P27 NATURAL CANCER TREATMENTS

 

The use of apoptosis inducing or cell necrosis therapeutic cancer treatments is a huge market. Everyone claims that they have a cure. Unfortunately, this is mostly hype and many substances have very little research and evidence of work in human studies.

All the substances that are listed below have had clinical research that has been performed by independent clinicians.

They are described with minimal hype and we have tried to clarify how they work, what they affect and what they are. These therapies are very disputed and show successes ranging from outstanding to downright disappointing. However, this is not always the case as there can be vast variations in the value and effectiveness of a therapeutic substance. This is due to the natural variation in person to person, cancer to cancer, lifestyle to lifestyle.

There is no one treatment that will work for everyone and dosages play an important roll in each individual assessment.

In case of a cancer diagnosis patients often jump to different treatments, desperate to use and test them. It is important to observe the effects and eliminate those who only cost money without having any beneficial effects. Therefore, it’s important for a practitioner as well as a coach to remain neutral and not to fall into the trap of hype. Asking for the aid of experienced practitioners in each field of treatment can greatly help discern the validity process required for a positive outcome.

Some treatments presented here can be used in different doses and concentrations as medical treatments. Please see the medical treatment section for clarifications, dosage and efficiency.

Artemisinin

Artemisinin, an antimalarial drug derived from the sweet wormwood plant, Artemisia annua.

Artemisinin contains an endoperoxide molecule part that can react with iron to form cytotoxic free radicals. Cancer cells contain significantly more intracellular free iron than normal cells and it has been shown that artemisinin and its analogs selectively cause apoptosis in many cancer cell lines. In addition, artemisinin compounds have been shown to have anti-angiogenic, anti-inflammatory, anti-metastasis and growth inhibition effects.

Artemisinin resulted in a 28% reduction of breast cancer cells treated only with artemisinin. Also, an amazing 98% decrease in breast cancer cells within 16 hours after treatment with artemisinin and an iron-enhancing molecule, transferrin. These treatments had no significant effect on normal human breast cells. This research pointed to the involvement of free iron in the toxic effect of artemisinin toward cancer cells, while basically sparing healthy cells. (‘Selective toxicity of dihydroartemisinin and holotransferrin toward human breast cancer cells,’ Life Sciences 70 {2001 pp. 49-56).

Artemisinin induces apoptosis in human cancer cells

Artemisinin is effective against a wide variety of cancers as shown in a series of successful experiments. The most effective is leukemia and colon cancer. Intermediate activities were also shown against melanoma, breast, ovarian, prostate, CNS and renal cancer. Although artemisinin is insoluble in water, it is able to cross the blood/brain barrier (the water soluble artesunate is the weakness among the derivates) and may be particularly suitable for curing brain tumors, together with Poly-MVA (an metalo-vitamin).

Artemisinin is not a stand-alone chemotherapeutic agent. A combination of nutritional supplements (such as green tea, CoQ10 and pancreatic enzyme) as well as a good anti-cancer diet is required.

ART (artemisinin) may be administered orally, with a 32 percent bioavailability as compared to injections. It is highly bound to membranes. Laboratory measurement of its serum level is therefore not exact.

Cautions:

• No artemisinin should be taken within 30 days of radiation therapy because of possible free iron leaks to the surrounding tissues after radiation therapy
• Preliminary laboratory studies include: CBC, reticulocyte count, liver function test, ferritin, TIBC, ESR, C reactive protein and appropriate tumour markers. If the iron load is low, supplementing iron for a few days can be considered prior to starting artemisinin
• Tumour markers may increase during the initial stages as the tumour starts breaking down
• Vitamin E may work against the effectiveness of ART in vitro. However, this has not been shown to be a concern in human clinical cases.
Artemisinin should always be taken with food. Cod liver oil , cottage cheese or fish oil may be administered at the same time to enhance absorption. Generally, 400 to 800 mg per day can be used for at least 6 to 12 months. After that, it can be tapered off slowly.

Always take Artemisinin 2-3 hours aside from other antioxidants such as vitamin C.

Always check with your health care professional prior to starting this herb.

Research Studies:

Singh, N. P., & Lai, H. C. (2004). Artemisinin induces apoptosis in human cancer cells. Anticancer Research, 24(4), 2277–2280.

Abstract:

Artemisinin is a chemical compound extracted from the wormwood plant, Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and retard the growth of implanted fibrosarcoma tumors in rats. In the present research, we investigated its mechanism of cytotoxicity to cancer cells.nnMATERIALS AND METHODS: Molt-4 cells, in complete RPMI-1640 medium, were first incubated with 12 microM of human holotransferrin at 37 degrees C in a humid atmosphere of 5% CO2 for one hour. This enhanced the iron supply to the cells. The cells were then pelleted and transferred to a complete RPMI-1640 containing 200 microM of an analog dihydroartemisinin (DHA) and incubation was started (0 h). In addition, some culture samples were treated with holotransferrin alone and some (controls) were assayed without neither holotransferrin nor DHA treatment. Cells were counted and DNA diffusion assay was used to evaluate apoptosis and necrosis in each sample at 0 h and at 1, 2, 4 and 8 h of incubation.nnRESULTS: DHA treatment significantly decreased cell counts and increased the proportion of apoptosis in cancer cells compared to controls (chi2=4.5, df=1, p<0.035). Addition of holotransferrin significantly further decreased cell counts (chi2=4.5, df=1, p<0.035) and increased apoptosis (chi2=4.5, df=1, p<0.035). No necrotic cells were observed.nnCONCLUSION: This rapid induction of apoptosis in cancer cells after treatment with DHA indicates that artemisinin and its analogs may be inexpensive and effective cancer agents.

Zhang, H. T., Wang, Y. L., Zhang, J., & Zhang, Q. X. (2014). Artemisinin inhibits gastric cancer cell proliferation through upregulation of p53. Tumour Biol., 35(2), 1403–9. http://doi.org/10.1007/s13277-013-1193-1

Abstract:

Recent population studies suggest that the use of artemisinin is associated with reduced incidence and improved prognosis of certain cancers. In the current study, we assessed the effect of artemisinin on gastric cancer cells (AGS and MKN74 cells). We found that artemisinin inhibited growth and modulated expression of cell-cycle regulators in these cells. Treatment with artemisinin was also associated with induction of p27 kip1 and p21 kip1, two negative cell-cycle regulators. Furthermore, we revealed that artemisinin treatment led to an increased expression of p53. Taken together, these results provide evidence for a mechanism that may contribute to the antineoplastic effects of artemisinin suggested by recent population studies and justify further work to explore potential roles for it in gastric cancer prevention and treatment.

Salvestrols

Salvestrols are a recently-discovered class of compounds naturally derived from plants called Phytoalexins. They are naturally produced in response to fungal attacks and are part of the plant’s immune system.

In 2002, Gerry Potter, Professor of Medicinal Chemistry at DeMonfort University Leicester School of Pharmacy, identified and outlined a nutritional rescue mechanism that linked specific compounds in some of the most common foods we eat with cancer cell death. This rescue mechanism hinged on the metabolic activity of a certain cytochrome P450 enzyme, CYP1B1.

Cytochrome P450 enzymes constitute a host of some 5,800 enzymes existing throughout nature. Fifty-seven cytochrome P450 enzymes exist in humans. They have the ability to make many toxins and drugs water soluble and thus clear them from the body. They are our natural ´detox´ mechanism.

Importantly, the CYP1B1 enzyme was found to be expressed by all cancers, regardless of oncogenic origin, while being absent from healthy tissue (Murray GI., et al; University of Aberdeen 1995). It has now been found throughout all stages of cancer and is widely regarded as a universal cancer marker.

When salvestrols are metabolised by CYP1B1, new compounds are produced that are anti-cancer agents and actually cause apoptosis, or death, in the cancer cell.

Salvestrols act as a natural rescue mechanism, ensuring our cells function correctly. Antioxidants strive to protect our cells from DNA damage but are ineffective once the damage is done. Salvestrols actively eliminate damaged cells, helping us heal before sufficient accumulation can make us sick.

In the Journal of Orthomolecular Medicine, Vol 25, No. 1, 2010 (with authors Brian A. Schaefer, D.Phil.,Catherine Dooner, B.A, M. Danny Burke, Ph.D, Gerard A. Potter, Ph.D) there was a presentation of case histories involving five cancers, breast; prostate; colon; liver; and Hodgkins lymphoma. To quote the authors, ‘Two of the cases show how rapid and dramatic the improvement can be when nutritional deficits are addressed. In each case of the five studies the patient used salvestrols to significant effect’.

Ideally we should be able to extract the salvestrols from the food we eat but there just aren’t enough in the average food we buy now.

Local and organic vegetables and fruits will have the highest content of salvestrols. Boiling leaches salvestrol out into the water and, unless the cooking water is included in the meal, all salvestrol will be lost. It’s better to steam, roast or stir-fry the vegetables to retain the most salvestrols as possible.

The salvestrol supplement is made from organically grown fruit. Mostly they are extracted in high concentrations from tangerine or orange peel and blueberries, and mixed with concentrated blackberry and strawberry powder.

None of the fruits used in salvestrol have been genetically modified, or treated with pesticides or anti fungal agents.

Salvestrol can be enhanced by biotin, niacin, magnesium and selenium as well as probiotics.

Research Studies:

Brian A Schaefer, D. P., 1, Gerard A. Potter, P., 2, Robbie Wood, BDS, D. O., R.C.S.(Eng), D. D. O. R. C. P. S., … M. Danny Burke. (2012). Cancer and Related Case Studies Involving Salvestrol and CYP1B1. Orthomolecular Medicine, 27(3), 131.

Ware, W. R. (2009). Nutrition and the prevention and treatment of cancer: association of cytochrome P450 CYP1B1 with the role of fruit and fruit extracts. Integrative Cancer Therapies, 8(1), 22–28. http://doi.org/10.1177/1534735408328573

Abstract:

Recommendations for a healthy or prudent diet include a large number of daily servings of fruits and vegetables, and these 2 classes of food are widely believed to assist in cancer prevention. One potential mechanism that is rarely mentioned in nutritional studies involves the cytochrome P450 enzyme CYP1B1, which appears to have the unique properties of being a universal cancer marker overexpressed in cancer cells and having the capability of converting various phytochemicals and synthetic chemicals into substances cytotoxic to these cells. Although these particular features of CYP1B1 have not gone unnoticed, there has been relatively little research aimed at exploiting them. Furthermore, therapeutic and preventive strategies currently being considered based on vaccines against the enzyme or inhibition without the generation of cytotoxins can be questioned because they do not take advantage of the unique properties of this enzyme. In addition, a few relevant case histories have been published that use specially designed fruit extracts containing substrates with demonstrated cytotoxic metabolic products, and these reports provide an initial confirmation of the potential of exploiting the unusual properties of this enzyme for cancer therapy.

Curcumin

‘No cancer has been found that is not affected by curcumin.’ (MD Anderson Cancer Center, Texas)

Curcumin is the natural pigment that gives the spice turmeric its yellow color. Not only does it have anticancer properties, it has the potential to improve heart health, lower cholesterol levels, and reduce Alzheimer's and diabetes risk.

The anti-cancer action of curcumin (turmeric):

• Importantly, the spice can stop the action of the enzyme COX-2 known to produce negative, inflammation causing localised enzymes (eicosanoids). Such inflammation is a known precursor to cancer
• It has also been shown to inhibit vascular epithelial growth factors. Every tumour needs a blood supply - the growth factors build one - but curcumin seems to stop them
• It has been shown to ´re-awaken´ a key tumour suppressor gene (p53 protein). This protein is needed for apoptosis, the normal process of cell suicide.
• Inhibit nuclear factor kappa beta (NF-kB). This is a protein produced by many cancers to block the signals to command it to stop proliferating.
• It has been shown to inhibit metastases
• It has been shown to kill cancer cells (B lymphoma cells)
• It prevents regrowth of cancer stem cells, which lie at the heart of many tumours
• It has been proven to reduce systemic inflammation and oxidative stress
• It boosts crucial cellular glutathione levels
• It has also been shown that curcumin has a strong synergistic effect against cancer with resveratrol and also with EGCG in green tea
• It can help prevent liver damage.
2010 research from St Louis has shown that it can turn off a protein called leptin, which causes liver damage. It has also been shown to be capable of detoxifying the liver. Thus curcumin may be of help in keeping the liver healthy during chemotherapy cancer treatments.

New studies show that curcumin from turmeric and piperine can lower the number of stem cells while having no effect on normal differentiated cells. When doses of over twenty times the potency of normal intake in diets were applied to the breast cancer cells, the cancerous cells decreased in number. This kind of potency can be made possible by taking dietary supplements. Limiting the number of stem cells is equivalent to limiting the chances for the cells to create tumours.

Unfortunately its bioavailability is extremely poor. Therefore the use of adjuvants are necessary to facilitate better bioavailability. Of the adjuvants Phospholipid complexes is the most successful form of curcumin. It showed with a almost 3 fold absorption rate in several studies and resulted in a marked increase in therapeutic outcomes.
Therefore when applying this information to the client at hand, it is important to note that the supplement she/he is currently taking is the best possible form available.

Recommended therapeutic dose is a min. of 400mg.

