CANCER TREATMENT PROTOCOLPlease read this before continuing on: |
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Every
cancer is different, and there are new tests (immuno-histochemistry)
available that look for specific mutations in the individual cancer cell in
order to help determine the best conventional and alternative therapies to
use. Whole-body
cytotoxic chemotherapy drugs are widely used in an attempt to kill the
metastasized tumor cells. However, conventional oncologists are failing to
incorporate newly published findings into their chemotherapy regimens that
could make chemotherapy more effective. Chemotherapy destroys immune
function, thereby condemning the cancer patient to the likelihood of a
recurrence of tumor metastasis, along with life-threatening infections. If
the immune system is unable to recognize and destroy metastasized cancer
cells, then the chances of achieving a permanent remission are remote. In
the 30 years that cancer chemotherapy has been used, it has proved effective
for relatively few cancers. The cancers that chemotherapy has been shown to
benefit include testicular cancer, choriocarcinoma, Hodgkin's disease,
leukemia and lymphoma. For the majority of cancers, however, chemotherapy has
been a failure. The Life Extension Foundation has identified methods of
making chemotherapy more toxic to cancer cells and less toxic to healthy cells. Please refer
to the Cancer Chemotherapy protocol for suggestions about making chemotherapy
more effective and how to protect healthy cells against injury and death from
highly toxic chemotherapy drugs. When
cancer is first diagnosed, the primary tumor often is too large for the
Foundation's Cancer Treatment Protocols to be effective by themselves. In
these cases, conventional cancer therapy (surgery and/or radiation) often is necessary to eradicate the primary tumor.
However, surgery and radiation place tremendous stress on the body that
severely weakens immune function and can put the body into a catabolic (wasting) state that leads to noticeable
weight loss. The Foundation's Cancer Treatment Protocol provides nutritional
and hormonal therapies that are needed to mitigate the damaging effects of
surgery/radiation therapy. Conventional cancer doctors seldom include any of
the nutritional support that is so desperately needed by the cancer patient. At
this time, the Life Extension Foundation does not have a good alternative for
conventional therapies when it comes to large primary tumors. Even the
advanced therapies used at offshore cancer clinics are usually not potent
enough to shrink large, primary tumors. It
is crucial for cancer patients to monitor the effectiveness of any cancer
therapy they are using under the care of a physician, preferably an
oncologist. Blood tests should be done monthly that measure tumor markers in
the blood and measure the effects of immune-boosting therapies on specific
immune components of the blood. We
cannot overemphasize the importance of monthly blood testing for all cancer
patients. Every patient responds differently to both conventional and
alternative cancer therapies. The results of blood tests provide critically important data to evaluate the
effectiveness of these therapies. Some
of the blood tests commonly used by doctors to evaluate different types of
cancers are: Type of Cancer Blood Test Ovarian cancer CA 125 Prostate cancer PSA and prolactin Breast cancer CA
27.29, CEA, alkaline phosphatase and
prolactin Colon,
rectum, liver, CEA,
GGTP stomach and other organ cancers Pancreatic CA 19.9, CEA, GGTP Leukemia,
lymphoma, CBC with differential, and Hodgkin's disease immune cell differentiation
and leukemia profile Lung
cancer CEA, CA 125, alkaline phosphatase PT, PTT and D-Dimer of fibrin Dr. Emil Schandl's Cancer
Profile, which has had an excellent track record for more than 10 years, is
strongly recommended for all cancers (refer to the Medical Testing Protocols for in-depth
information). For cancers that do not have an established blood tumor marker
test, one should use MRI, CAT scans, and other imaging diagnostics every 30
to 60 days to determine whether tumor shrinking is actually occurring. This
will provid some evaluation about the benefits of whatever therapy is being
used. While
you may have to rely on conventional cancer therapy to treat a primary tumor,
the nutrients and hormones in the Cancer Treatment protocol improve the
chances of bringing metastasized cancer cells under control. Melatonin may be the single most effective alternative cancer
therapy because it boosts immune function, suppresses free radicals, inhibits cell proliferation,
and helps to change cancer cells into normal cells. Nutrients
that have an inhibitory effect on cancer-cell proliferation include Vitamin-A (and synthetic Vitamin-A analogs) and such phytochemicals found in cruciferous vegetables
as sulforaphane, 3-indole-carbinol and isothiocyanate. Soy contains numerous
anti-cancer agents such as genistein and
other isoflavones. Vitamin-d3 inhibits
cancer cell growth and induces cancer cells to differentiate into normal
cells. The
best example of the effectiveness of Vitamin-A and beta-carotene in inhibiting cell proliferation
is in patients with cancer of the mouth. Vitamin-A or beta-carotene
supplementation puts most forms of early stage mouth cancer in remission as
long as these nutrients continue to be consumed. The
Foundation's Cancer Treatment Protocol is for most forms of cancer, including
metastasized prostate cancer. This
protocol assumes that the patient's primary tumor has been eradicated, at
least partially, by surgery or some other treatment. However, it may be
followed even if the primary tumor has not yet been eradicated. Here
is the Life Extension Foundation's Cancer Treatment Protocol: Step One: Arrange for monthly blood tests, to include: 1.
