BADEN BADEN CONGRESS OCT-31 to NOV-4-2019

 MEDEZINISH WOBE BADEN BADEN 2019

 KREBSKONGRESS

DEUTSCHE GESELLSCHAFT FUR ONKOLOGY

   (OCTOBER 31-NOVEMBER 4, 2019)

WITH THE COLLABORATION OF THE GERMAN SOCIETY OF ONCOLOGY.

This is an annual congress that attracts doctors from all over the world and where oncologists, medical doctors, and naturopaths meet in a friendly atmosphere. It is a very busy program with top lecturers from Germany, USA, Italy, Australia, Turkey, Austria with topics associated with cancer and other types of Integrative medicine. There are also several workshops in English of major interest. Many lectures are only in German language but also in English such as the ones on cancer.  Dr. Abdul Kadir Slocum from Istanbul Turkey present a topic on the Efficacy of Metabolically supported chemotherapy combined with Ketogenic Diet, Hyperthermia and Hyperbaric Oxygen Therapy for Stage IV Triple-Negative Breast Cancer. Prof. Dr. Wolfang Kostler of Vienna will present, “More cures for cancer by complementary oncology”. Dr. Young Ko from the USA will present, “New Information about anticancer technology”. Dr. Frederik Douwes is presenting, “New strategies for localized prostate cancer with thermo-hormone- therapy. In the last International Biobran Workshop 2016 held in Krakow, Poland an oncology nurse from England presented a very interesting lecture and a presentation of an impressive case from Dr. Slocum from his hospital in Istanbul. It should be of great interest to hear his lecture.

Figure 1: Dr. Frederic Douwes and Professor Serge Jurasunas at St. Georg Klinik in Munich, Germany

This year I was kindly invited by Dr. Frederik Douwes director of the St-George Klinic and President of the German Society of Oncology. In 2012 Dr. Douwes invited me to the 2nd International Congress on Complementary Oncology hold in Munich in June 2012 where I presented (Early on if not too soon ) a lecture on Molecular Markers and cancer.  (Available on SlideShare) However, since it now has been over 7 years since I have developed greater knowledge about the P53 tumor suppressor gene and other apoptotic players followed by clinical application with experience accumulated with a few hundred cases from my clinic.

My concern today is to present a lecture on ‘How to Target Breast Cancer through Apoptosis and the Immune System’ because it is a type of cancer that I have treated for more than several decades. We know how emotive this disease may become and how women may suffer from mutilation followed by chemotherapy/radiation. They may often have a disease recurrence after a period from 1 to 3 years for most and even longer for other patients.  Because of the limited time of my lecture 25minutes, I cannot offer a full presentation about breast cancer or about the molecular profile of the disease and how we can really approach breast cancer. More recently I fought with a case of Triple-Negative Breast Cancer with a nice 38-year-old woman, a mother of 3 children living in England that after having been subjected to a double mastectomy, followed by chemotherapy and radiation. She subsequently developed metastasis in her neck and ganglions. She came to my clinic in Portugal about 4 times and we tried our best to treat her. She had even gone, under my advice, to the St. George Klinic in Germany. She apparently had been improving from the treatment. She was very emotional and we know how this may have depressed the NK cells or even the P53 tumor suppressor gene and mutation.

 I spent considerable time helping her feel more confident, encouraging her to fight the disease. She was so thankful for my help. While she had apparently felt well after returning from the German clinic, one day she began to feel really bad from pain and sickness from her abdomen. She went into the hospital and was told that one of her kidney arteries was blocked and that she would be given blood-thinning tablets. Later on she was told that she may have also had a clot on her lung and needed to have emergency surgery to disperse it, but unfortunately she was made to wait too long in the ER before being called in and suddenly died from a pulmonary embolism. How could this be, since she was feeling well after returning from the German Clinic, the small tumor on her neck was noticeably reduced. This was a shocking situation and I believed that her regular conventional therapy not only was useless but contributed to her death.

Figure 2:  Case of Ellie My 39 Year-old English Patient with Triple Negative Breast Cancer with One of Her 2 Children Who Lost Their Mother

We can further say that the result of her molecular markers testing showed a very bad prognosis. A high level of mutated P53 protein, low activation of the P53 gene, a BcL2/Bax ratio of 0.06 (Very bad indeed) along with over-activated telomerase. What the test also showed was circulating cancer cells with an increased level of telomerase and probably CSCs.  However, her death could have been attributed to the consequences of the disease itself or her past chemotherapy! Could we have saved her without these problems?