Research Studies:

Ravindran, J., Prasad, S., & Aggarwal, B. B. (2009). Curcumin and cancer cells: how many ways can curry kill tumor cells selectively? The AAPS Journal, 11(3), 495–510. http://doi.org/10.1208/s12248-009-9128-x

Abstract:

Cancer is a hyperproliferative disorder that is usually treated by chemotherapeutic agents that are toxic not only to tumor cells but also to normal cells, so these agents produce major side effects. In addition, these agents are highly expensive and thus not affordable for most. Moreover, such agents cannot be used for cancer prevention. Traditional medicines are generally free of the deleterious side effects and usually inexpensive. Curcumin, a component of turmeric (Curcuma longa), is one such agent that is safe, affordable, and efficacious. How curcumin kills tumor cells is the focus of this review. We show that curcumin modulates growth of tumor cells through regulation of multiple cell signaling pathways including cell proliferation pathway (cyclin D1, c-myc), cell survival pathway (Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1), caspase activation pathway (caspase-8, 3, 9), tumor suppressor pathway (p53, p21) death receptor pathway (DR4, DR5), mitochondrial pathways, and protein kinase pathway (JNK, Akt, and AMPK). How curcumin selectively kills tumor cells, and not normal cells, is also described in detail.

Fathima, D. N. (2014). Curcumin -Role in Cancer, 6(11), 351–355.

Abstract:

Cancer is a hyper proliferative disorder which mainly arises from mutation of somatic cells. Cancer cells have the capacity to proliferate,transform and invade somatic cells. Recent studies have proved, this deadly disorder “Cancer” can now be inhibited by a liposoluble polyphenolic pigment “Curcumin” which is derived from Curcuma longa plant, commonly known has turmeric. The yellow colour of turmeric contains three curcumin namely diferuloylmethane, desmethoxycurcumin and bisdesmethoxycurcumin. Mainly diferuloylmethane helps in treatment of cancer. The main inhibitory effect of curcumin on tumor cells is by initiating benzo[a]pyrene and DMBA. The anticancer property of curcumin has an effect on many cell-signalling pathway involved in mutagenesis, oncogenes, cell cycle regulation, apoptosis, tumorigenesis. Curcumin is chemopreventive for various cancer.
Curcumin inhibits proliferation of tumor cells but not normal cells. Curcumin processes anticancer properties in variety of cancers such as head and neck squamous cell carcinoma, pancreatic carcinoma, colon cancer, breast adenocarcinoma, ovarian carcinoma, lung cancer cells etc.

Park, W., Ruhul Amin, a. R. M., Chen, Z. G., & Shin, D. M. (2013). New perspectives of curcumin in cancer prevention. Cancer Prevention Research, 6(5), 387–400. http://doi.org/10.1158/1940-6207.CAPR-12-0410

Abstract:

Numerous natural compounds have been extensively investigated for their potential for cancer prevention over the decades. Curcumin, from Curcuma longa, is a highly promising natural compound that can be potentially used for chemoprevention of multiple cancers. Curcumin modulates multiple molecular pathways involved in the lengthy carcinogenesis process to exert its chemopreventive effects through several mechanisms: promoting apoptosis, inhibiting survival signals, scavenging reactive oxidative species (ROS), and reducing the inflammatory cancer microenvironment. Curcumin fulfills the characteristics for an ideal chemopreventive agent with its low toxicity, affordability, and easy accessibility. Nonetheless, the clinical application of curcumin is currently compromised by its poor bioavailability. Here, we review the potential of curcumin in cancer prevention, its molecular targets, and mechanisms of action. Finally, we suggest specific recommendations to improve its efficacy and bioavailability for clinical applications.

Resveratrol

Resveratrol is a potent antioxidant chemical found in red wine, red grape skins, fruits, vegetables, legumes and weeds. It has been found to have the following actions and functions:

• Broad-spectrum antimicrobial
• Anti-infective
• Antioxidant
• Cardio-protective
• Anti-cancer.
Resveratrol has to been shown to induce apoptotic cell death in human leukemia cells as well as in some breast carcinoma cells.

A study done in China showed that resveratrol inhibited the proliferation of pancreatic cancer cells.

A study in India observed that resveratrol down-regulated PKM2 expression by inhibiting mTOR signaling and suppressed cancer metabolism, adjudged by decreased glucose uptake, lactate production (aerobic glycolysis) and reduced anabolism (macromolecule synthesis) in various cancer cell lines.

Research Studies:

Potter, G. a, Patterson, L. H., Wanogho, E., Perry, P. J., Butler, P. C., Ijaz, T., … Burke, M. D. (2002). The cancer preventative agent resveratrol is converted to the anticancer agent piceatannol by the cytochrome P450 enzyme CYP1B1. British Journal of Cancer, 86(5), 774–8. http://doi.org/10.1038/sj.bjc.6600197

Abstract:

Resveratrol is a cancer preventative agent that is found in red wine. Piceatannol is a closely related stilbene that has antileukaemic activity and is also a tyrosine kinase inhibitor. Piceatannol differs from resveratrol by having an additional aromatic hydroxy group. The enzyme CYP1B1 is overexpressed in a wide variety of human tumours and catalyses aromatic hydroxylation reactions. We report here that the cancer preventative agent resveratrol undergoes metabolism by the cytochrome P450 enzyme CYP1B1 to give a metabolite which has been identified as the known antileukaemic agent piceatannol. The metabolite was identified by high performance liquid chromatography analysis using fluorescence detection and the identity of the metabolite was further confirmed by derivatisation followed by gas chromatography-mass spectrometry studies using authentic piceatannol for comparison. This observation provides a novel explanation for the cancer preventative properties of resveratrol. It demonstrates that a natural dietary cancer preventative agent can be converted to a compound with known anticancer activity by an enzyme that is found in human tumours. Importantly this result gives insight into the functional role of CYP1B1 and provides evidence for the concept that CYP1B1 in tumours may be functioning as a growth suppressor enzyme.

Tang, Q., Li, G., Wei, X., Zhang, J., Chiu, J. F., Hasenmayer, D., … Zhang, H. (2013). Resveratrol-induced apoptosis is enhanced by inhibition of autophagy in esophageal squamous cell carcinoma. Cancer Letters, 336(2), 325–337. http://doi.org/10.1016/j.canlet.2013.03.023

Abstract:

The anti-cancer activity of resveratrol in human esophageal squamous cell carcinoma (ESCC) was investigated focusing on the role of autophagy and its effects on apoptotic cell death. We demonstrated that resveratrol inhibits ESCC cell growth in a dose-dependent manner by inducing cell cycle arrest at the sub-G1 phase and resulting in subsequent apoptosis. Mechanistically, resveratrol-induced autophagy in the ESCC cells is AMPK/mTOR pathway independent. Since both pharmacological and genetic inhibition of autophagy enhanced the resveratrol-induced cytotoxicity to the ESCC cells, this provided a novel strategy in potentiating the anti-cancer effects of resveratrol and other chemotherapeutic reagents in ESCC cancer treatment.

Honokiol

Honokiol is one of two compounds isolated from magnolia spp. bark, and is the most widely researched active constituent of the bark. In vivo studies suggest that honokiol’s greatest value is in its multiple anti-cancer actions.

In vitro research suggests honokiol has:

• Potential to enhance current anti-cancer regimens by inhibiting angiogenesis
• Promoting apoptosis
• Providing direct cytotoxic activity
• Down-regulating cancer cell signaling pathways
• Regulating genetic expression
• Enhancing the effects of specific chemotherapeutic agents
• Radio-sensitising cancer cells to radiation therapy
• Inhibiting multi-drug resistance.
Honokiol also shows potential in preventative health by reducing inflammation and oxidative stress, providing neurological protection, and regulating glucose; in mental illness, by its effects against anxiety and depression, and in helping regulate stress response signaling.

There is a need for research on honokiol to progress to human studies and on into clinical use.

Currently, honokiol is used by a growing number of practitioners in integrative treatment protocols for cancer and other conditions.

Research Studies:

Arora, S., Singh, S, G. a. P., Contreras, C. M., Panyam, J., & Singh, A. P. (2012). Honokiol: a novel natural agent for cancer prevention and therapy. Current Molecular …, 12(10), 1244–1252. http://doi.org/10.2174/156652412803833508

Abstract:

Honokiol ((3’,5-di-(2-propenyl)-1,1’-biphenyl-2,2’-diol) is a bioactive natural product derived from oxidative and anti-cancer properties of honokiol targets multiple signaling pathways including nuclear factor kappa B (NF-κB), signal transducers Magnolia spp . Recent studies have demonstrated anti-inflammatory, anti-angiogenic, anti- in vitro and in preclinical models. Honokiol and activator of transcription 3 (STAT3), epidermal growth factor receptor (EGFR) and mammalian target of rapamycin (m-TOR), which have great relevance during cancer initiation and progression. Furthermore, pharmacokinetic profile of honokiol has revealed a desirable spectrum of bioavailability after intravenous administration in animal models, thus making it a suitable agent for clinical trials. In this review, we discuss recent data describing the molecular targets of honokiol and its anti-cancer activities against various malignancies in pre-clinical models. Evaluation of honokiol in clinical trials will be the next step towards its possible human applications.

Fried, L. E., & Arbiser, J. L. (2009). Honokiol, a multifunctional antiangiogenic and antitumor agent. Antioxidants & Redox Signaling, 11(5), 1139–1148. http://doi.org/10.1089/ars.2009.2440

Abstract:

Honokiol is a small-molecule polyphenol isolated from the genus Magnolia. It is accompanied by other related polyphenols, including magnolol, with which it shares certain biologic properties. Recently, honokiol has been found to have antiangiogenic, antiinflammatory, and antitumor properties in preclinical models, without appreciable toxicity. These findings have increased interest in bringing honokiol to the clinic as a novel chemotherapeutic agent. In addition, mechanistic studies have tried to find the mechanism(s) of action of honokiol, for two major reasons. First, knowledge of the mechanisms of action may assist development of novel synthetic analogues. Second, mechanistic actions of honokiol may lead to rational combinations with conventional chemotherapy or radiation for enhanced response to systemic cancers. In this review, we describe the findings that honokiol has two major mechanisms of action. First, it blocks signaling in tumors with defective p53 function and activated ras by directly blocking the activation of phospholipase D by activated ras. Second, honokiol induces cyclophilin D, thus potentiating the mitochondrial permeability transition pore, and causing death in cells with wild-type p53. Knowledge of the dual activities of honokiol can assist with the development of honokiol derivatives and the design of clinical trials that will maximize the potential benefit of honokiol in the patient setting.

PolyMVA

Poly-MVA is a uniquely formulated dietary supplement containing a proprietary blend of the mineral palladium bonded to alpha-lipoic acid, Vitamins B1, B2 and B12, formyl-methionine, N-acetyl cysteine, plus trace amounts of molybdenum, rhodium, and ruthenium.

Proven actions:

• Aids in cellular energy production
• Supports liver detoxification
• Protects cell integrity
• Acts as a heavy metal chelator
• Acts as a powerful antioxidant
• Supports nerve and neurotransmittal function
• Enhances WBC function
• Assists in unblocking energy flow along meridians.

According to the inventor of Poly-MVA, this complex can alter the electrical charge of DNA molecules and other parts of cells. This activity is said to help repair damaged DNA and cause cancer cells to self-destruct, a process called apoptosis. Proponents have also claimed palladium allows lipoic acid, an antioxidant, to reach cells in the body it could not otherwise reach. The other components of Poly-MVA are said to complement these actions and to help restore nutrients needed for energy.

Research studies: 

Poly-MVA-Breakthrough-2020-Color-4-email

 

IP6

Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate found in food sources high in fibre content. Although there are limited human studies, IP6 showed clear anti-neoplastic properties in breast, colon, liver, leukemia, prostate, sarcomas, and skin cancer. In vitro studies also showed decreased cancer cell growth, increased apoptosis inhibition of tumor cell proliferation and reduced angiogenesis.

Research studies:

Vucenik, I., & Shamsuddin, A. M. (2009). Protection Against Cancer by Dietary IP 6 and Inositol. Nutrition and Cancer, 55(2), 109–125. http://doi.org/10.1207/s15327914nc5502

Abstract:

Inositol hexaphosphate (IP 6 ) is a naturally occur - ring polyphosphorylated carbohydrate, abundantly present in many plant sources and in certain high-fiber diets, such as cereals and legumes. In addition to being found in plants, IP 6 is contained in almost all mammalian cells, although in much smaller amounts, where it is important in regulating vital cel- lular functions such as signal transduction, cell prolifera- tion, and differentiation. For a long time IP 6 has been recog- nized as a natural antioxidant. Recently IP 6 has received much attention for its role in cancer prevention and control of experimental tumor growth, progression, and metastasis. In addition, IP 6 possesses other significant benefits for human health, such as the ability to enhance immune system, prevent pathological calcification and kidney stone formation, lower elevated serum cholesterol, and reduce pathological platelet activity. In this review we show the efficacy and discuss some of the molecular mechanisms that govern the action of this dietary agent. Exogenously administered IP 6 is rapidly taken up into cells and dephosphorylated to lower inositol phos - phates, which further affect signal transduction pathways re - sulting in cell cycle arrest. A striking anticancer action of IP 6 was demonstrated in different experimental models. In addi - tion to reducing cell proliferation, IP 6 also induces differenti - ation of malignant cells. Enhanced immunity and antioxidant properties also contribute to tumor cell destruction. Prelimi - nary studies in humans show that IP 6 and inositol, the pre - cursor molecule of IP 6 , appear to enhance the anticancer ef - fect of conventional chemotherapy, control cancer metastases, and improve quality of life. Because it is abun - dantly present in regular diet, efficiently absorbed from the gastrointestinal tract, and safe, IP 6 + inositol holds great promise in our strategies for cancer prevention and therapy. There is clearly enough evidence to justify the initiation of full-scale clinical trials in humans.

