Transcript Slide 1

CANCER – A Better Approach
By Steve Hines, N.D. N.E.
Co-Founder with Dr. Elio Rivera, M.D. of
WHAT IS CANCER?
• CANCER OCCURS WHEN THE NORMAL LIFE SPAN OR
THE LIFE & DEATH CYCLE OF CELLS IS DISRUPTED.
– Example: The life span for skin cells is 30 days. Toward the
end of its life, the current cell begins the process of
replication. When replication is complete, the old cell
should die and the new cell should take its place. But if
the old cell doesn’t die on time and both cells continue to
live, they will divide again in 30 days. This is the
beginning of a tumor.
WHAT CAUSES CANCER?
• Some Contributing Factors:
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Toxins
Genetics
Hormones or Hormone Mimicking Compounds
Nutritional Deficiencies
Infections
Hypoxia
Hyper-coagulation
Genetically Engineered Foods
Bad Dentistry
• My observations have shown Chronic Inflammation to be
the greatest promoter, although the inflammation is usually
the result of one or more of the above!
HOW IS IT DIAGNOSED?
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Palpation, Physical exam
Biopsies (Do they spread cancer?)
Cancer markers (blood test)
Scans
HOW IS IT TREATED?
• CONVENTIONAL TREATMENTS:
– Chemotherapy
– Biological Response Modifiers
– Anti-VEGf Therapies
– Hormonal Blockade
– Surgery
– Radiation
CHEMOTHERAPY:
Standard vs. Conventional
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5-Fu (inhibition of thymidylate synthase)
Adriamycin (intercalating DNA)
Bleomycin (DNA cleavage)
Cisplatin (alkylating agent): Damages all
cells!
Xeloda (inhibits DNA synthesis)
Cyclophosphamide (nitrogen mustard
alkylating agent)
HOW EFFECTIVE IS CHEMOTHERAPY?
• Study published in the journal Clinical
Oncology in December 2004, produced
astounding results:
– For all cancers chemotherapy has an average 5year survival success rate of just over 2 percent!
(See Table, next)
CHEMOTHERAPY
Natural Alternatives:
 I.V. Vitamin C (Cytotoxic oxidant at high
concentration)
 Mistletoe (Tyrosine Kinase activity)
 Artesunate (converts iron into intracellular free
radical)
 Amygdalin/B-17 (Caspase 3 and 9 activity)
 Pacific Yew tree extract (Tubulin disrupter)
 Camptotheca acuminatea (Cytotoxic)
 Periwinkle (tubulin disruption) Vincristine origin
 I2RA Intracellular redox recycling agent
(proprietary)
BIOLOGICAL RESPONSE MODIFIERS
• Biological response modifiers (BRMs):
– Substances that stimulate the body's response to
infection and disease. The body naturally
produces small amounts of these substances.
Scientists can produce some of them in the
laboratory in large amounts for use in treating
cancer. Interferon, interleukin-2 (IL-2), and several
types of colony- stimulating factors (CSF, GM-CSF,
G-CSF) are currently available with many more
being developed.
• Most Botanical extracts are BRMs by nature!
ANTI -VEGf THERAPIES
• These drugs inhibit the formation of blood
vessels to cancer cells.
– Conventional agents:
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Avastin (angiogenesis inhibitor)
Thalidomide (angiogenesis inhibitor)
Revlimid (angiogenesis inhibitor)
Sorafenib (angiogenesis inhibitor)
Sutent (epidermal growth factor inhibitor)
REPORT: Avastin And Taxol For Breast Cancer
March 23, 2006, 7:25 AM CT
• Avastin, an anti-angiogenesis drug is now showing
promise in the treatment of patients with metastatic
breast cancer. A new research led by Dr Robin Zon, of
Michiana Hematology-Oncology, PC in South Bend,
Indiana has shown that combining Avastin with Taxol
improves outcome in patients with metastatic breast
cancer. The study has shown that a combination of
Avastin and Taxol is more effective in prevention of
progression of breast cancer compared to using Taxol
alone.
Report (cont)
• Avastin is an anti-angiogenesis drug that works by blocking
the formation of new blood vessels and growing cancer cells.
Some claim that the combination of chemotherapy and
Avastin works better by facilitating chemotherapy delivery to
the cancer cells.
• This new research studied effectiveness of Avastin in
combination with Taxol. The study enrolled a total of 722
patients with advanced breast cancer. The study found that
combination of Avastin and Taxol was capable of keeping the
cancer stable for a period of 11.4 months in women who
received the drug combo compared to 6.11 months in
patients who had only been given Taxol.
