STOPPING METASTASES IS PARAMOUNT
Is it possible to stop cancer spreading?
We are told that 9 out of 10 people that die from cancer die from metastases...not the original primary tumour.
Most cancer victims choose chemotherapy.
Most cancer deaths (almost all) are due to metastases.
It follows that chemotherapy fails to stop cancer spreading in millions of cases!
Below I reveal a number of substances and approaches that can often halt cancer and even reverse it, even when all hope looks to be gone.
Cannabis compound stops spread of breast cancer:
Another great natural substance that can halt matastases is PECTIN...
Pectin induces apoptosis in human prostate cancer cells: correlation of apoptotic function with pectin structure
Extract from study:
Cancer therapy is aimed at either the primary tumor or metastatic cells. Because of the differences in the response of primary and metastatic cancers, most therapies do not address both cancer types. Pectin, a natural plant polysaccharide present in all higher plant cell walls, and thus in all fruits and vegetables and in most plant derived foods, is a compound that appears to be able to inhibit cancer metastasis and primary tumor growth in multiple types of cancer in animals. Although pectins were initially recognized as compounds capable of inhibiting metastatic lesions (Heitman et al. 1992; Platt and Raz 1992; Pienta et al. 1995; Nangia-Makker et al. 2002), more recently, pectins have been shown to reduce primary tumor growth (Nangia-Makker et al. 2002). It has been suggested that the inhibitory effects of pectin on metastatic lesions in the lung are mediated through their binding to galectin-3 (a galactoside-binding lectin). Galectins are specific carbohydrate-binding proteins present on the surface of cancer cells. Galectins facilitate cell–cell interactions by binding to galactose-containing molecules on neighboring cancer cells. In human colon, stomach and thyroid cancers, the amount of galectin increased with the progression of cancer. Blocking galectin-3 expression in highly malignant human breast, papillary, and tongue carcinoma cells led to reversion of the transformed phenotype and suppression of tumor growth in nude mice (Honjo et al. 2000, 2001). It has been proposed that the pH-modified CP blocks binding of galectins, and thus, inhibits tumor cell–cell interactions. The potential impact of blocking galectin action includes inhibition of the aggregation of cancer cells to each other and to normal cells, thus inhibiting metastatic lesions. However, LNCaP cells do not express galectin-3 (Ellerhorst et al. 1999,2002; Califice et al. 2004; our unpublished observations), suggesting that the apoptotic effects of pectins reported here are due to mechanisms not mediated through galectin-3.
The major goals of the present research were two-fold: (i) to identify pectins that are capable of inducing death of prostate cancer cells and (ii) to determine the structure of the pectin that is responsible for such biological effects. Initial experiments demonstrated that among the pectins tested, only FPP induced apoptosis. The pH-modified CP, PeS, is similar to the modified CP that has been shown to inhibit metastatic lesions and to induce apoptosis in multiple myeloma cells (Chauhan et al. 2005). Significantly, PeS did not induce appreciable apoptosis in prostate cancer cells, agreeing with published data showing no cytotoxic effects of pH-modified pectin on prostate cancer cells and xenografts (Pienta et al. 1995). Thus, the main thrust of the present research was to characterize the structure–function relationships of the apoptotic pectin FPP. Most of the published reports on the anticancer effects of pectin utilized pectins that were modified by alterations in pH in an effort to fragment pectin structure to facilitate biological effects in the systems under study. This procedure, in addition to fragmenting the pectin, may affect the structure of the pectin and thus its function. FPP was not produced by pH treatment, but rather was produced by heating CP. We therefore utilized several methods to correlate the biological function of FPP with its structure and compared FPP structure with that of PeS and CP, which were not apoptotic.
As a first step, the size and glycosyl residue composition and linkage of the different pectins were compared. Our results did not show any significant differences between the glycosyl residue composition or linkages of FPP compared with PeS and CP, indicating that differences in apoptotic activity among the three pectin preparations were not due to differences in the major types of pectin present. Also, there was no correlation in the size of the pectins and their apoptotic activity. As pectins consist of HG and RG, we hypothesized that one or more of these polysaccharides in FPP was responsible for its apoptotic effects. However, experiments testing the apoptotic effects of HG, RG-I, and RG-II, indicated that these individual structural components were not by themselves responsible for the apoptosis-inducing activity of FPP. We therefore conclude that the apoptosis-inducing activity of FPP is related to some structural constituent not detected by the above analyses.