Tumor marker test-The type of cancer dictates the type of test used. Some
cancers do not have a specific tumor marker test available. The CA Profile is not organ specific and has been shown to be
effective in monitoring the progression and regression of cancer. 2.
Immune cell subset test
(This is an expensive test.) 3.
Complete blood chemistry - to
include all standard liver, thyroid, heart and kidney function tests. This is
a low-cost test. These
blood tests must be taken on a regular basis under the supervision of a
physician in order to follow scientifically the Foundation's Cancer Treatment
Protocol. It's the best way of knowing whether what you are taking is
working, and/or whether significant toxicity is developing. This is no time
to guess! Since
you will be having these tests performed monthly, you should price-shop for
the best deal. The Life Extension Foundation now offers these tests at
discount prices. Step Two: Total nutritional support 1.
Life Extension Mix -The standard daily dose
involves three tablets, three times a day. Also available in powder or
capsule form to be taken in three divided doses. 2.
Life Extension Herbal Mix-powder only. One
tablespoon early in the day. 3.
Super selenium complex. One
tablet, two times a day. 4.
Green Tea capsules
(decaffeinated)-Four to
10 capsules a day in divided doses. 5.
Coenzyme Q10-oil filled capsules, 200 to 400
mg early in the morning. 6.
Garlic- Kyolic Galic Formula 105, four
capsules a day; and PureGar (high allicin Garlic), four 900-mg capsules a day
with meals. 7.
Essential fatty acids-Mega EPA fish oil
or Udo's Choice Ultimate
Oil. Highest tolerable doses. Suggested dose is 12 Mega EPA caps or two
tablespoons of Udo's Choice Ultimate Oil daily. Some studies suggest not
taking these oils if you have prostate cancer. 8.
Vitamin-C-Capsules or powder. Highest tolerable dose of pharmaceutical grade
Vitamin-C to be taken throughout the day. 9.
Phyto-Food powder.
One to two tablespoons daily. Juicing organic vegetables is an alternative to
Phyto-Food powder. 10.
L-carnitine capsules (600 mg)-Four capsules early in the day.
Use Acetyl-L-carnitine if affordable. 11.
Curcumin-four
500-mg capsules daily. 12.
Conjugated linoleic acid (CLA)-10
500-mg capsules in two divided doses Step Three: Boosting immune function 1.
If the immune system is weakened enough, cancer cells can survive and
multiply. The most critical part of the immune system is the thymus gland, a
small organ just below the breast bone that governs the entire system. There
are two products that promote healthy thymic activity: a)
Thymic Protein A has been
shown in laboratory and animal experiments to cause the T-4 lymphocyte to
mature, thereby initiating a specific cell-mediated immune response. Thymic Protein A is a protein that has been shown
to be a stimulant in animal models for the production of interleukin-2.
Interleukin-2 production by T-4 cells is the benchmark measurement for T-cell
maturity and initiation of immune response. A
daily dose of four micrograms of Thymic Protein A may strengthen the immune
system through its T-cell "programming" role. The more T-cells that
are properly functioning, the more immune response may be mounted against
metastasized cancer cells. Initial
reports from those undergoing chemotherapy indicate that Thymic Protein A has
maintained their total white blood count at acceptable levels during the
therapy. (It is well known among oncologists that chemotherapy and radiation
often will induce a drop in white blood count to dangerous levels, which may
dictate cessation of therapy.) Healthy people can take one packet every day
or every other day. Those with disease whose treatment is dependent on a
strong immune system may need three packets a day for several months. b)
Another product, Thymex, provides extracts of fresh, healthy tissue from the
thymus and other glands that produce the disease-fighting cells of our immune
system. The
primary ingredient in Thymex is
immunologic tissue from the thymus gland. Also included in Thymex is tissue
from the lymph nodes and spleen that produces the white blood cells that
engage in life or death combat with invading organisms in our bloodstream
under the "instruction" of the thymus gland. Thymex
is a synergistic formula that contains herbal activators and a full
complement of natural homeopathic nutrients, in addition to fresh, healthy
thymus, lymph and spleen tissues. Thymex is a professional formula normally
dispensed through doctor's offices. Thymex has been extensively used to
amplify the immune potentiating effect of DHEA
replacement therapy. According to a physician most familiar with DHEA, thymus extract is required to obtain the immune
system-boosting benefit of DHEA. 2.