This is the reason I decided to deliver this lecture in memory of this patient. I believe that women diagnosed with breast cancer and especially TNBC should think twice before having a double mastectomy and look immediately for complementary treatment. Also as mentioned P53 is mutated in 80 % of TNBC and according to a recent study by a team of researchers from Ireland restoring P53 mutation to normal function may be a new way of treating TNBC.  I am convinced that a double mastectomy is barbaric and not a solution as we have here one example among so many other cases.

COMPLEMENTARY BREAST CANCER THERAPIES

My lecture on breast cancer is based on the P53 tumor suppressor gene and P53 mutation as the main hallmark in cancer. P53 is not only associated with apoptosis but also with a number of other factors associated with cancer such as glycolysis and immune defense and seems to be the major key to cancer. What I am going to present is at the edge of Science and of Oncology, being the only way you can understand and treat cancer. If we look at the number of doctors and clinics, of books where each one offers the cure for cancer, we realize that for most it is without any serious basis of how to understand and treat cancer from a molecular standpoint. Do you have the necessary information about apoptotic tumor suppressor genes, inhibitors of apoptosis, angiogenic markers, transcription factors, inflammatory cytokines, etc.…involved with the disease? What about P53 mutation? That makes an overwhelming difference between a normal low activated P53 and low level of P53 protein compared to a high level of mutated P53 protein. How can you follow up on the disease and know if your therapy is really functioning? How can you find out about a risk of recurrence or an existing recurrence not yet diagnosed? If you do a molecular markers testing then you can know well in advance, which places us well in advance and far ahead of regular Oncologists that are totally unable to predict a recurrence.  The so-called regular hospital checkup for women with breast cancer recurrence is a totally false premise that does not inform the risk of recurrence ahead of time, but only after recurrence has already been activated.

MY ABSTRACT:

 1- Targeting Apoptosis and Immune function in Breast cancer.

Apoptosis should be the first step toward targeting in a comprehensive treatment. Cancer and disease progression are modulated by a number of tumor suppressor genes such as P53 Bax, P21 as well as anti-apoptotic genes such as BcL2 and Survivin. One of the most intriguing potential master regulators which directly control the transcription of genes involved in cancer growth, proliferation and metastasis is the P53 tumor suppressor gene, known as the guardian of our genome. Specifically, this is the gene that triggers apoptosis. P53 is also associated with the regulation of glycolysis pathways. Recently it has been shown that P53 inhibits the Warburg effect by reducing glycolysis and enhancing oxidative phosphorylation via upregulation of genes including Tigar and SC02  (Synthesis of cytochrome oxidase) as well as inhibiting the expression of glucose transporters GLUT 1, GLUT3 and GLUT 4.  SC02 increases mitochondrial respiration and Tigar inhibits glycolysis.  Most articles I have read on cancer and cellular respiration do not mention the role of P53 in modulating cellular respiration.

P53 may play an important role in the Tumor Microenvironment since some recent studies shown that P53 inactivation or mutation alters the immune landscape of the TME toward pro-tumor inflammation whereas P53 reactivation or restoration changes the milieu of TME to promote anti-tumor immunity.  It has been demonstrated that P53 activity potentially regulates host immune function and modulate the immunological landscape of the TME.

(Read about, “Tumor Suppressor P53 in Host Immune Response and the Tumor”, Online) 

P53 mutations are known to gain additional oncogenic functions and can exert additional tumor-promoting functions being able to upregulate a number of transcription factors involved in breast cancer metastasis including the NF-KB, Pten, Id4, E2F1, E-Cadherin, EGFR, TGF-B and Telomerase activity. Crosstalk takes place between P53 and the various other transcription factors. Cancer stem cells harbor P53 mutation and other characteristics like overactive Telomerase. This suggests that its activation is an early event in cancer progression.

Recent studies have shown that P53 is a regulator of Telomerase activity. Loss of function or mutation increases the activity of Telomerase in cancer cells that become very resistant. If more overactive than P53, cancer cells may turn into a cancer stem-cell-like state with an indeterminate lifespan length, not to say immortality. For instance, if telomerase activity is increasing, the normal P53 gene also dramatically increases its activity above telomerase, so it may be regulated so as not to become overactive.