Shafie, N. H., Esa, N. M., Ithnin, H., Saad, N., & Pandurangan, A. K. (2013). Pro-apoptotic effect of rice bran Inositol Hexaphosphate (IP6) on HT-29 colorectal cancer cells. International Journal of Molecular Sciences, 14(12), 23545–23558. http://doi.org/10.3390/ijms141223545

Abstract:

Inositol hexaphosphate (IP6), or phytic acid is a natural dietary ingredient and has been described as a "natural cancer fighter", being an essential component of nutritional diets. The marked anti-cancer effect of IP6 has resulted in our quest for an understanding of its mechanism of action. In particular, our data provided strong evidence for the induction of apoptotic cell death, which may be attributable to the up-regulation of Bax and down-regulation of Bcl-xl in favor of apoptosis. In addition, the up-regulation of caspase-3 and -8 expression and activation of both caspases may also contribute to the apoptotic cell death of human colorectal adenocarcinoma HT-29 cells when exposed to IP6. Collectively, this present study has shown that rice bran IP6 induces apoptosis, by regulating the pro- and anti-apoptotic markers; Bax and Bcl-xl and via the activation of caspase molecules (caspase-3 and -8).

Shamsuddin, A. M., Vucenik, I., & Cole, K. E. (1997). IP6: A novel anti-cancer agent. Life Sciences, 61(4), 343–354. http://doi.org/10.1016/S0024-3205(97)00092-1

Abstract:

Inositol hexaphosphate (InsP6 or IP6) is ubiquitous. At 10 gM to 1 mM concentrations, IP6 and its lower phosphorylated forms (IP1-5) as well as inositol (Ins) are contained in most mammalian cells, wherein they are important in regulating vital cellular functions such as signal transduction, cell proliferation and differentiation. A striking anti-cancer action of IP6 has been demonstrated both in vivo and in vitro, which is based on the hypotheses that exogenously administered IP6 may be internalized, dephosphorylated to IP1-5, and inhibit cell growth. There is additional evidence that Ins alone may further enhance the anti-cancer effect of IP6. Besides decreasing cellular proliferation, IP6 also causes differentiation of malignant cells often resulting in a reversion to normal phenotype. These data strongly point towards the involvement of signal transduction pathways, cell cycle regulatory genes, differentiation genes, oncogenies and perhaps, tamer suppressor genes in bringing about the observed anti-neoplastic action of IP6.

Green Tea

Epigallocatechin-3-gallate (EGCG), the major polyphenolic component of green tea, has been demonstrated to possess anti-inflammatory, antioxidant, anti-mutagenic, anti-proliferative, apoptotic and anti-carcinogenic properties. These characteristics have been extensively studied in both in vitro and vivo studies.

The findings of these studies are very conclusive and no adverse side effects have been noted

Exciting research studies have been published on green tea and its anti-cancer qualities. A recent study from Japan demonstrates that green tea goes way beyond its role as a well-known antioxidant. If the study is confirmed, it will propel the ancient beverage squarely into the middle of 21st century science. One of the factors that set cancer cells apart from normal cells is that they have telomerase, an enzyme that maintains telomeres on the ends of DNA. Most normal cells do not have telomerase to maintain their telomeres. Every time a normal cell divides, telomeres are lost. When all the telomeres are gone, the cell dies. Cancer cells' ability to maintain their telomeres may be the secret to their immortality. Consequently, inhibiting telomerase and causing cancer cells' telomeres to shorten has become a focus of cancer therapy. The first natural telomerase inhibitor has been discovered, green tea. Japanese researchers have been able to show that green tea extract (ECGC) inhibits telomerase of cancer cells in two different types of cancers in the test tube: leukemia and the solid tumor type. Within a month of treatment, some of the cancer cells began dying and within three months most were dead. The experiment has been repeated several times with the same result. Curiously, the telomeres of normal cells will remain unaffected. Extracts of green tea in pill form are now available.

Research Studies:

Li, X., Feng, Y., Liu, J., Feng, X., Zhou, K., & Tang, X. (2013). Epigallocatechin-3-gallate inhibits IGF-I-stimulated lung cancer angiogenesis through downregulation of HIF-1?? and VEGF expression. Journal of Nutrigenetics and Nutrigenomics, 6(3), 169–178. http://doi.org/10.1159/000355672

Abstract:

Numerous studies have shown that epigallocatechin-3-gallate (EGCG), a polyphenol component extracted from green tea, can inhibit the growth and induce apoptosis of various types of human tumor cells. In this study, we evaluated the inhibitory effects of EGCG on the proangiogenic capabilities of A549 cells.nnMETHODS: A549 cells starved in serum-free culture medium for 24 h were pretreated with EGCG at various concentrations (0, 10, 25, 50, and 100 μmol/l) for 1 h, followed by the addition of insulin-like growth factor-I (IGF-I) at the final concentration of 40 ng/ml and continued culturing for an additional 16 h. The in vitro angiogenesis analyzing test kit with ECMatrix™ gel was used to detect the formation of capillary tube-like structures. The mRNA expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) was determined by real-time PCR. The protein expression of HIF-1α and VEGF was detected by Western blotting and ELISA, respectively.nnRESULTS: EGCG significantly inhibited the formation of capillary tube-like structures on the surface of ECMatrix induced by IGF-I both in vitro and in vivo and reduced the level of hemoglobin in Matrigel plugs. In addition, EGCG was shown to significantly inhibit the IGF-I-induced upregulation of HIF-1α protein expression. Meanwhile, EGCG at the concentration of 25 and 100 μmol/l exhibited obvious inhibitory effects on IGF-I-induced VEGF expression (p < 0.01).nnCONCLUSION: Our results suggest that EGCG has potent inhibitory effects on tumor angiogenesis induced by IGF-I in human non-small cell lung cancer cells, which may possibly contribute to the downregulation of HIF-1α and VEGF expression.

Khan, N., & Mukhtar, H. (2011). Cancer and metastasis: prevention and treatment by green tea. Cancer Metastasis Reviews, 29(3), 435–445. http://doi.org/10.1007/s10555-010-9236-1.Cancer

Abstract:

Metastasis is the most deadly aspect of cancer and results from several interconnected processes including cell proliferation, angiogenesis, cell adhesion, migration, and invasion into the surrounding tissue. The appearance of metastases in organs distant from the primary tumor is the most destructive feature of cancer. Metastasis remains the principal cause of the deaths of cancer patients despite decades of research aimed at restricting tumor growth. Therefore, inhibition of metastasis is one of the most important issues in cancer research. Several in vitro , in vivo , and epidemiological studies have reported that the consumption of green tea may decrease cancer risk. ( − )-Epigallocatechin-3-gallate, major component of green tea, has been shown to inhibit tumor invasion and angiogenesis which are essential for tumor growth and metastasis. This article summarizes the effect of green tea and its major polyphenolic compounds on cancer and metastasis against most commonly diagnosed cancer sites.

Calcium D-Glucarate

Glucorinidation, one of the phase two liver detox pathways, is primarily responsible for the clearance of chemical carcinogens from the environment and estrogenic tumour promoters produced by the body. Calcium D-Glucarate has a profound anticancer effect by increasing glucoronidation and thereby lowering endogenous levels of estrogens. Increasing glucoronidation reduces carcinogens and promoting agents, which are excreted, at least in part, as glucuronide conjugates. In over twenty animal studies with induced cancer in rats, show that Calcium-D-Glucarate supplementation, after treatment with the carcinogen, inhibits tumour development by over 60%.

Research Studies:

Abou-Issa, H; Moeschberger, M; el-Masry, W; Tejwani, S; Curley, Jr, R W; Webb, T. E. (1995). Relative efficacy of glucarate on the initiation and promotion phases of rat mammary carcinogenesis. Attiki, Greece : International Institute of Anticancer Research, 15(3), 805.

Abstract:

The independent effects of the potential cancer chemopreventive agent calcium glucarate (CGT) when fed (128 mmol/kg diet) during the initiation (I), promotion (P) or (I+P) phases of 7,12-dimethylbenzanthracene-induced rat mammary carcinogenesis, was compared to that of the known chemopreventive agent N-(4-hydroxyphenyl) retinamide (4-HPR) fed (2.0 mmol/kg diet) during these same phases. CGT and especially 4-HPR both significantly increased tumor latency when fed during the P-phase. When fed during I, P or I+P phases mammary tumor incidence was reduced compared to the controls 33%, 42% and 67% by 4-HPR and 18%, 42% and 50% by CGT. Similarly, tumor multiplicity was significantly reduced by either agent. For example, as compared to the corresponding control, when fed during the I, P or I+P phases 4-HPR reduced tumor multiplicity 63, 34 and 63%, while CGT reduced tumor multiplicity 28, 42 and 63% respectively. CGT, like 4-HPR, acts on both the I and P phases with the effect being maximal when fed during P and I+P phases.

Walaszek, Z; Szemraj, J; Narog, M; Adams, A K; Kilgore, J; Sherman, U; Hanausek, M. (1997). Metabolism, uptake, and excretion of a D-glucaric acid salt and its potential use in cancer prevention. Medline, 21(2), 176.

Abstract:

D-Glucaric acid (GA) is a nontoxic, natural compound. One of its derivatives is the potent beta-glucuronidase inhibitor D-glucaro-1,4-lactone (1,4-GL). The goal of this study was to demonstrate the in vivo formation of 1,4-GL from a D-glucarate salt and determine its metabolism, uptake by selected organs, and excretion following oral administration of potassium hydrogen D-[14C]glucarate to male and female Sprague-Dawley rats. 1,4-GL increases detoxification of carcinogens and tumor promoters/progressors by inhibiting beta-glucuronidase and preventing hydrolysis of their glucuronides. 1,4-GL and its precursors, such as potassium hydrogen D-glucarate and calcium D-glucarate, may exert their anticancer action, in part, through alterations in steroidogenesis accompanied by changes in the hormonal environment and the proliferative status of the target organ. Thus, GA derivatives may be useful as new or adjuvant cancer preventive and therapeutic agents. In our study, 1,4-GL was found to be formed from the D-glucarate salt in the stomach of rats. It was apparently absorbed from the gastrointestinal tract, transported with the blood to different internal organs, and excreted in the urine and to a lesser extent in bile. There were no significant differences in the metabolism of PHG between male and female rats. Thus, formation of 1,4-GL from D-glucaric acid derivatives may be prerequisite for their inhibition of chemical carcinogenesis in rodents and prevention of breast, prostate, and colon cancer in humans.

Fucoidan

Fucoidan is a long chain carbohydrate found in seaweed (especially brown algae). The apoptotic effect of focoidan on cancer cells has been thoroughly examined in over 600 scientific studies; in vitro, in vivo and human studies. Fucoidan also works on a genetic level changing DNA expression in cancer cells, activating anti-cancerous genes and imitating apoptosis.

Research Studies:

Han, Y., Lee, J. H., & Lee, S. H. (2015). Antitumor Effects of Fucoidan on Human Colon Cancer Cells via Activation of Akt Signaling, 23(3), 225–232.

Abstract:

We identified a novel Akt signaling mechanism that mediates fucoidan-induced suppression of human colon cancer cell (HT29) proliferation and anticancer effects. Fucoidan treatment significantly inhibited growth, induced G1-phase-associated upregulation of p21WAF1 expression, and suppressed cyclin and cyclin-dependent kinase expression in HT29 colon cancer cells. Additionally, fucoidan treatment activated the Akt signaling pathway, which was inhibited by treatment with an Akt inhibitor. The inhibition of Akt activation reversed the fucoidan-induced decrease in cell proliferation, the induction of G1-phase-associated p21WAF1 expres - sion, and the reduction in cell cycle regulatory protein expression. Intraperitoneal injection of fucoidan reduced tumor volume; this enhanced antitumor efficacy was associated with induction of apoptosis and decreased angiogenesis. These data suggest that the activation of Akt signaling is involved in the growth inhibition of colon cancer cells treated with fucoidan. Thus, fucoidan may serve as a potential therapeutic agent for colon cancer.

Boo, H. J., Hong, J. Y., Kim, S. C., Kang, J. Il, Kim, M. K., Kim, E. J., … Kang, H. K. (2013). The anticancer effect of fucoidan in PC-3 prostate cancer cells. Marine Drugs, 11(8), 2982–2999. http://doi.org/10.3390/md11082982

Abstract:

Fucoidan, a sulfated polysaccharide, has a variety of biological activities, such as anti-cancer, anti-angiogenic and anti-inflammatory. However, the mechanisms of action of fucoidan as an anti-cancer agent have not been fully elucidated. The present study examined the anti-cancer effect of fucoidan obtained from Undaria pinnatifida in PC-3 cells, human prostate cancer cells. Fucoidan induced the apoptosis of PC-3 cells by activating both intrinsic and extrinsic pathways. The induction of apoptosis was accompanied by the activation of extracellular signal-regulated kinase mitogen-activated protein kinase (ERK1/2 MAPK) and the inactivation of p38 MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt. In addition, fucoidan also induced the up-regulation of p21Cip1/Waf and down-regulation of E2F-1 cell-cycle-related proteins. Furthermore, in the Wnt/β-catenin pathway, fucoidan activated GSK-3β that resulted in the decrease of β-catenin level, followed by the decrease of c-myc and cyclin D1 expressions, target genes of β-catenin in PC-3 cells. These results suggested that fucoidan treatment could induce intrinsic and extrinsic apoptosis pathways via the activation of ERK1/2 MAPK, the inactivation of p38 MAPK and PI3K/Akt signaling pathway, and the down-regulation of Wnt/β-catenin signaling pathway in PC-3 prostate cancer cells. These data support that fucoidan might have potential for the treatment of prostate cancer.

