Preventing and Controlling Cancer

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Low-carbohydrate ketogenic diets may aid control of certain cancers by keeping glucose and insulin levels low throughout the day, and vegan diets of moderate protein content can decrease blood levels of insulin-like growth factor-I (IGF-I), a hormone which promotes proliferation and survival in many cancers. Hence, it is proposed that ketogenic vegan diets, high in fat, moderate in plant protein, and very low in carbohydrates, comprised primarily of healthful whole foods, may represent a practical strategy for slowing or even temporarily reversing the spread of some cancers.

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A signaling molecule known as cyclic AMP (cAMP) is produced in many cancers, and makes them more aggressive. Adrenergic hormones (adrenaline, noradrenaline), as well as hormones produced by the pro-inflammatory cox-2 enzyme, boost cAMP production in many cancers. Hence, drugs which block cox-2 activity, or which inhibit receptors for adrenergic hormones, may have potential for cancer prevention and control. Drugs known as beta-blockers inhibit the activity of adrenergic hormones, and some studies show that cancer patients taking certain forms of these drugs have improved survival. Hence, beta-blockers may have a future as adjuvant therapies for cancer, and might also reduce cancer risk.

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An enzyme known as CK2 is highly active in a high proportion of aggressive cancers, and functions in numerous ways to make cancers more aggressive and harder to kill. Drugs which target this enzyme are currently being developed in hopes that they can become safe and effective therapies for cancer. Certain widely distributed phytonutrients – known as flavones and flavonols – have the potential to inhibit CK2 in concentrations that might conceivably be achieved via oral administration. It is proposed that this phenomenon may account, at least in part, for the demonstrated ability of these compounds to slow the growth of human cancers implanted in mice; hence, these compounds may merit serious clinical evaluation as cancer-retardant agents.

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Pancreatic adenocarcinomas tend to generate both superoxide and nitric oxide, and both of these factors aid the survival and spread of the cancer. This essay raises the possibility that a portion of this effect is mediated by peroxynitrite, which forms spontaneously when superoxide and nitric oxide react. If so, high-dose folate might be useful for treating this cancer, as intracellularly folates can scavenge radicals derived from peroxynitrite. Spirualina also may be helpful, by inhibiting the enzymatic complex that is the chief source of the superoxide.

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Cancer scientists at State University of New York have developed a protein that can punch holes in the walls of cancer cells, leading to their death. This phenomenon appears to be selective to cancer cells, and is more likely to work in cancers that are advanced and aggressive. Continual infusion of this protein suppresses the growth of pancreatic cancer in mice – without evident harm to the mice — so this protein may have potential as a very novel cancer drug.

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The most recent epidemiology on cadmium suggests that exposure to this toxic metal may be responsible for a high proportion of cases of breast and pancreatic cancer in people who have not experienced industrial cadmium exposure. It also suggests that cadmium boosts oxidative stress throughout the body, an effect which likely mediates much of its toxicity.

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Anti-angiogenic strategies for controlling cancer – measures which slow cancer growth and spread by blocking the growth of new blood vessels required for tumor expansion – were initially considered to have great promise, but in practice have usually had only a modest impact on survival statistics owing to adaptations by the cancer that help it to survive in a low oxygen environment and increase its ability to elicit blood vessel growth. In particular, increased activity of the protein hypoxia-inducible factor-1 (HIF-1) is evoked by anti-angiogenic therapy, and helps the cancer to adapt in this way. This essay describes a range of feasible measures that might be employed to suppress HIF-1 activity in cancers, potentially making anti-angiogenic therapy more effective.

Published in Medical Hypotheses 2010;74(5):789-97.

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Within cancer cells, vitamin C (ascorbate) performs the key function of controlling the activity of hypoxia-inducible factor-1 (HIF-1), a protein which helps cancer cells to thrive in low oxygen conditions and makes them much more aggressive. But there is evidence that in at least some cancers, their ascorbate content is too low to optimally control HIF-1 activity – and unfortunately simply ingesting more vitamin C is unlikely to correct the problem. However, the vitamin C metabolite dehydroascorbic acid can get into cancer cells efficiently – and once inside the cell is rapidly converted to ascorbate. So it is proposed that regular intravenous infusions of dehydroascorbic acid could be employed to optimize the ascorbate content of cancers, and thereby help control their aggressiveness.

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Recent analyses of large controlled trials evaluating daily low-dose aspirin reveal that this strategy is associated with a notable reduction in cancer mortality. There is reason to suspect that this reflects aspirin’s ability to inhibit the pro-inflammatory enzyme cox-2. This essay reviews a number of additional measures that are suspected to decrease cancer risk – including spirulina, phase 2-inductive phytochemicals, melatonin, vitamin D, soy isoflavones, vegan diets, leanness, exercise, and a low dietary omega-6/omega-3 ratio – and notes that at least a part of their protection may be afforded by a reduction in cox-2 activity. While maintaining a focus on cox-2, this article provides an overall summary of practical strategies for cancer prevention.

