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