Graviola

Graviola contains natural compounds that have cytotoxic activity. Studied since the early 1990s, empirical evidence shows that chemical extracts attack and destroy cancer cells. In vitro studies have shown that it effectively targets and kills malignant cells in twelve different types of cancer, including colon, breast, prostate, lung, and pancreatic cancer. It has been shown to decrease the expression of cancer promoting genes and cause selective apoptosis of cancerous cells. Some studies have shown that it is several times as cytotoxic as chemotherapy drugs, however it only targets cancer cells.

Research Studies:

Torres, M. P., Rachagani, S., Purohit, V., Pandey, P., Joshi, S., Moore, E. D., … Batra, S. K. (2012). Graviola: A novel promising natural-derived drug that inhibits tumorigenicity and metastasis of pancreatic cancer cells in vitro and in vivo through altering cell metabolism. Cancer Letters, 323(1), 29–40. http://doi.org/10.1016/j.canlet.2012.03.031

Abstract:

Pancreatic tumors are resistant to conventional chemotherapies. The present study was aimed at evaluating the potential of a novel plant-derived product as a therapeutic agent for pancreatic cancer (PC). The effects of an extract from the tropical tree . Annona Muricata, commonly known as Graviola, was evaluated for cytotoxicity, cell metabolism, cancer-associated protein/gene expression, tumorigenicity, and metastatic properties of PC cells. Our experiments revealed that Graviola induced necrosis of PC cells by inhibiting cellular metabolism. The expression of molecules related to hypoxia and glycolysis in PC cells (i.e. HIF-1α, NF-κB, GLUT1, GLUT4, HKII, and LDHA) were downregulated in the presence of the extract. . In vitro functional assays further confirmed the inhibition of tumorigenic properties of PC cells. Overall, the compounds that are naturally present in a Graviola extract inhibited multiple signaling pathways that regulate metabolism, cell cycle, survival, and metastatic properties in PC cells. Collectively, alterations in these parameters led to a decrease in tumorigenicity and metastasis of orthotopically implanted pancreatic tumors, indicating promising characteristics of the natural product against this lethal disease.

Dai, Y., Hogan, S., Schmelz, E. M., Ju, Y. H., Canning, C., & Zhou, K. (2011). Selective growth inhibition of human breast cancer cells by graviola fruit extract in vitro and in vivo involving downregulation of EGFR expression. Nutrition and Cancer, 63(5), 795–801. http://doi.org/10.1080/01635581.2011.563027

Abstract:

The epidermal growth factor receptor (EGFR) is an oncogene frequently overexpressed in breast cancer (BC), and its overexpression has been associated with poor prognosis and drug resistance. EGFR is therefore a rational target for BC therapy development. This study demonstrated that a graviola fruit extract (GFE) significantly downregulated EGFR gene expression and inhibited the growth of BC cells and xenografts. GFE selectively inhibited the growth of EGFR-overexpressing human BC (MDA-MB-468) cells (IC(50) = 4.8 μg/ml) but had no effect on nontumorigenic human breast epithelial cells (MCF-10A). GFE significantly downregulated EGFR mRNA expression, arrested cell cycle in the G0/G1 phase, and induced apoptosis in MDA-MB-468 cells. In the mouse xenograft model, a 5-wk dietary treatment of GFE (200 mg/kg diet) significantly reduced the protein expression of EGFR, p-EGFR, and p-ERK in MDA-MB-468 tumors by 56%, 54%, and 32.5%, respectively. Overall, dietary GFE inhibited tumor growth, as measured by wet weight, by 32% (P < 0.01). These data showed that dietary GFE induced significant growth inhibition of MDA-MB-468 cells in vitro and in vivo through a mechanism involving the EGFR/ERK signaling pathway, suggesting that GFE may have a protective effect for women against EGFR-overexpressing BC.

Haelan 951®

Haelan 951 is a fermented soy product. These are known to contain high concentrations of the isoflavone, genistein, and other compounds that exhibit anticancer activity. Haelan 951 has shown to prevent angiogenesis, block enzymatic activity, tumour reduction, and boosting of the immune system. The joint treatment of Haelan 951 and chemotherapy has been well studied and patients show favourable outcomes, reducing the side effects of chemo drugs and increasing lifespan.

Be careful the taste is terrible and many patients refuse to drink it.

Research Studies:

Chen, J., Stavro, P. M., & Thompson, L. U. (2009). Dietary Flaxseed Inhibits Human Breast Cancer Growth and Metastasis and Downregulates Expression of Insulin-Like Growth Factor and Epidermal Growth Factor Receptor Dietary Flaxseed Inhibits Human Breast Cancer Growth and Metastasis and Downregulates Expre, (783016864), 37–41. http://doi.org/10.1207/S15327914NC432

Abstract:

The effect of a fermented soy milk product (FSP) on various human breast carcinoma cell lines was investi- gated, and it was shown to have a growth-inhibitory effect, especially on MCF-7 cells. Thus the MCF-7 cell line was used to study the mechanism of action. In female severe combined immune deficiency mice implanted with MCF-7 cells, pretreatment with FSP significantly inhibited tumor growth. The inhibitory effect of FSP on MCF-7 cells seemed to be caused by the additive effects of a wide variety of con- stituents. The active components of FSP are mainly in the wa- ter phase, and the lipid-soluble fraction, which includes the soy isoflavones such as genistein and daidzein, is relatively ineffective. A variety of methods were used to demonstrate that FSP caused apoptotic cell death in MCF-7 cells. FSP in- duced generation of reactive oxygen species (ROS). Growth inhibition and ROS generation induced by FSP could be in- hibited by catalase and deferoxamine, indicating that the ROS production probably was the cause of this apoptotic cell death. This study suggests that FSP retards tumor growth in vivo and can trigger apoptosis in vitro. It may, therefore, be a potential nutritional supplement in chemotherapy.

Klein, A., He, X., Roche, M., Mallett, A., Duska, L., Supko, J. G., & Seiden, M. V. (2006). Prolonged stabilization of platinum-resistant ovarian cancer in a single patient consuming a fermented soy therapy. Gynecologic Oncology, 100(1), 205–209. http://doi.org/10.1016/j.ygyno.2005.08.006

Abstract:

Background. Women with ovarian cancer who experience disease progression during or within 6 months of first-line treatment with platinum-based anticancer drugs are considered to have platinum-resistant tumors. These patients have an unfavorable prognosis, and they frequently seek complementary and alternative therapies (CAM). Historically, this represents an understudied and underreported component of ovarian cancer treatment. Case. This report describes the case of a woman with rapidly progressive, platinum-resistant ovarian cancer. Upon initiating self-directed treatment with Haelan951®, a commercially available fermented soy beverage, she entered into a phase of prolonged disease stabilization including improvement in the serum tumor marker CA-125. Conclusion. Fermented soy products are known to contain high concentrations of the isoflavone, genistein, and other compounds that exhibit anticancer activity in preclinical models. This case report supports the prospective evaluation of alternative therapies such as these in patients with platinum-refractory ovarian cancer.

Modified Citrus Pectin

Modified citrus pectin (pH-modified), a soluble complex polysaccharides rich in galactoside residues, derived from citrus fruit, has been shown to interfere with cell-cell interactions, exhibit anti-mutagenic activity, inhibit cancer metastasis and proliferation, with no evidence of toxicity or other serious side effects. Modified citrus pectin has a modulatory effect on the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in macrophages. Modulation of iNOS and COX-2 are important in cancer chemoprevention and anti-inflammation. However, the primary anti-cancerous effect displayed by modified citrus pectin is its ability to bind to receptors on cancerous cells spontaneous metastasis.

Research Studies:

Glinsky, V. V., & Raz, A. (2009). Modified citrus pectin anti-metastatic properties: one bullet, multiple targets. Carbohydrate Research, 344(14), 1788–1791. http://doi.org/10.1016/j.carres.2008.08.038

Abstract:

In this minireview, we examine the ability of modified citrus pectin (MCP), a complex water soluble indigestible polysaccharide obtained from the peel and pulp of citrus fruits and modified by means of high pH and temperature treatment, to affect numerous rate-limiting steps in cancer metastasis. The anti-adhesive properties of MCP as well as its potential for increasing apoptotic responses of tumor cells to chemotherapy by inhibiting galectin-3 anti-apoptotic function are discussed in the light of a potential use of this carbohydrate-based substance in the treatment of multiple human malignancies.

Hossein, G., Keshavarz, M., Ahmadi, S., & Naderi, N. (2013). Synergistic effects of PectaSol-C modified citrus pectin an inhibitor of galectin-3 and paclitaxel on apoptosis of human SKOV-3 ovarian cancer cells. Asian Pacific Journal of Cancer Prevention, 14(12), 7561–7568. http://doi.org/10.7314/APJCP.2013.14.12.7561

Abstract:

Galectin-3 (Gal-3) is a carbohydrate-binding protein which is thought to be involved in cancer progression but its contribution to epithelial ovarian cancer (EOC) remains unclear. The present study sought to determine the role of Gal-3 in chemoresistance of the human SKOV-3 ovarian cancer cell line to paclitaxel (PTX) using recombinant human Gal-3 (rhGal-3) and PectaSol-C modified citrus pectin (Pect-MCP) as a specific Gal-3 competitive inhibitor. Our results showed 41% increased cell proliferation, 36% decreased caspase-3 activity and 33.6% increased substrate-dependent adhesion in the presence of rhGal-3 compared to the control case (p<0.001). Treatment of cells with a non-effective dose of PTX (100nM) and 0.1% Pect-MCP in combination revealed synergistic cytotoxic effects with 75% reduced cell viability and subsequent 3.9-fold increase in caspase-3 activity. Moreover, there was 39% decrease in substrate-dependent adhesion compared to control (p<0.001). These results suggest that inhibition of Gal-3 could be a useful therapeutic tool for combination therapy of ovarian cancer.

Proteolytic Enzymes

Proteolytic enzymes (or proteases) refer to the various enzymes that digest protein. Proteolytic enzymes have a long history of use in cancer treatment. In 1906, John Beard, the founder of the theory ‘cancer as metabolic disease’ reported success with enzyme treatment on cancer patients. Currently, Nicholas Gonzalez, an M.D. in New York ,uses proteolytic enzymes as foundational component for his treatment of advanced pancreatic cancer patients. Some of the most common proteolytic enzymes include: pancreatic proteases chymotrypsin and trypsin; bromelain (pineapple enzyme), papain (papaya enzyme), fungal proteases and serrapeptase. Cancer cells are characterised by uncontrolled cell growth. In John Beard’s theory he discovered that pancreatic enzymes are responsible for the inhibitions of uncontrolled cell growth of the placenta. As he found many similarities between placental cells and cancer, he hypothesised that cancer inhibition is linked to the utilisation, production or abundance of proteolytic enzymes. The mechanism of this is linked with the enzymes’ ability to digest proteins. Proteolytic enzymes remove the protective coating from cancer cells, allowing white blood cells to identify and attack them.

Research Studies:

Béez, R., Lopes, M. T. P., Salas, C. E., & Hernández, M. (2007). In vivo antitumoral activity of stem pineapple (Ananas comosus) bromelain. Planta Medica, 73(13), 1377–1383. http://doi.org/10.1055/s-2007-990221

Abstract:

Stem bromelain (EC 3.4.22.32) is a major cysteine proteinase, isolated from pineapple ( Ananas comosus) stem. Its main medicinal use is recognized as digestive, in vaccine formulation, antitumoral and skin debrider for the treatment of burns. To verify the identity of the principle in stem fractions responsible for the antitumoral effect, we isolated bromelain to probe its pharmacological effects. The isolated bromelain was obtained from stems of adult pineapple plants by buffered aqueous extraction and cationic chromatography. The homogeneity of bromelain was confirmed by reverse phase HPLC, SDS-PAGE and N-terminal sequencing. The in vivo antitumoral/antileukemic activity was evaluated using the following panel of tumor lines: P-388 leukemia, sarcoma (S-37), Ehrlich ascitic tumor (EAT), Lewis lung carcinoma (LLC), MB-F10 melanoma and ADC-755 mammary adenocarcinoma. Intraperitoneal administration of bromelain (1, 12.5, 25 mg/kg), began 24 h after tumor cell inoculation in experiments in which 5-fluorouracil (5-FU, 20 mg/kg) was used as positive control. The antitumoral activity was assessed by the survival increase (% survival index) following various treatments. With the exception of MB-F10 melanoma, all other tumor-bearing animals had a significantly increased survival index after bromelain treatment. The largest increase ( approximately 318 %) was attained in mice bearing EAT ascites and receiving 12.5 mg/kg of bromelain. This antitumoral effect was superior to that of 5-FU, whose survival index was approximately 263 %, relative to the untreated control. Bromelain significantly reduced the number of lung metastasis induced by LLC transplantation, as observed with 5-FU. The antitumoral activity of bromelain against S-37 and EAT, which are tumor models sensitive to immune system mediators, and the unchanged tumor progression in the metastatic model suggests that the antimetastatic action results from a mechanism independent of the primary antitumoral effect.