Cancer patients usually have elevated cortisol levels that can suppress
immune function. Take one to two tablets of KH3 daily on an empty stomach
first thing in the morning, and one or two KH3 tablets in the mid-afternoon on an empty stomach to
suppress the damaging effects of cortisol. 3.
DHEA can also
suppress dangerously high cortisol levels while boosting immune function via
other mechanisms. Doctors usually prescribe at least 25 mg per day of DHEA
for their male cancer patients and a minimum of 15 mg a day of DHEA for
females. Your monthly or bimonthly DHEA-S and immune cell subset tests and tumor marker tests
will determine if DHEA is producing a beneficial effect. Do not use DHEA if you have prostate cancer or estrogen-sensitive
breast cancer. 4.
Melatonin boosts immune function via several mechanisms of
action. It also exerts an inhibitory effect on cancer cell proliferation and
induces the differentiation of cancer cells into normal cells. Melatonin
should be taken every night in doses ranging from 3 to 40 mg. CAUTION: Some doctors are under the impression that
leukemia, Hodgkin's disease, and lymphoma patients should avoid melatonin
until more is known about its effects on these forms of cancer. If melatonin
is tried in these types of cancer, tumor blood markers should be watched
closely for any sign that melatonin is promoting tumor growth. 5.
Show your oncologist the information in this book regarding the use of the
FDA-approved drugs interleukin-2 or interferon and melatonin. Studies
document that low doses of interleukin-2 or alpha interferon combined with
high doses of melatonin (10 to
50 mg nightly) are effective against advanced, normally untreatable cancers.
Ask your doctor to prescribe these agents: a)
Interleukin-2 at a dose of 3 million units injected subcutaneously six out of
every seven days for six weeks. And one month later: b)
Alpha interferon at a dose of 100,000 to 300,000 units injected
subcutaneously six out of seven days for six weeks. Subcutaneous injections
can be self-administered at home. CAUTION: Breast cancer patients should not use
interleukin-2. While low-dose IL-2 and high-dose melatonin have been shown to
be effective against many forms of cancer, interleukin-2 could promote breast
cancer cell division. Breast cancer patients are encouraged to take 10 to 50
mg of melatonin nightly (See the Breast Cancer protocol). This
immune-boosting program should be adjusted if the immune cell subset test or
the CA Profile fails to
show marked improvement in the patient's immune function. For example, if
there are too many T-suppressor cells, 800 mg a day of the drug Tagamet (now
available over the counter) can lower the T-suppressor cell activity.
T-suppressor cells often are elevated in cancer patients, which prevents them
from mounting a strong immune response to the cancer. Step Four: Inhibiting cancer cell proliferation 1.
Water-soluble Vitamin-A liquid in doses
of 100,000 to 300,000 IU a day should be used for several months. CAUTION: Monthly blood tests can help ascertain if toxicity
is occurring in response to these high doses of Vitamin-A. Do not take
Vitamin-A if you have thyroid cancer or suffer severe thyroid deficiency.
Refer to theVitamin-A Precautions before
taking vitamin A. 2.
Melatonin taken to
boost immune function also inhibits cancer cell proliferation. 3.
Mega Soy Extract. Five
700-mg capsules four times a day. Soy may be effective in treating certain cancers.
Genistein is the most substantiated soy isoflavone that produces multiple cancer-inhibiting
effects. Genistein has been shown to work especially well against certain
leukemias and cancers of the skin, prostate and brain. CAUTION: For most cancers, the determining factor of whether
soy may work is if your cancer cells carry a mutated
p53 tumor suppressor gene, or carry functional p53. If functional p53 is
present, then soy genistein will probably not
work. In small-cell lung cancer, however, it was recently determined that
genistein's growth inhibitory effects were independent of p53 function. Only
specialized tumor cell tests (immuno-histochemistry) can determine the p53
status of your particiular cancer. Estrogen-receptor positive breast cancer patients should avoid high
doses of genistein. 4.