• Researchers say that this presents yet another option for
patients with advanced breast cancer. "These results are good
news for people with breast cancer," said Zon who presented
the results of the trial sponsored by the U.S. National Cancer
Institute at the 5th European Breast Cancer Conference in
Nice, France.
ALTERNATIVE/NATURAL AGENTS
• Increasing oxygen to the cells of the body
• Vitamin D3 (angiogenesis inhibitor)
• Bromelain (anti-coagulant/antiinflammation)
• Lumbrokinase (anti-coagulant)
ALTERNATIVE/NATURAL AGENTS
• Turmeric (anti-coagulant/anti-inflammatory)
• Genestein (anti-angiogenisis, blocks type 1 &
2 estrogen receptors.
• Access copper/zinc ratios/repair imbalance
• Hyper Cellular Respiration Therapy
• Treat infections
• Diet
DIET
 Some common components of the Oriental diet also act as
mild Angiogenesis Inhibitors. In particular, the following
food items contain significant inhibitors and have been
suggested as part of a healthy diet for this and other
benefits as well:
 Soy products such as tofu and tempeh both contain genistein an
inhibitor of angiogenesis (AGI).
 Agaricus Blazei mushrooms with AGI effects.
 Products such as Ambrotose, a proprietary formula derived from
Aloe Vera, have shown to enhance natural immunity as well as AGI
properties. This product is distributed by the Manna Tech
Corporation. No cancer patient should be without this product!
DIET (cont)
– Reishi Mushrooms/Trametes Versicolor/Maitake and
Phellinus Linteus all have AGI as well as immune
modulating properties.
– Green Tea extract contains Catechins.
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Agi activity
Immune modulating,
Anti-Carcinogenic
Apoptosis Inducing
Numerous other properties.
– Resveratrol found in Japanese Knotweed and Red wine
extract has AGI as well as P53 suppressor gene rescue
properties. The p53 gene is almost always mutated in
cancer. Resveratrol aids in normalizing this gene!
HORMONAL THERAPY
These drugs either block or alter the binding
of hormones to their respective receptors or
alter hormones from being converted to
various metabolites.
Conventional agents:
Tamoxifen (anti-estrogen)
Evista (selective estrogen receptor modulator)
Femara (aromatase inhibitor)
Arimidex (aromatase inhibitor)
*Problems: Most of these agents lose effectiveness in 3 months !
ALTERNATIVE/NATURAL AGENTS
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Genestein (isoflavones, phytoestrogens)
IC-3 (aromatase inhibitor)
Dim (aromatase inhibitor)
Red Clover (Angiogenisis) (anti-estrogen)
Scutellaria Baicalensis (induces apoptosis)
Red root (increases T-cell acivity, anti-estrogen)
Iodine (alters disposition of homones)
*Benefits: Most of these botanicals work synergistically with
each other and with pharmaceuticals and inhibit resistance!
ALTERNATIVE THERAPIES & STRATEGIC
PLANNING
• Know your enemy! Essential lab tests can help plan
your cancer battle plan!
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The Greek test (chemo sensitivity test)
Copper/Zinc Cerruloplasmin
Ferritin, Serum iron, Total Iron Binding Capacity
Vascular Endothelial Growth Factor (VEGf)
C-reactive Protein
Fibrinogen
D-Dimer
Cox-2
CBC
ALTERNATIVE THERAPIES
• Detoxification
– Far infrared Sauna
– Hyperbaric Oxygen
– Colonics/Coffee Enemas
– BEMER (pulsed electromagnet field therapy)
– Gallbladder/Liver Flushes
– Natural Sunlight Exposure
– Ozone Saunas
– Calcium D-Glucarate
ALTERNATIVE THERAPIES
• Toxicity and Infections
– Gi-02 panel (Diagnostechs clinical laboratories)
– Root Canals, Mercury fillings, Cavatations
– Heavy metals, Mercury, Lead, Cadmium, Arsenic,
Iron!