Dhandayuthapani, S., Perez, H. D., Paroulek, A., Chinnakkannu, P., Kandalam, U., Jaffe, M., & Rathinavelu, A. (2012). Bromelain-Induced Apoptosis in GI-101A Breast Cancer Cells. Journal of Medicinal Food, 15(4), 344–349. http://doi.org/10.1089/jmf.2011.0145

Abstract:

Bromelain is a proteolytic enzyme extracted from the stems and the immature fruits of pineapple that was found to be antitumorigenic in different in vitro models. Bromelain has been reported to promote apoptosis, particularly in breast cancer cells, with the up-regulation of c-Jun N-terminal kinase and p38 kinase. Our study was designed to determine if bromelain could induce apoptosis in GI-101A breast cancer cells. GI-101A cells were treated with increasing concentrations of bromelain for 24 hours. The effect of bromelain for inducing cell death via activation of the apoptosis mechanism in GI-101A cells was further determined by using caspase-9 and caspase-3 assays along with the M30-Apoptosense assay to measure cytokeratin 18 (CK18) levels in the cytoplasm of the cultured cancer cells. A dose-dependent increase in the activities of caspase-9 and caspase-3 coinciding with elevation of CK18 levels was found in bromelain-treated cells compared with control cells. Furthermore, the apoptosis induction by bromelain was confirmed by DNA fragmentation analysis and 4,6'-diamino-2-phenylindole dihydrochloride fluorescence staining of the nucleus. Our results indicate an increase in apoptosis-related cell death in breast cancer cells with increasing concentrations of bromelain.

Protocel, Cancell, Cantron and Entelev

Sheridan’s Formula, Jim’s Juice, JS–114, JS–101, 126–F, Crocinic Acid, Entelev, Protocel, and Cantron are all products with extremely similar composition under different brand names. First made about 70 years ago by a chemist called James Sheridan, there is very little evidence supporting its claims. The composition of the formula is a mystery and so is its mechanism of action. The producers claim that it changes the action potential of the cells membrane’s thereby changing its energy production and starving cancer cells. The theory is quite flawed with unsupported claims and biological mistakes. Along with cancer, Protocel etc. has been claimed to cure AIDS, herpes, chronic fatigue syndrome, lupus, endometriosis, Crohn’s disease, fibromyalgia, diabetes, emphysema, scleroderma, Lou Gehrig disease, multiple sclerosis, cystic fibrosis, muscular dystrophy, Parkinson disease, Alzheimer’s disease, hemophilia, high and low blood pressure, mental illness, some forms of epilepsy and asthma.

Protocel's effect can be stopped by a number of substances such as: Vitamin C , Vitamin E, Selenium
Thyroid support products, SOD, CoEnzyme Q10
"sea greens" such as spirulina, algae, plankton, chlorella, kelp

These claims seem unsubstantiated and the belief that a treatment can aid in so many different ways in such a complex human biological system seems unfounded and ridiculous.

Laetrile

Laetrile, vitamin B17 and amygdalin are all different names for the same product. Laetrile is particularly prevalent in the seeds of bitter almond, apricot, blackthorn, cherry, nectarine, peach and plum. The most common source of laetrile is the apricot kernel. When we introduce laetrile into the body it will be broken down by the enzyme rhodanese. This enzyme is found in large quantities throughout the body but it is not present wherever there are cancer cells. Rhodanese breaks down vitamin B17 into thiocynate and benzoic acid, which is beneficial in nourishing healthy cells. They form the metabolic pool for vitamin B12 production. The body will expel any excess via urination.

Since cancer cells do not contain any rhodanese enzyme, hydrogen cyanide cannot be broken down into harmless byproducts. When vitamin B17 comes into contact with the enzyme glucosidase, which is only prevalent in cancer cells, it will cause a chemical reaction between the hydrogen cyanide and benzaldehyde to synergistically produce a poison that destroys and kills cancer cells. Hydrogen cyanide has been proven to be chemically inert and non-toxic when consumed through food or a refined pharmaceutical, such as laetrile. To use laetrile in the form of apricot kernels is not recommended; in several incidence it caused internal bleeding. However, if a client decides to do it anyway it is important to ensure that they are free of molds which produce Aflatoxins, which is very toxic and carcinogenic to humans.

Laetrile treatment has to be shown very successful when given IV (intravenous).

Research Studies:

Chen, Y., Ma, J., Wang, F., Hu, J., Cui, A., Wei, C., … Li, F. (2013). Amygdalin induces apoptosis in human cervical cancer cell line HeLa cells. Immunopharmacology and Immunotoxicology, 35(1), 43–51. http://doi.org/10.3109/08923973.2012.738688

Abstract:

Amygdalin, a naturally occurring substance, has been suggested to be efficacious as an anticancer substance. The effect of amygdalin on cervical cancer cells has never been studied. In this study, we found that the viability of human cervical cancer HeLa cell line was significantly inhibited by amygdalin. 4,6-Diamino-2-phenyl indole (DAPI) staining showed that amygdalin-treated HeLa cells developed typical apoptotic changes. The development of apoptosis in the amygdalin-treated HeLa cells were confirmed by double staining of amygdalin-treated HeLa cells with annexin V-FITC and propidium iodide (PI) along with increase in caspase-3 activity in these cells. Further studies indicated that antiapoptotic protein Bcl-2 was downregulated whereas proapoptotic Bax protein was upregulated in the amygdalin-treated HeLa cells implying involvement of the intrinsic pathway of apoptosis. In vivo, amygdalin administration inhibited the growth of HeLa cell xenografts through a mechanism of apoptosis. The results in the present study suggest that amygdalin may offer a new therapeutic option for patients with cervical cancer.

Makarević, J., Rutz, J., Juengel, E., Kaulfuss, S., Reiter, M., Tsaur, I., … Blaheta, R. A. (2014). Amygdalin blocks bladder cancer cell growth in vitro by diminishing cyclin A and cdk2. PloS One, 9(8), e105590. http://doi.org/10.1371/journal.pone.0105590

Abstract:

Amygdalin, a natural compound, has been used by many cancer patients as an alternative approach to treat their illness. However, whether or not this substance truly exerts an anti-tumor effect has never been settled. An in vitro study was initiated to investigate the influence of amygdalin (1.25-10 mg/ml) on the growth of a panel of bladder cancer cell lines (UMUC-3, RT112 and TCCSUP). Tumor growth, proliferation, clonal growth and cell cycle progression were investigated. The cell cycle regulating proteins cdk1, cdk2, cdk4, cyclin A, cyclin B, cyclin D1, p19, p27 as well as the mammalian target of rapamycin (mTOR) related signals phosphoAkt, phosphoRaptor and phosphoRictor were examined. Amygdalin dose-dependently reduced growth and proliferation in all three bladder cancer cell lines, reflected in a significant delay in cell cycle progression and G0/G1 arrest. Molecular evaluation revealed diminished phosphoAkt, phosphoRictor and loss of Cdk and cyclin components. Since the most outstanding effects of amygdalin were observed on the cdk2-cyclin A axis, siRNA knock down studies were carried out, revealing a positive correlation between cdk2/cyclin A expression level and tumor growth. Amygdalin, therefore, may block tumor growth by down-modulating cdk2 and cyclin A. In vivo investigation must follow to assess amygdalin's practical value as an anti-tumor drug.

Black Cumin

Black cumin seed oil from the Nigella sativa plant has also been found to kill cancer cells. The ingredient thymoquinone (TQ) has anti-cancer properties that suppress the growth and lead to apoptosis of cancer cells. Since 1959 there have been over 200 different studies regarding the treatment of cancer with Nigella sativa. Black cumin seed oil has had enormous success in tumour therapy without the negative side effects of common chemotherapy. Research found that it increased the growth rate of bone marrow cells by 250% while inhibiting tumour growth by 50%. It stimulated immune cells and raised the interferon production, which protects cells from the effects of cell destroying viruses. One study even concluded that black bumin seed oil is more effective against many strains of bacteria than antibiotics. Black seed oil capsules were used in a study at I.I.M.E.R. Panama city, Florida, to reveal that the majority of people who took black seed oil displayed a 72% increase in helper-to-suppressor T-cell ratio, as well as an increase in natural killer cell functional activity. Therefore, black cumin seed oil may be an important part of a cancer patient’s treatment.

Research Studies:

Shafiq, H., Ahmad, A., Masud, T., & Kaleem, M. (n.d.). Cardio-protective and anti-cancer therapeutic potential of Nigella sativa, (13).

Abstract:

Nigella sativa is the miraculous plant having a lot of nutritional and medicinal benefits, and attracts large number of nutrition and pharmacological researchers . N. sativa seed composition shows that it is the blessing of nature and it contains and many bioactive compounds like thymoquinone, α - hederin, alkaloids, flavonoids, antioxidants, fatty acids many other compounds that have positive effects on curing of different diseases. Several medicinal properties of N. sativa like its anti - cancer, anti - in flammatory, anti - diabetic, antioxidant activities and many others are well acknowledged. However, this article focuses on activity of N. sativa against cardiovascular diseases and cancer. For gathering required data the authors went through vast number of articles using search engines like Science direct, ELSEVIER , Pub Med, Willey on Line Library and Google scholar and the findings were classified on the basis of relevance of the topic and were reviewed in the article. N. sativa is rich source of different biologically active compounds and is found effective in controlling number of cardiovascular diseases and various cancers both in vivo and in vitro studies

Sulforaphane

Sulforaphane (SFN), a substance formed from two constituents of brassica vegetables, have shown to provide cancer prevention through a number of mechanisms including the up regulation of detoxification enzymes and epigenetic changes. These changes have been thoroughly studied and show statistical significance in most cases. The epigenetic effect that SFN displays is rare and of key importance for changing the outcomes of a patient. Fresh broccoli contains myrosinase, an enzyme which, in the presence of water, converts the glucosinolate glucoraphanin into the bioactive compound SFN. This process, although seemingly simple, makes supplementation of SFN extremely complicated.

Proven actions of Sulforaphane:

• Modulates cell cycle
• Anti-inflammatory
• Functions as inhibitor of phase 1 liver enzymes and inducer of phase 2 liver enzymes.
• Aids in the detoxification of mutagens and xenobiotics
• Reduce the carcinogenicity of many environmental toxins by boosting the genetic expression of important detoxifying enzymes.
• Protects DNA from oxidative damage caused by toxins, thereby preventing the initial changes that can lead to cancer.
• Encourage cancer cells to commit suicide
• Suppresses genes that create the new blood vessels (angiogenesis) that support rapid growth of tumors.
• Can turn off genes that promote the spread of cancer.
Source:

Broccoli sprouts yield more SFN than any other known plant and contain 10–100 times the concentration of glucoraphanin of mature broccoli. Mature broccoli also do not contain as much myrosinase enzyme, reducing the percentage of SFN produced. Erucic acid is a lipid found in broccoli seeds and has been linked to myocardial lipidosis, myocardial necrosis and impaired oxidative phosphorylation in animal studies. Broccoli seeds contain 28% lipids, but broccoli sprouts contain only about 1% lipids. Therefore, broccoli sprouts contain the most glucoraphanin and myrosinase.

Processing:

Several of the studies have shown that it is necessary for myrosinase to be present to optimise SFN yield. Although it has been documented that some endogenous bacteria can convert glucoraphanin to SFN, for broccoli sprout supplement to demonstrate bioactivity in vivo, it must retain both the glucoraphanin and myrosinase enzyme. Cooking, freezing and extraction are the primary processes leading to loss of myrosinase. Because the reaction between the glucoraphanin and myrosinase is initiated in the presence of moisture, the conversion of glucoraphanin to SFN may be complete before the extraction process is finished. Although glucoraphanin is stable over a long period of time, SFN is not. Therefore, many seed extracts found on the market have little or no therapeutic effect as they lack the essential myrosinase enzyme. The ideal broccoli sprout ingredient contains separately compartmentalised glucoraphanin and myrosinase that react at, or close to, the time of ingestion.

As seen above, the complications for broccoli sprout supplementation are extensive. However, there are supplements on the market that provide powdered (capsule) glucoraphanin and myrosinase which activates upon exposure to moisture. These supplements must be an olive green in color to ensure they are from properly sprouted broccoli. However, the ingestion of fresh broccoli sprouts has shown to be extremely effective vs inactive extracts. Therefore, an increase in broccoli sprouts in the diet may be a fundamental dietary change.

Research Studies:

Li, Y., & Zhang, T. (2013). Targeting cancer stem cells with sulforaphane, a dietary component from broccoli and broccoli sprouts. Future Oncology (London, England), 9(8), 1097–103. http://doi.org/10.2217/fon.13.108

Abstract:

Many studies have supported the protective effects of broccoli and broccoli sprouts against cancer. The chemopreventive properties of sulforaphane, which is derived from the principal glucosinolate of broccoli and broccoli sprouts, have been extensively studied. Recent research into the effects of sulforaphane on cancer stem cells (CSCs) has drawn lots of interest. CSCs are suggested to be responsible for initiating and maintaining cancer, and to contribute to recurrence and drug resistance. A number of studies have indicated that sulforaphane may target CSCs in different types of cancer through modulation of NF-κB, SHH, epithelial-mesenchymal transition and Wnt/β-catenin pathways. Combination therapy with sulforaphane and chemotherapy in preclinical settings has shown promising results. In this article, we focus on the effects of sulforaphane on CSCs and self-renewal pathways, as well as giving a brief review of recent human studies using broccoli sprout preparations.