Whey protein
concentrate powder. 30 to 60 grams a day (one to two scoops). Whey protein
concentrate inhibits cancer cell glutathione levels, making cancer cells more vulnerable to free
radical destruction than normal cells. Step Five: Inducing cancer cell differentiation Cancer
cells are aberrant, transformed cells that proliferate (divide) more rapidly
than normal cells until they kill the patient. Inducing cancer cells to
"differentiate" back into normal cells is a primary objective of
cancer researchers. 1.
The Total Nutritional Support protocol supplies nutrients like beta-carotene
and the phytochemicals found in fresh fruits and vegetables that induce
cancer cell differentiation into normal cells and inhibit cancer cell
proliferation. 2.
Melatonin , which
boosts immune function and inhibits cancer cell proliferation, also induces
cancer cell differentiation. 3.
Vitamin-d3 and its analogs may be the most effective therapies to induce cancer
cell differentiation. Vitamin-d3 can
cause too much calcium to be absorbed into the bloodstream, so the monthly
blood chemistry test, which includes serum calcium levels and kidney and
liver function tests, is crucial to guard against Vitamin-d3
overdose. A daily dose of 2,000 to 3,000 IU of Vitamin-d3 is suggested.
Increase Vitamin-d3 if blood
tests show blood calcium levels are not being affected and parathyroid
hormone (PTH) levels are not suppressed. Decrease or eliminate Vitamin-d3
supplementation if hypercalcemia occurs. Underlying kidney disease precludes
high-dose Vitamin-d3 supplementation. Note
the importance of competent, professional guidance by a physician. Monthly
blood testing is mandatory when taking high doses of Vitamin-A or Vitamin-d3.
Step Six: Preventing cancer cell metastasis Modified citrus pectin interferes with cancer cell
communication, enhances killer cell activity, and inhibits cancer cell
metastasis. Suggested dose of this powder is 15 grams a day. Step Seven: Call the Life Extension Foundation If
following the above protocols does not result in significant immune
enhancement, improvements in blood tumor markers, tumor shrinkage, weight
stabilization, and an overall improvement in well being within two months,
please call the Life Extension Foundation at 1-800-544-4440 or order OnLine for
other, more aggressive options. It
is impossible to fit a description about the mechanisms of action of all the
nutrients and hormones in this Cancer Treatment protocol. That would require
a separate book. What follows are some recent reports that substantiate some
components of the Cancer Treatment protocol. The inclusion of certain
nutrients in the following descriptions does not mean that they are more
important than nutrients like Vitamin-C and selenium, whch are not discussed
because of lack of space. Conjugated
linoleic acid (CLA) has been shown both in vitro and in animal models to have
strong anti-tumor activity. Particular effects have been observed on the
growth and metastatic spread of mammary tumors. A study investigated the
effect of dietary CLA on the growth of human
breast adenocarcinoma cells in immuno-deficient mice. CLA inhibited the
development and growth of mammary tumors. Moreover, CLA completely abrogated the spread of breast cancer
cells to lungs, peripheral blood and bone marrow. These results indicate the
ability of dietary CLA to block both the local
growth and systemic spread of human breast cancer via mechanisms independent
of the host immune system. CLA
has been shown to inhibit initiation and promotion stages of carcinogenesis
in several experimental animal models. A study of mice with skin tumors
showed that CLA inhibited tumor yield. This study confirmed previous studies
showing that CLA inhibits tumor promotion in a manner that is independent of
its cancer-prevention effects. Genistein
has shown significant cell-inhibiting effects in many different types of
cancer. A study was conducted to examine the role genistein played in growth
factors such as protein tyrosine kinase and thymidine incorporation into
cancer cells. Genistein
suppressed protein tyrosine kinase activity and the subsequent growth
stimulatory incorporation of thymidine into cancer cells. The scientists
speculated that genistein has
potential value in the prevention and treatment of some tumors in vivo. In
other studies, genistein has shown anti-angiogenesis properties, cancer cell
adhesion-inhibition properties, estrogen-receptor blocking properties and
apoptosis-inducing effects. An investigation into the effect of soy genistein on the growth and
differentiation of human melanoma cells showed that genistein significantly
inhibited cell growth. Some studies suggest that genistein may enhance the
efficacy of certain chemotherapy regimens. Curcumin and genistein both have been shown to inhibit the
growth of estrogen-positive human breast cancer cells induced by pesticides.