ALTERNATIVE THERAPIES
• Stress Reduction and Management
– Heart math program
– Moderate exercise
– Prayer
SCIENCE NEWS
• Study Of Hypoxia And New Gene Reveals EarlyStage Action Of P53 Tumor Suppressor:
– ScienceDaily (Jan. 17, 2005) - Philadelphia, PA –
Researchers have known for a decade that the p53 tumor
suppressor gene is important for killing cells as they
proliferate under low-oxygen conditions inside tumors. As
tumors grow they outstrip their oxygen supply. If a cell has
a normal p53 gene, the p53 protein will eliminate
cancerous cells, keeping tumor growth at bay. Under
conditions of stress to the cell – such as radiation or
chemotherapy and hypoxia – p53 normally eliminates
tumors.
SCIENCE NEWS
• Study (cont)
– Hypoxia, however, induces p53 to mutate: The less oxygen, the more
mutations in the p53 gene, so cancer cells are not killed; instead, they
proliferate. A team led by Wafik El-Deiry, MD, PhD, Associate
Professor, Departments of Medicine, Genetics, and Pharmacology with
the Abramson Cancer Center of the University of Pennsylvania,
discovered a gene related to p53 called Bnip3L that can also cause cell
death. The gene is turned on by p53 and a second transcription factor
called hypoxia inducible factor, or HIF. The team silenced Bnip3L in
cells with normal p53 and exposed cells to low oxygen conditions. In
cell culture and in an animal model with implanted tumor cells, the
researchers showed that tumors with silenced Bnip3L grew more
aggressively in low oxygen conditions than cells and tumors with intact
Bnip3L. El-Deiry and first author Peiwen Fei, MD, PhD, a post-doctoral
fellow, report their findings in the December issue of Cancer Cell.
SCIENCE NEWS
• Study (cont)
– "From this, we predict in humans that another reason for tumor
growth is the silencing of Bnip3L," says El-Deiry. "We think one of the
ways that p53 suppresses tumors at their earliest stages is by turning
on Bnip3L, and that's new. There is no information at present about
how p53 works in the earliest stages of tumor growth, especially as
the growth begins to outstrip the supply of nutrients and oxygen."
– Understanding how cells die after they are starved for oxygen is
important for fighting cancer as well as other diseases. "Down the
road we would like to find strategies to turn Bnip3L back on to restore
the ability to die under hypoxia now that we know how it happens in
the first place," says El-Deiry.
This work was funded by the Howard Hughes Medical Institute and by
grants from the National Institutes of Health.
DIFFERENT TYPES OF CHEMOTHERAPY
DRUGS
• Chemotherapy drugs can be divided into several groups based
on factors such as how they work, their chemical structure,
and their relationship to another drug. Some chemotherapy
drugs are grouped together because they were derived from
the same plant. Because some drugs act in more than one
way, they may belong to more than one group. Knowing how
the drug works is important in predicting side effects. This
helps oncologists decide which drugs are likely to work well
together. If more than one drug will be used, this information
also helps them plan exactly when each of the drugs should
be given (in which order and how often).
DIFFERENT TYPES OF CHEMOTHERAPY
DRUGS
• ALKYLATING AGENTS
– Alkylating agents directly damage DNA to prevent the cancer cell
from reproducing. As a class of drugs, these agents are not phasespecific; in other words, they work in all phases of the cell cycle.
Alkylating agents are used to treat many different cancers, including
acute and chronic leukemia, lymphoma, Hodgkin disease, multiple
myeloma, sarcoma, as well as cancers of the lung, breast, and ovary.
– Because these drugs damage DNA, they can cause long-term damage
to the bone marrow. In a few rare cases, this can eventually lead to
acute leukemia. The risk of leukemia from alkylating agents is "dosedependent," meaning that the risk is small with lower doses, but
goes up as the total amount of drug used gets higher. The risk of
leukemia after alkylating agents is highest 5 to 10 years after
treatment.
DIFFERENT TYPES OF CHEMOTHERAPY
DRUGS
• Many different types of ALKYLATING AGENTS :
– Nitrogen Mustards:
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Mechlorethamine (Nitrogen Mustard)
Chlorambucil
Cyclophosphamide (Cytoxan®)
Ifosfamide Melphalan
– Nitrosoureas:
• Streptozocin
• Carmustine (BCNU)
• Lomustine
– Alkyl Sulfonates:
• Busulfan
DIFFERENT TYPES OF CHEMOTHERAPY
DRUGS
• Types of ALKYLATING AGENTS (cont) :
– Triazines:
• Dacarbazine (DTIC)
• Temozolomide (Temodar®)
– Ethylenimines:
• Thiotepa
• Altretamine (Hexamethylmelamine)
*The platinum drugs (cisplatin, carboplatin, and oxalaplatin) are sometimes
grouped with alkylating agents because they kill cells in a similar way. These
drugs are less likely than the alkylating agents to cause leukemia.