Both P53 and Telomerase play a key role in tumor development, causing cancer cells to resemble a cancer stem-cell-like state.

(L.Ying Cao, Michael C, Berndt, John W Funder, Jun-Ping Liv. Molecular Interreaction between telomerase and tumor suppressor protein P53 in vitro. Oncogene 18, 6785-6794.1999)

P53 IS THE MASTER REGULATOR OF APOPTOSIS, OXIDATIVE PHOSPHORYLATION AGAINST GLYCOLYSIS, CONTROLS A MYRIAD OF TRANSCRIPTION FACTORS, INCLUDING TELOMERASE ACTIVITY, AND PLAYS A KEY ROLE IN THE IMMUNE DEFENSE OF THE TME. WHEN MUTATED GAINS AN ONCOGENIC FUNCTION WHICH IS THE MAIN CAUSE OF TUMOR GROWTH, INVASION, METASTASIS, etc.….

THEREFORE ACTIVATING OR RESTORING P53 IS THE MAJOR IMPORTANT STEP WHEN TREATING CANCER.

At the moment we are working with cancer patients looking to observe the result of P53 Telomerase testing to measure the ratio between the two, before and after the treatment. If the result showed activated telomerase over P53 then it indicates overactive telomerase with a significant risk to develop the cancer stem-cell-like state (mentioned above).

One Recent Example:

Our patient originally had a good ratio, however, in a case of cancer remission testing showed a very high risk of disease recurrence. At that moment the anti-tumor activity was above the pro-tumor activity.

P53 tumor suppressor gene: 15.188 units/ul of plasma. (Reference range =100 units). Indeed this gene showed a very active indication of the destruction of pre-cancerous, cancer cells.

Telomerase activity: 6,475 u/ul of plasma.

Ratio: P53/Telomerase = 1.2

The patient is still taking Biobran, Curcumin, Genistein and Vitamin D.  We believe that the gene is highly active also to keep down telomerase activity.

Another Example:

Test results showed a bad ratio in a case of breast cancer remission but with a risk of relapse, previously diagnosed at a Montreal hospital. 

P53 gene expression: N.D. (Not detectable)

P53 normal protein level: N.D.

Mutated protein: N.D.

Telomerase activity: 1.860 u/ul of plasma

While too low to have a ratio, yet testing had shown an increased population of cancer cells with active telomerase, with no detectable destruction. Here we may have CSCs since the P53 gene expression is not activated producing either protein. These cells have an extended lifespan, being very resistant to apoptosis and chemotherapy.  The non-activated P53 gene expression and highly activated Telomerase had shown that the patient had cancerous cells but probably not yet in a tumor formation as indicated by the low level of the Vesicular Endothelium Growth Factor (10 units/ul of plasma – Reference range: 50 units.) 

New work developed at the Salk Institute for Biological Studies had found that cancer cells resembling stem cells need not be part of the original tumor, but rather may emerge during later stages of tumor development facilitated by the loss of P53 which cannot be clearer, hence explaining the tumor resistance to anticancer treatment. In even more advanced case, to the contrary cancer cells begin to invade even quicker.

CANCER IN A STEM-CELL-LIKE STATE, ARE RESPONSIBLE FOR RELAPSE AND METASTASIS AND ARE IMPLICATED IN NEARLY ALL TYPES OF TUMORS

1- TUMOR GROWTH

2- DISSEMINATION

3- TUMOR RELAPSE

4-RESISTANCE TO APOPTOSIS

5-DISSEMINATION OF MORE METASTASIS AFTER EXCESSIVE CHEMOTHERAPY

 Such cells may be responsible for relapse and metastasis by giving rise to new tumors through a process of self-renewal capabilities and differentiation. CSCs are very resistant because they develop a DNA repair mechanism more rapidly than normal cells and thus repair quickly, even after being damaged by chemotherapy. They develop and display pro-survival factors that inhibit apoptosis by chemotherapeutic agents. They maintain an undifferentiated state to the contrary of other differentiated cancer cell subsets. They use MDR pumps to extrude amphiphilic chemotherapeutic agents such as Taxanes, Anthracyclines, etc...

Normal differentiated cancer cells can increase the volume of local tumors but lack the ability to self-renew and are sensitive to chemotherapy. However, CSCs are highly resistant and possess the ability to self-renew and differentiate, which enables them to originate metastases that chemotherapy cannot destroy.