Published in Medical Hypotheses 2012;78(1):45-57.

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This essay reviews the evidence currently available on macrophage activated factor (GcMAF) as a treatment for cancer, and on serum nagalase as a putatively universal marker for cancer. Studies by Yamamoto and colleagues suggest that, when cancer is in a micrometastatic form follwing therapeutic extirpation of visible tumors, weekly injection of GcMAF may enable the macrophage-orchestrated immune response to eliminate the residual cancer cells, effectively achieving a cure. Repeated assays of serum nagalase may enable monitoring of cancer status during such therapy, revealing whether the therapy is working, and providing guidance as to how long the therapy should be continued. Much further research is required to confirm these possibilties. The use of GcMAF in conjunction with other agents that boost the tumor-kiling potential of macrophages may be a promising approach to cancer immunotherapy that should be evaluated.

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There is now strong reason to suspect that a natural protein, made in our bodies to boost the microbe- and cancer-fighting abilities of immune cells known as macrophages, can help to cure cancer when injected repeatedly by cancer patients who have minimal disease following successful surgery, chemotherapy, or radiotherapy.  This agent – macrophage activating factor (abbreviated as “GcMAF”) also may have the potential to slow cancer spread in patients with more advanced cancers, although this is more speculative.  And the good news is that, although GcMAF hasn’t yet received drug approval (and may be unlikely to, owing to the fact that it is a natural compound), it currently can be ordered via email from several chemical companies, who ship it in a form suitable for intramuscular administration (much like insulin). More

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Prostate epithelium, and some early prostate cancers, appear to require higher concentrations of folic acid than most other tissues to support a maximal rate of cellular multiplication. Therefore, a low-folate diet and/or low doses of the folate antagonist methotrexate may have the potential to slow the onset and growth of early stage prostate cancer – a possibility that could be tested clinically.

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Concentrations of statins much higher than those achieved clinically have potentiated the cancer-killling efficacy of many cytotoxic chemotherapeutic agents in cell culture studies or mice, but would be toxic if sustained in humans. This essay proposes that administration of very-high-dose statins for just several days prior to and following a dose of chemotherapy might achieve worthwhile chemopotentiation without unacceptable toxicity, and that this strategy merits clinical evaluation. Concurrent administration of tocotrienols may amplify response to such a regimen.

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This document cites a number of nutraceutical or drug measures that have potential for slowing the growth of colorectal cancer and/or improving its responsiveness to chemotherapy. Abstracts of scientific publications pertinent to these suggestions are appended.

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This document cites a number of nutraceutical or drug measures that have potential for slowing the growth of melanoma and/or improving its responsiveness to chemotherapy. Abstracts of scientific publications pertinent to these suggestions are appended.

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This document cites a number of nutraceutical or drug measures that have potential for slowing the growth of prostate cancer and/or improving its responsiveness to chemotherapy. Abstracts of scientific publications pertinent to these suggestions are appended.

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Despite the development of novel chemotherapy regimens which are prolonging life in many patients with multiple myeloma, long term prognosis remains poor owing to the onset of chemoresistance. However, a number of available drugs have the potential to render this cancer more sensitive to chemotherapeutic agents, as suggested by the research abstracts posted here.

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Epithelial ovarian cancer accounts for more deaths than any other gynecological cancer. If surgery fails to achieve a cure, chemotherapy is usually effective initially, but most cancers eventually evolve to resistance and progress. This essay discusses a number of nutraceuticals, drugs, or other strategies that have potential for amplifying or restoring response to chemotherapy drugs, and/or for slowing cancer spread.

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This document cites a number of nutraceutical or drug measures that have potential for slowing the growth of prostate cancer and/or improving its responsiveness to chemotherapy. Abstracts of scientific publications pertinent to these suggestions are appended.

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The great majority of prostate cancers remain dependent on effective activity of the androgen receptor – even cancers that no longer respond to androgen-antagonist measures and hence are characterized as “androgen-independent”. It may however prove feasible to durably inhibit androgen receptor activity with specially targeted drugs now being developed, while suppressing expression of the androgen receptor with measures that suppress activity of the pro-inflammatory transcription factor NF-kappaB.

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For cancers that can be biopsied, it is now feasible to assess their sensitivities to chemotherapy drugs in the laboratory, before chemotherapy is done. This can often help oncologists to choose agents capable of effectively controlling the cancer, while avoiding the needless toxicity associated with use of ineffective drugs. This article suggests that, in an analogous manner, lab testing could be used to determine which adjuvant agents could best potentiate response to chosen chemotherapies.

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