Sarkar, R., Mukherjee, S., Biswas, J., & Roy, M. (2012). Sulphoraphane, a naturally occurring isothiocyanate induces apoptosis in breast cancer cells by targeting heat shock proteins. Biochemical and Biophysical Research Communications, 427(1), 80–85. http://doi.org/10.1016/j.bbrc.2012.09.006

Abstract:

Heat shock proteins (HSPs) are involved in protein folding, aggregation, transport and/or stabilization by acting as a molecular chaperone, leading to inhibition of apoptosis by both caspase dependent and/or independent pathways. HSPs are overexpressed in a wide range of human cancers and are implicated in tumor cell proliferation, differentiation, invasion and metastasis. HSPs particularly 27, 70, 90 and the transcription factor heat shock factor1 (HSF1) play key roles in the etiology of breast cancer and can be considered as potential therapeutic target. The present study was designed to investigate the role of sulphoraphane, a natural isothiocyanate on HSPs (27, 70, 90) and HSF1 in two different breast cancer cell lines MCF-7 and MDA-MB-231 cells expressing wild type and mutated p53 respectively, vis-à-vis in normal breast epithelial cell line MCF-12F. It was furthermore investigated whether modulation of HSPs and HSF1 could induce apoptosis in these cells by altering the expressions of p53, p21 and some apoptotic proteins like Bcl-2, Bax, Bid, Bad, Apaf-1 and AIF. Sulphoraphane was found to down-regulate the expressions of HSP70, 90 and HSF1, though the effect on HSP27 was not pronounced. Consequences of HSP inhibition was upregulation of p21 irrespective of p53 status. Bax, Bad, Apaf-1, AIF were upregulated followed by down-regulation of Bcl-2 and this effect was prominent in MCF-7 than in MDA-MB-231. However, very little change in the expression of Bid was observed. Alteration in Bcl-2 Bax ratio resulted in the release of cytochrome c from mitochondria and activation of caspases 3 and 9 which are in agreement with apoptotic index values. Sulphoraphane therefore can be regarded as a potent inducer of apoptosis due to HSP modulation in breast cancer cells.

Diindolylmethane DIM

DIM and other plant indoles are found in cruciferous vegetables such as brocoli, cauliflower, cabbage, and kale.

DIM stimulates estrogen to be broken down into its beneficial or good estrogen metabolites know as the 2-hydroxy estrogens. When DIM increases the good estrogen metabolites then there is a simultaneous reduction in the levels of undesirable or bad estrogen metabolites. These include the 16-hydroxy and 4-hydroxy estrogens, which are not antioxidants and can actually cause cancer.

Indole 3 Carbinol I3C, promoted as supplement, turns out not to be active in our body until it is converted into DIM. DIM is formed as I3C combines with itself, in a process that occurs only if just the right amount of stomach acid is present. DIM is found in cruciferous vegetables such as broccoli, cauliflower, cabbage, and kale.

Research Studies:

Semov, A., Iourtchenco, L., Liu, L. F., Li, S., Xu, Y., Su, X., … Alakhov, V. (2012). Diindolilmethane (DIM) selectively inhibits cancer stem cells. Biochemical and Biophysical Research Communications, 424(1), 45–51. http://doi.org/10.1016/j.bbrc.2012.06.062

Abstract:

Epidemiologic studies repeatedly have shown chemopreventive effects of cruciferous vegetables. Indole-3-carbinol (I3C) and its metabolite diindolylmethane (DIM) were identified in these plants as active ingredients and theirs anti-tumor activities were confirmed in multiple in vitro and in vivo experiments. Here, we demonstrate that DIM is a selective and potent inhibitor of cancer stem cells (CSCs). In several cancer cell lines, DIM inhibited tumor sphere formation at the concentrations 30-300 times lower than concentrations required for growth inhibition of parental cells cultured as adherent culture. We also found that treatment with DIM overcomes chemoresistance of CSCs to cytotoxics, such as paclitaxel, doxorubicin, and SN-38. Pre-treatment of tumor spheres with DIM before implantation to mice significantly retarded the growth of primary tumors compared to tumors formed by untreated tumor spheres. The concentrations of DIM required to suppress CSCs formation are in the close range to those achievable in human plasma after oral dosing of the compound. Therefore, DIM can potentially be used in cancer patients, either alone, or in combinations with existing drugs.

Banerjee, S., Kong, D., Wang, Z., Bao, B., Hillman, G. G., & Sarkar, F. H. (2011). Mutation Research / Reviews in Mutation Research Attenuation of multi-targeted proliferation-linked signaling by 3 , 3 0 -diindolylmethane ( DIM ): From bench to clinic. Mutation Research-Reviews in Mutation Research, 728(1-2), 47–66. http://doi.org/10.1016/j.mrrev.2011.06.001

Abstract:

Emerging evidence provide credible support in favor of the potential role of bioactive products derived from ingesting cruciferous vegetables such as broccoli, brussel sprouts, cauliflower and cabbage. Among many compounds, 3,3 0 -diindolylmethane (DIM) is generated in the acidic environment of the stomach following dimerization of indole-3-carbinol (I3C) monomers present in these classes of vegetables. Both I3C and DIM have been investigated for their use in preventing, inhibiting, and reversing the progression of cancer – as a chemopreventive agent. In this review, we summarize an updated, wide-ranging pleiotropic anti-tumor and biological effects elicited by DIM against tumor cells. It is unfeasible to point one single target as basis of cellular target of action of DIM. We emphasize key cellular and molecular events that are effectively modulated in the direction of inducing apoptosis and suppressing cell proliferation. Collectively, DIM orchestrates signaling through Ah receptor, NF- k B/Wnt/Akt/mTOR pathways impinging on cell cycle arrest, modulation of key cytochrome P450 enzymes, altering angiogenesis, invasion, metastasis and epigenetic behavior of cancer cells. The ability of DIM to selectively induce tumor cells to undergo apoptosis has been observed in preclinical models, and thus it has been speculated in improving the therapeutic efficacy of other anticancer agents that have diverse molecular targets. Consequently, DIM has moved through preclinical development into Phase I clinical trials, thereby suggesting that DIM could be a promising and novel agent either alone or as an adjunct to conventional therapeutics such as chemo-radio and targeted therapies. An important development has been the availability of DIM formulation with superior bioavailability for humans. Therefore, DIM appears to be a promising chemopreventive agent or chemo-radio-sensitizer for the prevention of tumor recurrence and/or for the treatment of human malignancies.

Cannabis Oil

It has been known for a long time that cannabis oil contains cancer-fighting properties. Investigators are studying the anti-cancer capabilities of cannabis, as a growing body of preclinical and clinical data concludes that cannabinoids can reduce the spread of specific cancer cells via apoptosis (programmed cell death) and by the inhibition of angiogenesis (the formation of new blood vessels).

‘Run From The Cure - The Rick Simpson Story’ is a full-length video documentary that can be found on YouTube.

Rick Simpson states:

‘I have been providing people with instructions on how to make Hemp Oil medicines for about 8 years. The results have been nothing short of amazing. Throughout man’s history hemp has always been known as the most medicinal plant in the world. Even with this knowledge, hemp has always been used as a political and religious football.

The current restrictions against hemp were put in place and maintained, not because hemp is evil or harmful, but for big money to make more big money, while we suffer and die needlessly.

Look at a proposal such as this: If we were allowed to grow hemp in our backyards and cure our own illnesses, what do you think the reaction of the pharmaceutical industry would be to such a plan?

Many large pharmaceutical companies, that still exist today, sold hemp-based medicines in the 1800s and early 1900s. They knew then what I have recently found out. Hemp oil, if produced properly, is a cure-all that the pharmaceutical industry can’t patent.’

In March of 2011, The National Cancer Institute quietly added a summary of marijuana’s medicinal benefits to their treatment database.

Noted statement:

‘The potential benefits of medicinal cannabis for people living with cancer include antiemetic effects, appetite stimulation, pain relief and improved sleep. Though no relevant surveys of practice patterns exist, it appears that physicians caring for cancer patients who prescribe medicinal cannabis predominantly, do so for symptom management.”

Laboratory tests conducted in 2008 by a team of scientists formed as a joint research effort between Spain, France and Italy, were published in The Journal of Clinical Investigation. These test results illustrated that the active ingredient in marijuana, known as tetrahydrocannabinol or THC, can function as a cure for brain cancer by inducing human glioma cell death through stimulation of autophagy.

Marijuana is typically high in THC (delta-9 tetrahydrocannabinol) -- the compound responsible for the plant’s notorious psychoactive effect -- and low in CBD (cannabidiol) content. Both THC and CBD are known as cannabinoids.

Cannabis oil ingestion is being recommended for the destruction of cancer cells within the body, not for recreational use. Healing results from ingestion of the oil from the marijuana buds, not from smoking the buds. The high heat from a burning marijuana cigarette can destroy the 'medicinal qualities' contained within the cannabis buds. Furthermore, when smoking marijuana, carbon monoxide and tar are produced as byproducts of combustion and therefore increase the risk of introducing toxic elements into the body.

Please be aware that in many countries the use of marijuana is illegal. Merely having possession of marijuana can result in serious legal consequences.

Research Studies:

Ramer, R., Bublitz, K., Freimuth, N., Merkord, J., Rohde, H., Haustein, M., … Hinz, B. (2012). Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1. FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 26(4), 1535–48. http://doi.org/10.1096/fj.11-198184

Abstract:

Cannabinoids inhibit cancer cell invasion via increasing tissue inhibitor of matrix metalloproteinases-1 (TIMP-1). This study investigates the role of intercellular adhesion molecule-1 (ICAM-1) within this action. In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 μM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase. Up-regulation of ICAM-1 mRNA by CBD in A549 was 4-fold at 3 μM, with significant effects already evident at 0.01 μM. ICAM-1 induction became significant after 2 h, whereas significant TIMP-1 mRNA increases were observed only after 48 h. Inhibition of ICAM-1 by antibody or siRNA approaches reversed the anti-invasive and TIMP-1-upregulating action of CBD and the likewise ICAM-1-inducing cannabinoids Δ(9)-tetrahydrocannabinol and R(+)-methanandamide when compared to isotype or nonsilencing siRNA controls. ICAM-1-dependent anti-invasive cannabinoid effects were confirmed in primary tumor cells from a lung cancer patient. In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6% for CBD + ICAM-1 antibody]. Overall, our data indicate that cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness.

Shrivastava, A., Kuzontkoski, P. M., Groopman, J. E., & Prasad, A. (2011). Cannabidiol Induces Programmed Cell Death in Breast Cancer Cells by Coordinating the Cross-talk between Apoptosis and Autophagy, 22(10), 1161–1173. http://doi.org/10.1158/1535-7163.MCT-10-1100

Abstract:

Cannabidiol (CBD), a major nonpsychoactive constituent of cannabis, is considered an antineoplastic agent on the basis of its in vitro and in vivo activity against tumor cells. However, the exact molecular mechanism through which CBD mediates this activity is yet to be elucidated. Here, we have shown CBD-induced cell death of breast cancer cells, independent of cannabinoid and vallinoid receptor activation. Electron micro- scopy revealed morphologies consistent with the coexistence of autophagy and apoptosis. Western blot analysis confirmed these findings. We showed that CBD induces endoplasmic reticulum stress and, subse- quently, inhibits AKT and mTOR signaling as shown by decreased levels of phosphorylated mTOR and 4EBP1, and cyclin D1. Analyzing further the cross-talk between the autophagic and apoptotic signaling pathways, we found that beclin1 plays a central role in the induction of CBD-mediated apoptosis in MDA-MB- 231 breast cancer cells. Although CBD enhances the interaction between beclin1 and Vps34, it inhibits the association between beclin1 and Bcl-2. In addition, we showed that CBD reduces mitochondrial membrane potential, triggers the translocation of BID to the mitochondria, the release of cytochrome c to the cytosol, and, ultimately, the activation of the intrinsic apoptotic pathway in breast cancer cells. CBD increased the generation of reactive oxygen species (ROS), and ROS inhibition blocked the induction of apoptosis and autophagy. Our study revealed an intricate interplay between apoptosis and autophagy in CBD-treated breast cancer cells and highlighted the value of continued investigation into the potential use of CBD as an antineoplastic agent.

Pure CBD oil

Pharmaceutical strength marijuana is now available legally to the four corners of the globe because Cannabidiol (CBD) has no illegal THC. Of the more than 85 cannabinoids so far identified in the cannabis plant, CBD is the second most common after tetrahydrocannabinol (THC). Unlike THC, CBD is non-psychotropic and therefore doesn’t cause a euphoric high.

Cannabinoids, including CBD, interact with your body’s endocannabinoid system, or ECS. The ECS is a system of receptors found in all mammals. These receptors are located in the brain and nervous system throughout the body, specifically CB1 and CB2 receptors.

Numerous studies have shown the ECS to be directly involved in the processes that keep our bodies balanced day to day, including: appetite, pain sensation, mood, memory, immune system functions, and inflammation control.

Actions of CBD:

• Anti-inflammatory: Modulation of inflammatory response via multiple pathways, including suppression of overactive immune cells, suppression of pro-inflammatory cytokines and chemokines at inflammatory sites, and enhanced T cell activity.
• Provides stress adaption and release of its physiological effects.
• Neuroprotective: Recent research on cannabidiol shows it to be neuroprotective in those with multiple sclerosis and other neurological conditions such as Lyme disease, epilepsy, Parkinson’s disease and spinal cord injury; exerting this effect by supporting the regulation of inflammatory response in the nerves and muscles.
• Anti-tumour activity through suppressing carcinogenesis.
Researchers at the University of Milan in Naples, Italy, reported in the Journal of Pharmacology and Experimental Therapeutics that non-psychoactive compounds in marijuana inhibited the growth of glioma cells in a dose-dependent manner, and selectively targeted and killed malignant cells through apoptosis. "Non-psychoactive CBD produce[s] a significant anti-tumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent."

According to Dr. Allan Frankel, "Cannabidiol will be used to treat chronic pain, anxiety and other mood disorders, as well as being a neuro-protectant and a very helpful anti-cancer drug." CBD is an extremely powerful anti-inflammatory. While inflammation is normally treated with corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDS), the improvements in quality and understanding of CBD content increases the opportunity for inflammation and associated pain to be treated with CBD.