However, these cells still have a capacity to differentiate, to become less aggressive through using some dietary agents like Genistein and Curcumin or reactivated P53 wild type or even to reverse P53 mutation to a normal P53 tumor suppressor gene.  Of course we are just at the beginning of this study taking place in our clinic with patients.  We need more cases prior to publication, but I am also planning an article for the next issue of the Townsend Letter, the magazine of Alternative Medicine (USA).

I have been a frequent contributor to the Townsend Letter for over 20 years, having published many articles on cancer. The Townsend Letter is read by medical doctors and naturopaths not only in North America but also in Europe, Australia, and South Africa, etc.  I often suggest that doctors subscribe to the Townsend Letter since it offers high-quality articles where we can learn from other like-minded colleagues.  For instance, the special August/September Cancer issue published each year should be read by all doctors concerned with cancer treatment.  This year (August 2019), my article is based on the following subject:

NK CELL-BASED IMMUNOTHERAPY IN THE TREATMENT OF CANCER TARGETING A NEW ARABINOXYLAN RICE COMPOUND (KNOWN IN EUROPE AS BIOBRAN). It should interest all the doctors working with cancer and the immune system.  If you cannot get the article, let me know and I will send you a copy of the article fully illustrated in color.

P53 MUTATION AND BREAST CANCER

P53 is the most mutated gene in our body and more than half of all cancers harbor P53 mutation, while 15-40% of breast cancer and 80% of Triple-Negative Breast Cancer exhibit P53 mutations that as explained above, help to drive cell migration, invasion, angiogenesis, while increasing resistance to chemotherapy with poor prognostic and overall limited survival. A normal P53 is associated with much less aggressive breast cancer better outcome and usually increased survival compared to patients with P53 mutation.  P53 testing should be included together with the classical diagnostic of Breast cancer.  Mutations in the P53 gene or increased expression of the mutant P53 protein have been described as prognostic factor for many types of cancer including Breast cancer. Mutant P53 is an early event in aggressive breast cancer since it operates independently of the oncogenic function. P53 controls the cell cycle and apoptosis by inhibiting BcL2 expression and activating Bax expression.  However BcL2 is upregulated in 70% of breast cancers, Bax is down-regulated in 1/3 of breast cancers increasing resistance to chemotherapy, and associated with the worst prognosis.  While BcL2 and Bax are regulated by the P53 gene as previously explained, activated telomerase can also be responsible for BCL2 upregulation and Bax downregulation.  Without these important factors obtained through blood testing, we can hardly have a complete diagnosis and be able to follow up on the results of the treatment.

COMPLEMENTARY BREAST CANCER THERAPIES

Today, targeting P53 has become a primary beneficial treatment for breast cancer by increasing its function, increasing the level of normal protein to promote apoptosis or by reversing a mutant P53 to a normal P53 tumor suppressor gene which is more difficult to achieve.  In the first case, increasing the expression of the P53 gene and of the level of normal protein increase death of cancer cells by apoptosis since also it may increase the expression of Bax, another tumor suppressor.  Secondly by reversing mutant P53 to normal function not only increases apoptosis but also decreases the oncogenic function and the aggressivity of the tumor.

-Important is the fact that WT P53 is a key negative regulator of aromatase and, hence estrogen production in the breast cancer microenvironment. Therefore this plays a key role in breast cancer treatment.

When I started over 12 years ago I had no experience of what can target mutant P53 protein so I began some research starting to experiment with some natural compounds that I felt could be effective. I quickly achieved success by reinvigorating P53 gene expression, by reversing mutant P53 protein to normal P53 WT protein, thus having reversed the oncogenic process and increasing apoptosis.

Here are some products I have used to reverse P53 mutation:

Fish peptide, Anoxe (a low molecular antioxidant compound made from modified vegetables and seeds), with strong anti-inflammatory effects and other pharmaceutical properties, Live Yeast Cells, Chlorella Growth Factor (CGF), and Selenium. I found that these compounds, especially fish peptides, a short chain of amino acids can contribute to reverse mutant P53 and activate p53 gene expression. Some proteins contained in Selenium, Live Yeast Cells, and CGF can inter-react with P53 genes in the body.