When curcumin and genistein were added to breast cancer cells, a synergistic
effect resulted in a total inhibition of cancer cell growth caused by
pesticide-induced estrogenic activity. This study suggested that the
combination of curcumin and genistein in the diet has the potential to reduce
the proliferation of estrogen-positive cells induced by mixtures of
pesticides or estrogen. Since it is difficult to remove pesticides completely
from the diet, and since both curcumin and soy genistein are not toxic to
humans, their inclusion in the diet in order to prevent hormone-related
cancers deserves consideration. Curcumin appears
to function via several different mechanisms to inhibit cancer cell
proliferation. Genistein
appears to be especially effective against prostate cancers. One study showed
that genistein inhibited the proliferation and expression of the in vitro
invasive capacity of tumoral prostatic cells. In a cell culture system,
genistein appeared to be cytotoxic and inhibitory to PC-3 cells. The more
aggressive the prostate cancer cell culture studies, the more genistein was effective, both with respect to proliferation
rate and inhibition of growth factors. Angiogenesis
(new blood vessel growth) is a key step in tumor growth, invasion and
metastasis. To date, a number of anti-angiogenic agents have been identified.
In animal models, treatment with angiogenesis inhibitors has proven
anti-tumor effects. Early clinical experience with angiogenic inhibitors
indicates that optimal anti-angiogenic therapy in the future will likely be
based on their long-term administration to cancer patients in adjunct to
surgery, radiotherapy and conventional chemotherapy. Differentiation-inducing
agents such as genistein, retinoids and Vitamin-d analogs inhibited tumor cell induced angiogenesis
in vitro and in vivo. Simultaneous administration of retinoids and 1,25-Dihydroxy Vitamin-d3 led to a synergistic
inhibition of tumor associated angiogenesis in mice. Recently, these
compounds have been shown to induce and act in concert with natural
angiogenic inhibitors such as interferons. A
study was conducted to determine if genistein can induce human breast
adenocarcinoma cell maturation and differentiation. Treating these cells with
genistein resulted in growth inhibition accompanied by increased cell
maturation. These maturation markers were optimally expressed after nine days
of treatment with genistein. Both estrogen receptor-positive and estrogen
receptor-negative cells became differentiated in response to genistein, which
is a crucial step in inducing cancer cell apoptosis (programmed cell death). Despite this study, we do not recommend that women with estrogen
receptor-positive breast cancer use soy genistein because of the following
evidence. The
Foundation has made a preliminary determination that women with
estrogen-receptor positive breast cancer should not take soy supplements
based on evidence that an estrogenic growth effect could occur in some forms
of estrogen-receptor positive breast cancer. Until more is known about the
effects of soy phytoestrogens in this type of cancer, compounds such as
genistein should be avoided in those with estrogen-receptor positive breast
cancer. One
study tested the effects of naturally occurring flavonoids on the
proliferation of an estrogen receptor-positive human breast cancer cell line.
