth of most cancers studied in a dose-dependent fashion.

  6. Green tea extract; promotes apoptosis in almost every cancer cell line studied; blocks the aryl hydrocarbon receptor, which activates oncogenes (cancer promoting genes); inhibits VEGF (a potent factor that helps cancer cells develop their blood supply).

Treatments are individualized and are specific to the patient and the patients' cancer. It is not unusual to alter treatment as the cancer mutates. As mentioned earlier, the goal is to convert an acutely progressive terminal illness (in the case of stage IV cancer) into a chronic disease that the individual can live with.

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