So far I have performed such testing on a few hundred cancer patients and have demonstrated that some selected natural compounds can really not only increase the expression of the P53 gene and protein level but also reverse the production of mutated or misfolded P53 protein using selected natural compounds.  Therefore when I treat cancer patients I am in position to determine the real situation, give a prognostic, choose the best treatment and have a follow up of the case with this new innovative testing, done regularly. This is what we call SCIENCE or scientific medicine.

The second important approach is the immune system. We especially focus on Natural Killer Cells which are seen as our first line of defense against cancer and are associated with breast cancer and breast cancer recurrence. Cancer patients have less activated NK cells compared to healthy individuals. From10% (often less) to 30% maximum while ranging from 60-75% and even more in healthy individuals. NK cell activity decreases even more during chemotherapy and radiotherapy with fewer defenses and less efficiency.  NK cells when activated can not only quickly kill cancer cells but also can activate other immune cells like macrophages, lymphocytes and contribute to mature dendritic cells. By producing cytokines that also inhibit angiogenesis, there are hundreds of papers that already have shown the important role of NK cells in the prevention and treatment of cancer, especially related to breast cancer.  You can read my new article published in the Cancer special issue of Townsend Letter, August/September 2019.

Figure 3: TGF-β  induces EMT to MTE-Associated with Migration and Invasion of Cancer Cells to the Lung Tissues and Bones.   

TWO MAIN NATURAL COMPOUNDS IN THE TREATMENT OF BREAST CANCER

The suggested therapies in my lecture include Genistein and Curcumin because both target most of the cancer mechanisms including multiple signaling pathways, apoptotic and anti-apoptotic genes, and the immune system. Curcumin and Genistein inhibit EGF and EGFR mediated signaling pathway that is overexpressed in breast cancer when P53 is mutated and involved in cancer progression. Curcumin and Genistein also block the excessive TGFB receptor signaling that induces epithelial to mesenchymal transition during invasion and metastasis process especially bone metastasis in breast cancer. TGFB also increases angiogenesis and blocks the immune system. More importantly, both can inhibit telomerase activity, therefore being the 2 most important dietary compounds together with Biobran to include in the treatment of breast cancer.

TARGETING TELOMERASE IS ONE IMPORTANT FACTOR IN THE TREATMENT OF CANCER SINCE IT ALSO CONTRIBUTES TO CHEMOTHERAPY EFFICACY BY DECREASING THE RESISTANCE OF CSCs

Other suggested supplementation to include in breast cancer treatment:

Artemisia

Melatonin

Indole-3-carbinol

Alpha-Lipoic Acid

Vitamin D3

Selenium

IMPORTANT FACTS ABOUT THE RELATIONSHIP BETWEEN VITAMIN D AND P53 IN CANCER CELLS

Vitamin D3 may have anticancer benefits especially by inducing cell cycle change and apoptosis, however, the effects of vitamin D are under the control of the VDR gene which encodes a nuclear receptor that mediates the effects of vitamin D3 and thus has potential tumor suppressor activity. Dysfunction or mutation of P53 may be one cause of VDR dysregulation and thus needs to be reactivated in order for patients in order to have benefit taking Vitamin D3 since we perfectly understand that just prescribing Vitamin D3 in a patient with P53 dysfunction is totally inefficient.

IMMUNO-ONCOLOGY

Biobran is a functional food made by a special process that utilizes modified rice bran cultivated on shitake mushroom which is quickly absorbed by the body, to activate immune cells. Arabinoxylan is the main ingredient of fiber but cannot be absorbed by the body because of a long chain of molecules and has no anticancer properties before being modified. After modification, the Arabinoxylan Rice Bran Compound is quickly absorbed in the body has a strong effect to increase immune cell activity, particularly NK cells.

Figure 4: Inhibiting Overactive Telomerase Improves Chemotherapy/ Radiation Treatment

I have been using Biobran for nearly 25 years in our cancer protocol and have been able to observe its superiority over other similar compounds. Having accumulated broad knowledge about RBAC having presented papers at a number of Biobran conferences, seminars, and workshops in Europe, I decided after being invited by the Daiwa Labs (The Japanese manufacturer of Biobran), to write my extensive experience, including a large introduction to immune defense, about Biobran itself, especially how it contributes to increasing chemotherapy effectiveness. Of course, the book also contains many other interesting chapters such about P53 and apoptosis, P53 and the immune system, about my experience with Live Blood Analysis, about what is cancer, about curcumin working in synergy with Biobran and of course a large chapter on clinical cases with proper documentation with references and illustrations

.