CHEMOTHERAPY DRUGS (cont)
• ANTIMETABOLITES
– Interfere with DNA and RNA growth by
substituting for the normal building blocks of
RNA and DNA.
– These agents damage cells during the S phase.
– They are commonly used to treat leukemias,
tumors of the breast, ovary, and the intestinal
tract, as well as other cancers.
CHEMOTHERAPY DRUGS (cont)
• Examples of ANTIMETABOLITES:
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5-Fluorouracil (5-FU)
Capecitabine (Xeloda®)
6-mercaptopurine (6-MP)
Methotrexate
Gemcitabine (Gemzar®)
Cytarabine (Ara-C®)
Fludarabine
Pemetrexed (Alimta®)
CHEMOTHERAPY DRUGS (cont)
• ANTI-TUMOR ANTIBIOTICICS:
– Anthracyclines
• Interfere with enzymes involved in DNA replication.
• Agents work in all phases of the cell cycle, so are widely used for
a variety of cancers.
• Major consideration: Can permanently damage the heart if given
in high doses. For this reason, lifetime dose limits are often
placed on these drugs.
– Examples of Anthracyclines:
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Daunorubicin
Doxorubicin (Adriamycin®)
Epirubicin
Idarubicin
CHEMOTHERAPY DRUGS (cont)
• Other ANTI-TUMOR ANTIBIOTICICS:
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Actinomycin-D
Bleomycin
Mitomycin-C
Mitoxantrone:
• Anti-tumor antibiotic similar to Doxorubicin in many ways,
including the potential for damaging the heart.
• This drug also acts as a Topoisomerase II inhibitor and can lead to
treatment-related leukemia.
• Mitoxantrone is used to treat prostate cancer, breast cancer,
lymphoma, and leukemia.
CHEMOTHERAPY DRUGS (cont)
• TOPOISOMERASE INHIBITORS:
– These drugs interfere with enzymes called Topoisomerases, which help
separate the strands of DNA so they can be copied.
– Used to treat certain leukemias, as well as lung, ovarian, gastrointestinal,
and other cancers.
• Examples of Topoisomerase I Inhibitors:
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Topotecan
Irinotecan (CPT-11)
Etoposide (VP-16)
Teniposide
Mitoxantrone also inhibits topoisomerase II
• Treatment with topoisomerase II inhibitors increases the risk of a second
cancer -- acute Myelogenous Leukemia. Secondary leukemia can be seen
as early as 2-3 years after the drug is given.
CHEMOTHERAPY DRUGS (cont)
• MITOTIC INHIBITORS:
– Often plant alkaloids and other compounds derived from natural
products.
– Can stop mitosis or inhibit enzymes from making proteins needed for
cell reproduction.
– Work during the M phase of the cell cycle, but can damage cells in all
phases.
– Used to treat many different types of cancer including breast, lung,
myelomas, lymphomas, and leukemias.
– These drugs are enzymes, and the proteosome inhibitor Bortezomib
(Velcade®), known for their potential to cause peripheral nerve
damage, which can be a dose-limiting side effect.
CHEMOTHERAPY DRUGS (cont)
• Examples of MITOTIC INHIBITORS:
– The Taxanes:
• Paclitaxel (Taxol®)
• Docetaxel (Taxotere®)
– Epothilones:
• Ixabepilone (Ixempra®)
– The Vinca Alkaloids:
• Vinblastine (Velban®)
• Vincristine (Oncovin®)
• Vinorelbine (Navelbine®)
– Estramustine (Emcyt®)
CHEMOTHERAPY DRUGS (cont)
• CORTICOSTEROIDS:
– Steroids are natural hormones and hormone-like drugs that are useful in
treating some types of cancer (lymphoma, leukemias, and multiple
myeloma), as well as other illnesses.
– When these drugs are used to kill cancer cells or slow their growth, they are
considered chemotherapy drugs.
– Corticosteroids are commonly used as anti-emetics to help prevent nausea
and vomiting caused by chemotherapy.
– Also used before chemotherapy to help prevent severe allergic reactions
(hypersensitivity reactions).
– When a corticosteroid is used to prevent vomiting or allergic reactions, it is
not considered chemotherapy.
– Examples include
• Prednisone
• Methylprednisolone (Solumedrol®)
• Dexamethasone (Decadron®)
CHEMOTHERAPY DRUGS (cont)
MISCELLANEOUS CHEMOTHERAPY DRUGS:
Some chemotherapy drugs act in slightly
different ways and do not fit well into any of the
other categories.