There is NO proper range of dosage of CBD established at the moment. Dosage ranges vary depending on the case. Cancer patients receive up to 1000mg per day in form of suppositories. See below three different dosage guides from three different sources.

• General Health: 2.5-15mg CBD by mouth daily / To treat chronic pain: 2.5-20 mg CBD by mouth daily / To treat sleep disorders: 40-160 mg CBD by mouth daily
• Finally, preliminary clinical trials suggest that high-dose oral CBD (150–600 mg/d) may exert a therapeutic effect for social anxiety disorder, insomnia and epilepsy, but also that it may cause mental sedation. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763649/
• To treat epilepsy, 200-300 milligrams of CBD has been taken by mouth daily for up to 4.5 months.
Sources of CBD:

There are many sources / companies which produce CBD oil and suppositories. Please make sure to use a high quality product. Some recommendations are below:

• Nanoemusified Colorado Hemp oil by Quicksilver Scientific (3mg per dose) https://www.purxpressions.com/store/cho-50-ml
• CBD Suppositories (each suppository 50mg) by Endoca https://www.endoca.com/en/p103-buy-cbd-supositories-500mg-cbd-oil-suppositories (delivery worldwide)
• Pure CBD Extra Strength Oil by ResultsRNA (33,3 mg per dose in 1000mg strength) https://www.resultsrna.com/pure-cbd-organic-hemp-seed-oil/
• Suppositories organic pure CBD (250mg per suppositories) contact Marcus (mf@trulyheal.com)

Glutathione

Glutathione is an important intercellular antioxidant that plays a vital role in drug detoxification (liver detox) or elimination, and in protecting cellular damage by free radicals and toxins. It also plays a crucial role in diverse biological processes from protein synthesis to enzyme catalysis, growth and division, functioning of immune cells and many more.

Glutathione selectively stimulates apoptosis (cell death) of malignant cells while leaving healthy cells unaffected.

Glutathione concentrations are sensitive to diet and nutritional status. As we age our ability to produce glutathione drastically diminishes, which makes it hard to keep up with the demand posed by oxidative stress.

Glutathione cannot be raised significantly by oral consumption of L-Glutathione or Liposomal Glutathione, but it can be raised through glutathione injections. Unfortunately, these treatments are very expensive and last for only a few hours after the initial injection. The best way to raise glutathione naturally is through it's precursors.

Spirulina is very effective in raising glutathione levels because it delivers all the essential and non-essential amino acids, which are needed for glutathione production.

Precursors of glutathione production are:

• N-A-C (N- acetyl cysteine)
• Vitamin B6
• Zinc
• Natural Whey Protein Powder contains three amino acids; cysteine, glycine and glutamic acid, which are needed by the body to produce glutathione.
• Alpha-Lipoic-Acid
• Glutamine

Research Studies:

Traverso, N., Ricciarelli, R., Nitti, M., Marengo, B., Furfaro, A. L., Pronzato, M. A., … Domenicotti, C. (2013). Role of glutathione in cancer progression and chemoresistance. Oxidative Medicine and Cellular Longevity, 2013. http://doi.org/10.1155/2013/972913

Abstract:

Glutathione (GSH) plays an important role in a multitude of cellular processes, including cell differentiation, proliferation, and apoptosis, and disturbances in GSH homeostasis are involved in the etiology and progression of many human diseases including cancer. While GSH deficiency, or a decrease in the GSH/glutathione disulphide (GSSG) ratio, leads to an increased susceptibility to oxidative stress implicated in the progression of cancer, elevated GSH levels increase the antioxidant capacity and the resistance to oxidative stress as observed in many cancer cells. The present review highlights the role of GSH and related cytoprotective effects in the susceptibility to carcinogenesis and in the sensitivity of tumors to the cytotoxic effects of anticancer agents.

Balendiran, G. K., Dabur, R., & Fraser, D. (2004). The role of glutathione in cancer. Cell Biochemistry and Function, 22(6), 343–352. http://doi.org/10.1002/cbf.1149

Abstract:

Glutathione is an abundant natural tripeptide found within almost all cells. Glutathione is highly reactive and is often found conjugated to other molecules via its sulfhydryl moiety. It instils several vital roles within a cell including antioxidation, maintenance of the redox state, modulation of the immune response and detoxification of xenobiotics. With respect to cancer, glutathione metabolism is able to play both protective and pathogenic roles. It is crucial in the removal and detoxification of carcinogens, and alterations in this pathway, can have a profound effect on cell survival. However, by conferring resistance to a number of chemotherapeutic drugs, elevated levels of glutathione in tumour cells are able to protect such cells in bone marrow, breast, colon, larynx and lung cancers. Here we present a number of studies investigating the role of glutathione in promoting cancer, impeding chemotherapy, and the use of glutathione modulation to enhance anti-neoplastic therapy.

Black salve

Black salve is also known as BEC5, black and yellow salve, escharotics, escharotic therapy, botanical salve, Curaderm and Cansema.

Black salve is a plant based, non-invasive treatment for skin cancer. There are many kinds of formulas, which can contain up to ten ingredients or more. Ingredients may include; chaparral (Larrea tridentata), bloodroot (Sanguinaria canadensis), DMSO (dimethyl sulfoxide), chickweed (Stellaria media), Indian tobacco (Lobelia inflata), comfrey (Symphytum officinale), myrrh (Commiphora myrrha), marshmallow (Althaea officinalis), mullein (Verbascum thapsus), Australian devils apple (Solanum Sodomaeum) and other herbs, oils and chemicals.

Although all the ingredients have therapeutic effects, one of the killing effects attributed by black salve is believed to be due to a plant sugar called rhamnose. Specific endogenous lectins are present in the plasma membranes of susceptible cancer cells, but they are not present in normal cells. Therefore, the sugar rhamnose of the glycoalkaloid gets bonded to the cancer cell. Subsequently, this enters the cancer cell and causes cell death by destroying the lysosome.

Black salve has been tested in several clinical trial in both Australia and great Britain. All showed at least an 80% success rate within 8 weeks.

However black salve is also quite dangerous and there are several incidences where it has caused damage to surrounding cells (something it claims not to do). Therefore, it is banned in most countries and is considered dangerous due to an increased risk of keloid scarring and bleeding. Black salve is not intended to treat any internal cancers including breast cancer. It is also cautioned against use for skin melanoma.

Black salve is a topical cream and to use it, simply liberally administer to the specific tumour site. Black salve can be used for a minimum of seven days up to 60 days, depending on the size of the cancer.

Research Studies:

Cham, B. E. (2013). Topical Curaderm BEC5 Therapy for Periocular Nonmelanoma Skin Cancers : A Review of Clinical Outcomes, 2013(May), 233–238.

Abstract:

Approximately 5 to 10 percent of all skin cancers occur in the periocular region. Basal cell carcinoma is the most frequent malignant periocular tumor, followed by squamous cell carcinoma, sebaceous gland carcinoma, and malignant melanoma. Nonmelanoma skin tumors at the periocular area often cause disfigurement with destruction of soft conjunctival tissue. Many therapeutic methods have been recommended to combat the morbidity and mortality associated with these lesions. Excisions with frozen-section control or Mohs micrographic surgery are regarded as the gold-standard treatments for periocular basal cell and squamous cell carcinomas. However, these treatment modalities have various limitations and reconstruction surgery is often associated with these treatment options. The chemotherapeutic agents solasodine rhamnosides in a cream formulation CuradermBEC5 are specific, effective and safe treatments for nonmelanoma skin cancers with excellent cosmesis. The antineoplastic mode of action is by apoptosis. In this review it is shown that CuradermBEC5 also treats periocular basal cell carcinoma and squamous cell carcinoma with impressive cosmetic outcomes and no reconstructive surgery is required.

Essiac Tea

Essiac is a product that is composed of four or more herbs, two of which (sheep sorrel and burdock root) are known to kill cancer cells. The other two herbs build the immune system and deal with detox and protecting the organs.

Essiac tea is a long proven method of curing cancer. It dates back to the 1920s and before.

In 1922 Rene Caisse, a Canadian nurse, healed her aunty of cancer. Inspired by the success she offered the recipe to anyone who asked for it. From 1922 to 1978 she helped thousands of people with her formula. The original formula contained eight herbs (burdock root, sheep sorrel, Turkish rhubarb root, red clover, watercress, blessed thistle, kelp and slippery elm bark).

There were never any formal studies conducted but success was reported in many cases for cancer, arthritis, circulatory problems, urinary tract infections, prostate irregularities and asthma.

It is important to find a good quality tea on the internet. Make sure the herbs are organic and the mixture definitely contains sheep sorrel.

There some precautions which need to be taken into account when drinking the tea:

• Pregnant, nursing or women trying to conceive should not drink the tea as some constituents of the herbs may increase blood flow to the pelvic region and stimulate menses
• The varying amounts of oxalic acids in the tea are irritating to the kidneys. Caution when kidney disease, kidney stones or kidney infections are present
• Properties in the tea promote peristalsis and can cause diarrhea
• Patients who have ulcers or colitis have to be careful as some properties f the herbs can be highly irritating to these conditions
• The tea contains varies amount of iron and should be avoided by patients with increased levels of iron in their blood
• It is known that at the beginning of a treatment tumour growth/enlargement is observed before the tumor begins to break down. Caution has to be taken with patients where a tumor growth could have dire consequences. This can be extremely detrimental in the brain tissue
• Constituents in the tea may have an effect on blood clotting
• Some of the constituents of the tea may influence insulin. Diabetics who are insulin dependent need to closely watch their BGL
• If a patient has osteoporosis, he/she has to be careful as oxalic acid can interfere with calcium metabolism.

Research Studies:

Leonard, S. S., Keil, D., Mehlman, T., Proper, S., Shi, X., & Harris, G. K. (2006). Essiac tea: Scavenging of reactive oxygen species and effects on DNA damage. Journal of Ethnopharmacology, 103(2), 288–296. http://doi.org/10.1016/j.jep.2005.09.013

Abstract:

Essiac, a tea reportedly developed by the Ojibwa tribe of Canada and widely publicized as a homeopathic cancer treatment, is prepared from a mixture of four herbs Arctium lappa, Rumex acetosella, Ulmus rubra and Rheum officinale. Each of these herbs has been reported to possess antioxidant and anti-cancer activity. Essiac itself has also been reported to demonstrate anti-cancer activity in vitro, although its effects in vivo are still a matter of debate. We prepared an extract of Essiac tea from a concentration of 25 mg/mL and boiled it for 10 min. From this preparation we used concentrations of 5, 10, 25 and 50% to measure Essiac effects. In this study, we examined the effects of Essiac on free radical scavenging and DNA damage in a non-cellular system, as well as the effects Essiac on lipid peroxidation using the RAW 264.7 cell line. We observed, using electron spin resonance, that Essiac effectively scavenged hydroxyl, up to 84% reduction in radical signal at the 50% tea preparation concentration, and superoxide radicals, up to 82% reduction in radical signal also at the 50% tea preparation concentration, as well as prevented hydroxyl radical-induced DNA damage. In addition, Essiac inhibited hydroxyl radical-induced lipid peroxidation by up to 50% at the 50% tea preparation concentration. These data indicate that Essiac tea possesses potent antioxidant and DNA-protective activity, properties that are common to natural anti-cancer agents. This study may help to explain the mechanisms behind the reported anti-cancer effects of Essiac.

Ottenweller, J., Putt, K., Blumenthal, E. J., Dhawale, S., & Dhawale, S. W. (2004). Inhibition of prostate cancer-cell proliferation by Essiac. Journal of Alternative and Complementary Medicine (New York, N.Y.), 10(4), 687–691. http://doi.org/10.1089/acm.2004.10.687

Abstract:

OBJECTIVE: To assess the ability of Essiac tea extracts (Essiac Canada International, Ottawa, Canada) to modulate cancer cell proliferation and immune responsiveness. DESIGN: A noncancerous transformed cell line was compared to a cancerous cell line and spleen cells that had been isolated from mice to examine proliferation responses mediated by the addition of an Essiac preparation. RESULTS: We found in vitro evidence of decreased proliferation of both noncancerous transformed (CHO) and cancerous prostate cell line (LNCaP) when Essiac was present in the culture media. A dose response for inhibition was demonstrated by a linear regression performed on the data for both the CHO and LNCaP cells. The percent inhibition of the LNCaP cells was higher than the percent inhibition of the CHO cells suggesting that Essiac may have a more selective effect on cancer cells than transformed cells. In addition, the effects of Essiac were examined in an immune T-lymphocyte proliferation assay. At low doses of Essiac, augmentation of proliferation of these T cells was demonstrated, but at higher doses Essiac was inhibitory to T-cell proliferation. The same doses of Essiac that stimulated spleen cells were inhibitory for LNCaP cell proliferation. CONCLUSIONS: Essiac preparations may be able to inhibit tumor cell growth while enhancing immune response to antigenic stimulation. This may be especially valuable in immune-suppressed individuals.

Shark Cartilage

Shark cartilage is proclaimed as a famous anti-cancer agent. It has been used for over ten years but unfortunately its effectiveness couldn’t be established over time.

Shark cartilage is said to;

• Prevents the activity of enzymes called matrix mettaloproteinases that are responsible for part of the angiogenesis process
• Can inhibit tumour progression
• Prevents bFGF-induced angiogenesis
• Acts as a shield against reactive oxygen species
• Has anti-inflammatory and analgesic effects
• Reduced the size of the tumour and the number of metastases in lab studies.
Shark cartilage is best taken in powdered form or frozen in bottles. Capsules of shark cartilage should not be used.

Treatment of cancer requires the high concentration of 1-2 gram shark cartilage per day for each kilogram of body weight as stated in literature.