To further understand the structure–function relationship of apoptotic pectin, FPP was specifically fragmented using endopolygalacturonase (EPG), which cleaves HG at contiguous nonesterified GalA residues. The cleavage of FPP with EPG did not have a major effect on its apoptotic activity. Thus, two methods were used to remove ester linkages from FPP prior to EPG treatment and thereby, make FPP more susceptible to EPG cleavage: chemical deesterification by mild base treatment and specific enzymatic hydrolysis of methyl esters by treatment with pectinmethylesterase (PME). Chemical deesterification of FPP resulted in significant loss of apoptosis suggesting that a base-sensitive structure, such as an ester linkage, is necessary for the apoptotic activity of FPP. Since specific cleavage of methyl esters by PME did not destroy FPP's apoptosis inducing activity, linkages other than methyl esters are required for apoptotic activity. Furthermore, PAGE analysis of intact and treated FPP showed that a polymeric/oligomeric FPP structure containing a base-sensitive linkage, and/or the specific base-sensitive linkage itself, is required for the apoptotic activity of FPP. Taken together the results suggest that an ester-based (or related) cross-link in pectin is important for the apoptosis-inducing activity of FPP.
The incubation of FPP with a nonspecific protease, with endo-α1,5-arabinase or with RNAse prior to cell treatment (data not shown), did not significantly affect FPP's apoptosis-inducing ability, suggesting that the apoptotic response is not due to the presence of proteins, α1,5-arabinan, or RNA within the pectin preparation. Significantly, we have been successful in generating the apoptosis-inducing capability in CP by heat treatment, a critical step in the production of FPP from the mother pectin. This supports our conclusion that a specific pectin structure and/or pectin-containing linkage is responsible for inducing apoptosis. The question of whether the heat treatment of CP causes a covalent or noncovalent modification of CP structure that leads to the apoptotic activity remains to be determined.
In conclusion, we provide the first evidence that specific structural characteristics of pectin are responsible for inducing apoptosis in cancer cells. Our results demonstrate that different extraction protocols may alter the structure of pectin and can lead to differences in pectin's apoptosis-inducing activity. Further experiments to identify the specific apoptotic structure in pectin will enable us to generate the smallest fragment that is capable of inducing apoptosis. A detailed understanding of structure–function relationships of such a fragment may lead to effective anti-cancer therapy. This is of particular therapeutic significance, as we have demonstrated that manipulating the structure of pectin results in a compound that is capable of inducing apoptosis in both androgen-responsive and androgen-independent prostate cancer cells. http://glycob.oxfordjournals.org/content/17/8/805.full
New Modified Citrus Pectin Slows Cancer Progression and Stops Cancer Cells in Their Tracks...