When treating cancer you have 3 main hallmarks to target in order to obtain positive results.

1- Apoptosis (P53, Bax, P21, etc...)

2- Angiogenesis. (VEGF, MPPs)

3- Immune defense (NK cells, dendritic cells, T-lymphocytes etc...)

Detoxification also has an important role, the same as targeting some transcription factors associated with inflammation and tumor growth. (Read my book, “Health and Disease Begin in the Colon”)

Nuclear Factor Kappa B. (NF-KB)

Cyclooxygenase 2 (COX2)

Cox2 expression was increased by 40-60% in breast cancer associated with the induction of angiogenic factors and inhibition of the immune system. It also increased the progression of estrogen-dependent breast cancer by autocrine and paracrine mechanisms or by indirect upregulation of aromatase activity.

In our protocol of breast cancer besides RBAC, we use a variety of dietary compounds such as Curcumin and Genistein that not only target apoptosis but most of the mechanisms of cancer as I will show in my lecture.  It includes apoptotic players, transcription factors such the NFKB, TGFB, and even Telomerase activity.

In fact, Genistein has been found to potentiate the antitumor activity of chemotherapeutic agents through regulation of NF-KB since some chemotherapeutic agents such as cisplatin, gemcitabine, and docetaxel induce the activation of NF-KB in cancer cells and may be responsible for drug resistance in cancer cells.  One other interesting factor is that Genistein reduces COX-2 activity which as explained is overactive in breast cancer with anti-apoptotic effects and inducing angiogenesis.  Genistein down-regulates the expression of MMP-9, MMP-2 and especially TGFB up-regulation of which was already explained associates with EMT to MET, especially in the dissemination of bone metastasis in breast cancer.

Genistein causes a reversion of the Epithelial-Mesenchymal Transition (EMT) phenotype by increasing levels of E-cadherin in membrane protein that is associated with increased cell-cell adhesion and thus reduced the invasive potential of metastasis.

P53 is a negative regulator of aromatase and, hence the production of estrogen in breast cancer microenvironment so again it can be implicated in breast cancer treatment. Slide 35 of my lecture shows how genistein and curcumin target the mechanisms of breast cancer. 

RBAC, Curcumin, and Genistein work in synergy with each other

but also with chemotherapy increasing its effectiveness with

better QOL as I fully explain in my book. As seen in one of my slides we considerably eliminate bone metastasis after 3 months of treatment in a case of breast cancer recurrence and getting worse with more metastasis dissemination after chemotherapy. Of course in case of overexpression of VEGF that stimulates blood vascularization such as in the case of a large breast tumor we use a special compound call C-Statin which is a naturally occurring plant extracted from field bindweed with strong anti-angiogenic properties. Before we use for nearly 20 years the Liquide cartilage extract in a frozen vial. (Too difficult now to obtain in Europe).  This combination therapy has demonstrated efficacy in treating breast cancer including tumor regression, diminution or total elimination of bone metastasis as I demonstrate with clinical case in my new book.

ADDITIONALLY:

For doctors looking to learn more about Naturopathic Medicine, Diet, Nutrition, P53,  colon care, the microbiome, detox program the value of food, Iridology, I invite you to read my book. It is fully illustrated with over 100 figures in color:

“Health and Disease Begin in the Colon”. (Available on Amazon)

My new upcoming book:

“Cancer Treatment Breakthrough. Immuno-Oncology Using Rice Bran Arabinoxylan Compound”. 

Soon to be published in the US and EU. It is a must for the doctor involved in the treatment of cancer. Will make the announcement on my blog. The book is published by Daiwa Laboratory Japan who manufactures Biobran|MGN3 (or Rice Bran Arabinoxylan).

Please view the presentation of my workshop on Immunology and Rice Bran Arabinoxylan Compound that I had planned to present at the Medizinische Woche Kresbskongress, but for some reason was deleted. Now I have the whole presentation available on SlideShare with several other lectures delivered over the past years.

Title: “New Modern Way to Approach Cancer using a Rice Bran Arabinoxylan Compound and Other Compounds in the Treatment of Cancer.”

www.slideshare.net/sheldonstein

For more information and to receive notification  about the release date of my new book book and how it can be obtained, I can be contacted directly through my email:

Sergejurasunas@gmail.com