The shark cartilage product AE-941 (Neovastat®) is one of the most researched products. It was under evaluation in three pivotal clinical studies with two phase III clinical trials in patients with lung and renal carcinoma, and a phase II clinical trial in patients with multiple myeloma. The trails were put on hold.

The treatment should be done under supervision because of dosage and eventual side effects.

Side effects may be: nausea, vomiting, upset stomach, changes in taste, or constipation.

Serious side effects may be: weakness, unusual tiredness, dizziness, increased thirst/urination, shakiness, mental/mood changes (e.g. confusion, nervousness).

Research studies:

Patra, D., & Sandell, L. J. (2012). Antiangiogenic and anticancer molecules in cartilage. Expert Reviews in Molecular Medicine, 14(April), e10. http://doi.org/10.1017/erm.2012.3

Abstract:

Cartilage is one of the very few naturally occurring avascular tissues where lack of angiogenesis is the guiding principle for its structure and function. This has attracted investigators who have sought to understand the biochemical basis for its avascular nature, hypothesising that it could be used in designing therapies for treating cancer and related malignancies in humans through antiangiogenic applications. Cartilage encompasses primarily a specialised extracellular matrix synthesised by chondrocytes that is both complex and unique as a result of the myriad molecules of which it is composed. Of these components, a few such as thrombospondin-1, chondromodulin-1, the type XVIII-derived endostatin, SPARC (secreted protein acidic and rich in cysteine) and the type II collagen-derived N-terminal propeptide (PIIBNP) have demonstrated antiangiogenic or antitumour properties in vitro and in vivo preclinical trials that involve several complicated mechanisms that are not completely understood. Thrombospondin-1, endostatin and the shark-cartilage-derived Neovastat preparation have also been investigated in human clinical trials to treat several different kinds of cancers, where, despite the tremendous success seen in preclinical trials, these molecules are yet to show success as anticancer agents. This review summarises the current state-of-the-art antiangiogenic characterisation of these molecules, highlights their most promising aspects and evaluates the future of these molecules in antiangiogenic applications.

Melatonin

Melatonin made by the body plays a large role in the daily rhythms of sleeping and waking. Some recent studies have found that people who work night shifts may be at increased risk for cancer, which could be linked to melatonin levels in the body.

Our biological clock resides in the suprachiasmatic nucleus of our brain (SCN), which is part of the hypothalamus. Based on signals of light and darkness, our SCN tells our pineal gland when it’s time to secrete melatonin.

Light comes in through the eyes and travels up the optic nerves to the SCN, which is exquisitely sensitive to cycles of light and darkness. When we turn on the light at night, we send misinformation to our brain believing it is daytime. Our pineal glands immediately cease its production of melatonin.

It doesn’t matter if the light is on for an hour or just seconds, the effect is the same. The melatonin pump doesn’t turn on again.

The yellow, orange and red wavelengths don’t suppress melatonin production the way white and blue wavelengths do. In fact, the range of light that inhibits melatonin is fairly narrow — 460 to 480 nm. Switching over to a low wattage bulb with yellow, orange, or red light protects the melatonin production. Using a salt lamp illuminated by a 5-watt bulb in this color range is a great alternative.

The hormone melatonin has many health benefits. It not only ensures better sleep but also reduces stress and anxiety, migraines and fights against cancer.

Melatonin effect on cancer:

• Powerful antioxidant and free radical scavenger that helps combat inflammation
• Inhibits the proliferation of a wide range of cancer cell types
• Triggers cancer cell apoptosis
• Interferes with the new blood supply tumours require for their rapid growth (angiogenesis)
• Can boost efficacy and decrease the toxicity of cancer chemotherapy
• Reduces the side effects of chemotherapy
• Enables one to overcome the lack of appetite and weight loss (cachexia)
• Has a calming effect on several reproductive hormones, which may explain why it seems to protect against sex hormone-driven cancers, including ovarian, endometrial, breast, prostate and testicular cancers
• Melatonin also boosts your production of immune stimulating substances such as interleukin-2.

Research Studies:

Mills, E., Wu, P., Seely, D., & Guyatt, G. (2005). Melatonin in the treatment of cancer: a systematic review of randomized controlled trials and meta-analysis. Journal of Pineal Research, 39(4), 360–6. http://doi.org/10.1111/j.1600-079X.2005.00258.x

Abstract:

Most observational studies show an association between melatonin and cancer in humans. We conducted a systematic review of randomized controlled trials (RCTs) of melatonin in solid tumor cancer patients and its effect on survival at 1 yr. With the aid of an information specialist, we searched 10 electronic databases from inception to October 2004. We included trials using melatonin as either sole treatment or as adjunct treatment. Prespecified criteria guided our assessment of trial quality. We conducted a meta-analysis using a random effects model. We included 10 RCTs published between 1992 and 2003 and included 643 patients. All trials included solid tumor cancers. All trials were conducted at the same hospital network, and were unblinded. Melatonin reduced the risk of death at 1 yr (relative risk: 0.66, 95% confidence interval: 0.59-0.73, I2=0%, heterogeneity P<or=0.56). Effects were consistent across melatonin dose, and type of cancer. No severe adverse events were reported. The substantial reduction in risk of death, low adverse events reported and low costs related to this intervention suggest great potential for melatonin in treating cancer. Confirming the efficacy and safety of melatonin in cancer treatment will require completion of blinded, independently conducted RCTs.

Seely, D., Wu, P., Fritz, H., Kennedy, D. a, Tsui, T., Seely, A. J. E., & Mills, E. (2012). Melatonin as adjuvant cancer care with and without chemotherapy: a systematic review and meta-analysis of randomized trials. Integrative Cancer Therapies, 11(4), 293–303. http://doi.org/10.1177/1534735411425484

Abstract:

Melatonin (MLT) is known to possess potent antioxidant, antiproliferative, immune-modulating, and hormone-modulating properties. Clinical evidence suggests that MLT may have a possible role in the treatment of cancer. The authors systematically reviewed the effects of MLT in conjunction with chemotherapy, radiotherapy, supportive care, and palliative care on 1-year survival, complete response, partial response, stable disease, and chemotherapy-associated toxicities.

CONCLUSION: MLT may benefit cancer patients who are also receiving chemotherapy, radiotherapy, supportive therapy, or palliative therapy by improving survival and ameliorating the side effects of chemotherapy.

Ellagic Acid

Ellagic acid is not a stand-alone cancer treatment but a very important supplementary natural nutrient. Raspberries, strawberries and blueberries contain ellagitannins, which, upon human consumption, are broken down into ellagic acid.

Ellagic acid affects cancer cells as follows:

• Leads to apoptosis of breast, pancreas, prostate, esophagus, skin and colon cancer cells
• Protects the p53 gene that is important for cancer prevention
• Exhibits antioxidant properties
• Inhibits COX-2
• Simulates anti-angiogenic activity
• Reduces tumor cell growth
• Accelerates the production of enzymes from the glutathione.
In addition, ellagic acid has antibacterial properties, protects the liver and binds carcinogenic molecules.

It would probably be a mistake to take ellagic acid supplements without also consuming many natural, whole, raw foods that contain ellagic acid in order to get necessary enzymes and other synergistic nutrients.

Research studies:

Vanella, L., Di Giacomo, C., Acquaviva, R., Barbagallo, I., Cardile, V., Kim, D. H., … Sorrenti, V. (2013). Apoptotic markers in a prostate cancer cell line: Effect of ellagic acid. Oncology Reports, 30(6), 2804–2810. http://doi.org/10.3892/or.2013.2757

Abstract:

Ellagic acid (EA) inhibits cell growth and induces apoptosis in cultured cells; however, the precise molecular mechanism involved in EA-induced apoptosis in prostate cancer cells is unknown. The aim of the present study was to delineate possible apoptotic pathway(s) involved in the EA-mediated chemotherapeutic effects in the LNCaP human prostatic cancer cell line. EA produced anti-proliferative effects through inhibition of rapamycin (mTOR) activation and a reduction in intracellular levels of β-catenin. Moreover, we demonstrated that EA induced apoptosis via downregulation of the anti-apoptotic proteins, silent information regulator 1 (SIRT1), human antigen R (HuR) and heme oxygenase-1 (HO-1). EA modulated the expression of apoptosis-inducing factor (AIF) resulting in a significant increase in reactive oxygen species (ROS) levels and the activation of caspase-3. Finally, we demonstrated that EA reduced both transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) levels. EA treatment resulted in the increased expression of the tumor suppressor protein p21 and increased the percentage of apoptotic cells. In conclusion, the results suggest that EA treatment represents a new and highly effective strategy in reducing prostate cancer carcinogenesis.

Papaya leaf juice

According to published research in the Journal of Ethnopharmacology published in 2010, researchers from US and Japan discovered that enzymes found in papaya leaf have dramatic cancer fighting properties against a wide range of tumours including cervical cancer, breast cancer, liver cancer, lung cancer, and pancreatic cancer. According to the study, papaya leaves are not known to have toxic effects and their consumption goes without side effects.

Papaya leaf consists of over 50 active ingredients to kill fungi, worms, parasites and bacteria.
Also contains important nutrients that support the immune system, including vitamins A, C, and E.

The recipe is from Harold W. Tietze in his book “Papaya The Medicine Tree”

Wash and partly dry several medium-size papaya leaves. Cut them up like cabbage and place them in a saucepan with 2 quarts/ litres of water. Bring the water and leaves to the boil and simmer without a lid until the water is reduced by half.Strain the liquid and bottle in glass containers.

The concentrate will keep in the refrigerator for three to four days. If it becomes cloudy, it should be discarded.
The recommended dosage in the original recipe is 3 Tablespoons/ 50ml three times a day.The leaves have also been reported successful used when dried and ground.

Pawpaw twigs contain acetogenins - active compounds that modulate the production of ATP in mitochondria of specific cells - which affects the viability of specific cells and the growth of blood vessels that nourish them. A recent clinical study with over 100 participants showed that the pawpaw extract, containing a mixture of acetogenins, supports the body's normal cells during times of cellular stress.

Acetogenins are also being active against worms, some viruses, fungi, and many cancer cell lines. When compared with conventional chemotherapy agents, they have worked comparably in cell culture and animal studies, but at far lower concentrations and with almost no toxicity to host animals.

However, pawpaw should not be used with any kind of thyroid stimulators (for example herbal thyroid activator KC-X) or with CoQ10 (coenzyme Q10)

Research studies:

Nguyen, T. T. T., Shaw, P. N., Parat, M.-O., & Hewavitharana, A. K. (2013). Anticancer activity of Carica papaya: a review. Molecular Nutrition & Food Research, 57(1), 153–64. http://doi.org/10.1002/mnfr.201200388

Abstract:

Carica papaya is widely cultivated in tropical and subtropical countries and is used as food as well as traditional medicine to treat a range of diseases. Increasing anecdotal reports of its effects in cancer treatment and prevention, with many successful cases, have warranted that these pharmacological properties be scientifically validated. A bibliographic search was conducted using the key words "papaya", "anticancer", and "antitumor" along with cross-referencing. No clinical or animal cancer studies were identified and only seven in vitro cell-culture-based studies were reported; these indicate that C. papaya extracts may alter the growth of several types of cancer cell lines. However, many studies focused on specific compounds in papaya and reported bioactivity including anticancer effects. This review summarizes the results of extract-based or specific compound-based investigations and emphasizes the aspects that warrant future research to explore the bioactives in C. papaya for their anticancer activities.

Otsuki, N., Dang, N. H., Kumagai, E., Kondo, A., Iwata, S., & Morimoto, C. (2010). Aqueous extract of Carica papaya leaves exhibits anti-tumor activity and immunomodulatory effects. Journal of Ethnopharmacology, 127(3), 760–7. http://doi.org/10.1016/j.jep.2009.11.024

Abstract:

AIM OF THE STUDY: Various parts of Carica papaya Linn. (CP) have been traditionally used as ethnomedicine for a number of disorders, including cancer. There have been anecdotes of patients with advanced cancers achieving remission following consumption of tea extract made from CP leaves. However, the precise cellular mechanism of action of CP tea extracts remains unclear. The aim of the present study is to examine the effect of aqueous-extracted CP leaf fraction on the growth of various tumor cell lines and on the anti-tumor effect of human lymphocytes. In addition, we attempted to identify the functional molecular weight fraction in the CP leaf extract.

RESULTS: We observed significant growth inhibitory activity of the CP extract on tumor cell lines. In PBMC, the production of IL-2 and IL-4 was reduced following the addition of CP extract, whereas that of IL-12p40, IL-12p70, IFN-gamma and TNF-alpha was enhanced without growth inhibition. In addition, cytotoxicity of activated PBMC against K562 was enhanced by the addition of CP extract. Moreover, microarray analyses showed that the expression of 23 immunomodulatory genes, classified by gene ontology analysis, was enhanced by the addition of CP extract. In this regard, CCL2, CCL7, CCL8 and SERPINB2 were representative of these upregulated genes, and thus may serve as index markers of the immunomodulatory effects of CP extract. Finally, we identified the active components of CP extract, which inhibits tumor cell growth and stimulates anti-tumor effects, to be the fraction with M.W. less than 1000.

CONCLUSION: Since Carica papaya leaf extract can mediate a Th1 type shift in human immune system, our results suggest that the CP leaf extract may potentially provide the means for the treatment and prevention of selected human diseases such as cancer, various allergic disorders, and may also serve as immunoadjuvant for vaccine therapy.

 

Further studying but not required: 

Book: Cancer-Free by Bill Henderson

Book: Shattering the Cancer Myth by Katrina Ellis