Examples include drugs such as
Lasparaginase.
OTHER TYPES OF CANCER DRUGS
• Other drugs and biological treatments are used to treat
cancer, but are not usually considered "chemotherapy."
• While chemotherapy drugs take advantage of the fact that
cancer cells divide rapidly, these other drugs target different
properties that set cancer cells apart from normal cells.
• They often have less serious side effects than those
commonly caused by chemotherapy drugs because they are
targeted to work mainly on cancer cells, not normal, healthy
cells. Many are used along with chemotherapy.
OTHER TYPES OF CANCER DRUGS (cont)
• TARGETED THERAPIES:
– As researchers have come to learn more about the inner
workings of cancer cells, they have begun to create new
drugs that attack cancer cells more specifically than
traditional chemotherapy drugs can.
– Most attack cells with mutant versions of certain genes,
or cells that express too many copies of a particular gene.
– These drugs can be used as part of primary treatment or
after treatment to maintain remission or decrease the
chance of recurrence.
CHEMOTHERAPY DRUGS (cont)
• TARGETED THERAPIES (cont):
– Only a handful of these drugs are available at this time.
– Examples include:
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Imatinib (Gleevec®)
Gefitinib (Iressa®)
Erlotinib (Tarceva®)
Sunitinib (Sutent®)
Bortezomib (Velcade®)
– Targeted therapies are a huge research focus and there
will likely many more developed in the future.
CHEMOTHERAPY DRUGS (cont)
• DIFFERENTIATING AGENTS:
– Drugs that act on the cancer cells to make them
mature into normal cells.
– Examples include:
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Retinoids
Tretinoin (ATRA or Atralin®)
Bexarotene (Targretin®)
Arsenic trioxide (Arsenox®)
HORMONE THERAPY
• Drugs in this category are sex hormones, or
hormone-like drugs, that alter the action or
production of female or male hormones. They are
used to slow the growth of breast, prostate, and
endometrial (uterine) cancers, which normally grow
in response to natural hormones in the body.
• These cancer treatment hormones do not work in
the same ways as standard chemotherapy drugs,
but rather by preventing the cancer cell from using
the hormone it needs to grow, or by preventing the
body from making the hormones.
HORMONE THERAPY(cont)
• EXAMPLES include:
– Anti-estrogens
• Fulvestrant (Faslodex®)
• Tamoxifen
• Toremifene (Fareston®)
– Aromatase Inhibitors
• Anastrozole (Arimidex®)
• Exemestane (Aromasin®)
• Letrozole (Femara®)
– Progestins
• Egestrol Acetate (Megace®)
HORMONE THERAPY(cont)
• Examples (cont):
– Estrogens
– Anti-Androgens
• Bicalutamide (Casodex®)
• Flutamide (Eulexin®)
• Nilutamde (Nilandron®)
– LHRH Agonists
• Leuprolide (Lupron®)
• Goserelin (Zoladex®)
IMMUNOTHERAPY
 Drugs that are given to people with cancer to
stimulate their natural immune systems to more
effectively recognize and attack cancer cells.
 Offer a unique method of treatment
 Often considered to be separate from
chemotherapy.
 Compared to other forms of cancer treatments,
(Surgery, Radiation Therapy, or Chemotherapy),
Immunotherapy is still relatively new.
IMMUNOTHERAPY
• Active & Passive Types of Immunotherapy:
– Active immunotherapies stimulate the body's
own immune system to fight the disease.
– Passive immunotherapies do not rely on the
body to attack the disease; instead, they use
immune system components (such as antibodies)
created outside of the body.
IMMUNOTHERAPY
• Other Types of Immunotherapies include:
– Monoclonal Antibody Therapy (Passive
Immunotherapies)
• Rituximab (Rituxan®)
• Alemtuzumab (Campath®)
– Non-specific Immunotherapies and Adjuvants (other
substances or cells that boost the immune response)
• BCG
• Interleukin-2 (IL-2)
• Interferon-alpha
IMMUNOTHERAPY
• Types of Immunotherapies (cont):
– Immunomodulating drugs
• Thalidomide
• Lenalidomide (Revlimid®)
– Cancer Vaccines (active specific
immunotherapies)
• Although several vaccines are being studied, as of
early 2009 there are no FDA-approved vaccines to
treat cancer.