Genistein inhibited cell proliferation, but this effect was reversed when
estrogen was added. The flavonoids hesperidin, naringenin and quercetin inhibited breast cancer
cell proliferation even in the presence of high levels of estrogen. These
flavonoids apparently exert their anti-proliferative activity via a mechanism
that is different from genistein. Women
with any type of breast cancer should test their serum estrogen levels to
make sure that too much estrogen is not present if they are taking high doses
of soy. Estrogen can combine with the phytoestrogen genistein to cause some
breast cancer cells to grow faster. Other studies, however, show that
genistein blocks certain types of estrogen-receptor sites, thus inhibiting
the proliferation of these types of breast cancer cells. Cancer
patients whose tumor cells have a mutant p53 oncogene are far more likely to
benefit from soy extract supplementation. Only a pathology examination of the
actual cancer cells can determine p53 status. An immuno-histochemistry test
can help to determine the p53 status of tumor cells. The following laboratory
can perform this new test: IMPATH
Laboratories 1010 Third Avenue, Suite 203 New York, N.Y. 10021 Phone:
1-800-447-5816 IMPATH
Laboratories measures mutant p53. If the test is positive, you have mutant
p53 and are more likely to benefit from soy extracts. If the test is
negative, this indicates that you have functional p53 and are less likely
to benefit from soy extracts. The Foundation realizes that many cancer
patients seeking to use soy supplements may find it difficult to have an
immuno-histochemistry test performed to ascertain p53 status. In order to
find out if you have p53, please contact your oncologist and ask him to
request this test from IMPATH. IMPATH is unable to provide information about
the likelihood of p53 expression on an individual basis without samples and
test requests from your treating oncologist. Because
all cancer therapies produce individual responses, the Foundation reiterates
its recommendation that all cancer patients have monthly blood tumor marker
tests to determine whether the therapies they are using are working. If, for
instance, tumor markers were to continue to elevate for 30 to 60 days after
initiating soy extract supplementation, discontinue its use and seek another
therapy immediately. Fish
oil may enhance the effectiveness of cancer chemotherapy drugs. A study
compared different fatty acids on colon
cancer cells to see if they could potentiate the effect of the chemotherapy
drug mitomycin C. Eicosapentaenoic acid (EPA) from fish oil was shown to make
colon cancer cells more vulnerable to mitomycin C without affecting normal
cells. The scientists found that EPA induced alternations of the fatty-acid
composition of cancer cells, which made them more vulnerable to chemotherapy
destruction. Although preliminary, these findings imply that EPA specifically enhances the chemosensitivity of
malignant cells. Fish oil has been shown to specifically induce apoptosis of
pancreatic cancer cells and to inhibit metastasis of breast and lung cancer
cells. Garlic is a well-established cancer preventing nutrient. A
study investigated aged garlic extract in an
effort to determine whether it could inhibit proliferation of cancer cells.
The proliferation and viability of erythroleukemia, hormone-responsive breast
and prostate cancer cell lines were evaluated. The eyrtholeukemia cells were
not significantly affected by the garlic extract, but the breast and prostate
cancer cell lines clearly were susceptible to the growth-inhibitory influence
of aged garlic extract. The anti-proliferative effect of aged garlic extract
was limited to actively growing cells. This study provided evidence that
garlic can exert a direct effect on established cancer cells. Aberrant
hyperproliferation is a late occurring event that precedes mammary
tumorigenesis in vivo. A study conducted on pre-cancer cells showed that EPA,
indole-3-carbinol (broccoli-cabbage extract) and green tea extract resulted in a 70 to 99 percent inhibition
of aberrant hyperprolifertion. Whey
protein concentrate has been studied for cancer prevention and treatment.
When different groups of rats were given a powerful carcinogen, those fed whey protein concentrate showed fewer tumors
and a reduced pooled area of tumors. The researchers found that whey protein
offered "considerable protection to the host" over that of other
proteins, including soy . Whey appears to inhibit the growth of breast cancer
cells at low concentrations. One clinical study with cancer patients showed a
regression in some patient's tumors when fed whey protein concentrate at 30
grams per day. As
noted in a related protocol, but worth repeating in this context, this led
researchers to discover a relationship between cancerous cells, whey protein concentrate and glutathione. Glutathione is an antioxidant that protects the
body against harmful compounds. It was found that whey protein concentrate
selectively depletes cancer cells of their glutathione, thus making them more
susceptible to cancer treatments such as radiation and chemotherapy. It
has been found that cancer cells and normal cells will respond differently to
nutrients and drugs that affect glutathione status. What is most interesting
is that the concentration of glutathione in tumor cells is higher than that
of the normal cells that surround it. This difference in glutathione status
between normal cells and cancer cells is believed to be an important factor
in cancer cells' resistance to chemotherapy. As the researchers put it,
"Tumor cell glutathione
concentration may be among the determinants of the cytotoxicity of many
chemotherapeutic agents and of radiation, and an increase in glutathione
concentration in cancer cells appears to be at least one of the mechanisms of
acquired drug resistance to chemotherapy." They
further state, "It is well-known that rapid glutathione synthesis in
tumor cells is associated with high rates of cellular proliferation.
Depletion of cancer cell glutathione in vivo decreases the rate of cellular
proliferation and inhibits cancer growth." The problem is, it's
difficult to reduce glutathione sufficiently in tumor cells without placing
healthy tissue at risk and putting the cancer patient in a worse condition.