Study Shows New Modified Citrus Pectin Works as Well as Chemo Without Toxicity and Improves Quality of Life in Advanced Disease
Better Health Publishing report that many people with cancer could be helped by anew form of Modified Citrus Pectin (MCP) that may work as well as chemotherapy
in advanced disease stages; yet without the dangerous toxicity. These published
findings of new capabilities for MCP have the potential to revolutionize cancer
treatment. Previous research with MCP has shown it to be effective in slowing the progression, metastasis and angiogenesis of several types of cancer. Now with further improvement in the modification process, more of the effective substance can be utilized by the body. The first human study described below was done with patients with late stage, breast, prostate, colorectal, kidney, pleural or lung, cervix/uterine cancer, liver, pharynx, pancreatic, stomach, melanoma and bile duct cancers. This landmark clinical trial was published in the peer-reviewed journal Clinical Medicine: Oncology, where it showed a significant improvement of quality of life and stabilization of disease for patients with advanced solid tumors. The results of the landmark advanced tumor study clearly demonstrate MCP's enhanced capabilities. "This is a very important breakthrough destined to help a lot of people," said Dr. Isaac Eliaz, a prominent doctor of Integrative Medicine and MCP researcher. "MCP may have the benefits similar to chemotherapy in advanced cancers, but without the side effects. This study sheds additional light on the potential benefits of MCP in cancer prevention and treatment." A background report on the development of MCP in integrative cancer healthcare is available through Better Health Publishing at the following url: www.betterhealthpublishing.org/mcpreport MCP, a natural substance modified from the peel of citrus fruit has been used during the past decade in integrative cancer therapy to help keep aberrant cells from clustering and blocking the formation of blood vessel attachment. The absorption into the blood stream is based on the size and weight of its molecules. MCP molecules bind to receptors on cancerous cells, preventing these cells from attaching to healthy tissue and blocking the formation of blood vessels to feed the cancerous cells. Once this has occurred, the cancer cells starve and die or are eliminated by the immune system. In the past, the enzymatic modification process produced too much total breakdown of the pectin molecules when it tried to achieve the effective low molecular weight absorbable chains. The new MCP also goes through an enzymatic process that reduces the pectin's molecular size and modifies it to better control the amount of total breakdown of the citrus pectin. These new developments led to an improved MCP, lower in weight, which allows it to be more systemic, circulating through the blood stream and allowing the body to absorb more of the effective molecules. Treatment and Scientific Data of Study: The treatment in the advanced tumor and previous studies consisted of the oral intake of five grams of MCP three times a day. One cycle of therapy was defined as four weeks of treatment. Objectives were clinical benefit (pain, functional performance, weight change), safety, tumor response (RESIST criteria) and quality of life. The results proved very exciting. Forty-nine patients (between 36 and 82 years old) with various advanced solid tumors were enrolled. Twenty-nine patients were evaluated for clinical benefit after two cycles of treatment. All patients tolerated the therapy well without any adverse effects. The results also demonstrated that after two cycles of oral intake of MCP, 6/29, (20.7%) had an overall clinical benefit with a stabilization or improvement of life quality. On intent to treat basis 11/49 patients (22.5%) showed a stable disease after two cycles and 12.3% had a SD for more than 24 weeks. One patient with advanced and hormonal resistant prostate cancer had a 50% decrease in PSA with significant improvement in his quality of life. Most of the patients had improvements in their life quality as reflected in the Karnofsky scores. The MCP used in the advanced tumor study is now commercially available in the US. It's called PectaSol-C and distributed by EcoNugenics, Santa Rosa, CA. About Better Health Publishing: Better Health Publishing, founded by Isaac Eliaz, M.D. is a publishing house that focuses on the publication of key works promoting health and wellness. The staff at Better Health Publishing believes that a natural and efficacious lifestyle is the cornerstone of a return to healthy and sustainable society. The works published by BHP strive to promote this concept and disseminate to the public a healthier choice. For more information on Dr. Eliaz, log onto www.dreliaz.org. For a free report on MCP log onto www.betterhealthpublishing.org/mcpreport
The above Modified Citrus Pectin is a very exciting substance (that I personally used myself when fighting cancer) which, - according to the book below, - works on cancer cells and frustrates their objective to grow and spread. I'm sure the above results could be greatly enhanced by including an aggressive anti-cancer diet, along with other key measures to maximise results.Published on Apr 16, 2015
Stage 4 cancer healed:
This is a wonderful insight into how the body can rally and reverse cancer naturally, given the right approach. This approach is not suggested for every or any particular case of cancer, but is an insight into the fact that radical change of diet and lifestyle can seriously impact cancer, despite the fact that surgery and radiotherapy had depleted her immune system, and managed to spread the cancer massively in a very short space of time. This approach obviously requires expert instruction, along with a well structured protocol that you follow to the letter..
Nutritional Oncology Research Institute (NORI)
NORI has researched and developed a unique approach to cancer therapy that is very simple, effective, low-cost, nontoxic and can be implemented at home. It is based on targeting common metabolic abnormalities present in nearly all types of cancer cells.
A methionine restricted diet combined with a nontoxic chemotherapeutic cocktail is a unique and powerful approach to treating and managing malignancies.