What is needed is a compound that can selectively deplete the cancer cells of
their glutathione , while increasing, or at least maintaining, the levels of
glutathione in healthy cells. This is exactly what whey protein appears to
do. This
research found that cancer cells subjected to whey proteins were depleted of
their glutathione and their growth was inhibited, while normal cells had an
increase in glutathione and increased cellular growth. These effects were not
seen with other proteins. Not surprisingly, the researchers concluded,
"Selective depletion of tumor cell glutathione may in fact render cancer
cells more vulnerable to the action of chemotherapy and eventually protect
normal tissue against the deleterious effects of chemotherapy." The exact
mechanism by which whey protein achieves this is not fully understood, but it
appears that it interferes with the normal feedback mechanism and regulation
of glutathione in cancer cells. It is known that glutathione
production is negatively inhibited by its own synthesis. Since baseline
glutathione levels in cancer cells are higher than that of normal cells, it
is probably easier to reach the level of negative-feedback inhibition in the
cancer cells' glutathione levels than in the normal cells' glutathione
levels. Molecular Oncology CAUTION: The following information is extremely technical.
The cooperation of your oncologist is vital to most cancer patients who seek
to use the following information in an attempt to save their lives: -
Determining RAS mutations. The
family of RAS proteins plays a central role in the regulation of cell growth
and integration of regulatory signals that govern the cell cycle and
proliferation. Mutant RAS genes were among the first oncogenes described for
their ability to transform cells to a cancerous phenotype. Mutations in one
of three genes (H, N and K-RAS) encoding RAS proteins have been intimately
associated with unregulated cell proliferation, and are found in an estimated
30 percent of all human cancers. The frequency of RAS mutations appears to
depend upon the specific tumor type analyzed. For example, 90 percent of
pancreatic carcinomas contain a mutated oncogenic RAS protein while RAS
mutations are rarely found in breast carcinomas. Approximately
one-third of liver cancers harbor a mutated RAS oncogene. Pravastatin, an
inhibitor of the rate-limiting enzyme of cholesterol synthesis, inhibits
growth of liver cancer cells. One of the possible mechanisms of pravastatin
inhibition of cell growth is that pravastatin may inhibit the activity of RAS
proteins. In a recently published study, patients with primary liver cancer
were treated either with the chemotheraputic drug 5-FU or a combination of
5-FU and 40 mg per day of pravastatin. Median survival was 26 months in the
combination therapy group, versus 10 months in the mono-therapy (5-FU) group.
The
highest incidences of RAS mutations are found in adeno-carcinomas of the
pancreas (90 percent), the colon (50 percent) and the lung; in thyroid tumors
(50 percent); in liver tumors (30 percent); and in myeloid leukemia (30
percent). If you have one of these cancers, you should consider requesting an
immuno-histochemistry for the mutated RAS oncogene or a biopsied specimen in
order to ascertain if the combination of chemotherapy and a statin drug may
be effective. -
Determining p53 status. Another
of the most widely studied molecular changes in epithelial malignancies is
mutation in the p53 tumor suppressor gene. A p53 mutation has been found in
approximately 50 percent of solid tumors. The p53 gene product is regarded as
a cell-cycle checkpoint, arresting progression through the G phase of the
mitotic cycle in response to cellular injury and allowing time for repair of
replication errors. Mutant p53 allows tumor cells to bypass the cell cycle
constraints that facilitate repair or promote apoptosis (programmed cell
death). P53
dysfunction promotes the spontaneous emergence of mutant cells and encourages
progression of cancer. Mutant p53 might restrict therapeutic efficacy since
many cancer drugs and radiotherapy operate via the induction of DNA damage
and p53 dependent apoptosis. Clinically, the presence of p53 mutations is
indeed associated with intransigence to treatment, and both in vitro and in
vivo studies with human cell lines and transplantable tumors have
demonstrated enhanced survival of p53 mutant or null cells in the face of
normally lethal concentrations of cytotoxic drugs and ionizing radiation. A
determination of p53 status, by an immuno-histochemistry, can help to
ascertain whether genotoxic chemotherapy and/or radiotherapy are likely to
work, and can even help determine whether natural therapies such as soy
genistein will be effective. In
a recently published study, genistein was shown to inhibit growth and induce
differentiation in human melanoma cells in vitro. The effects of genistein
were regulated by cellular p53. Functional p53-containing cells were not
suppressed by genistein. However, mutant p53-containing cells were
significantly more sensitive to genistein's inhibitory and
cell-differentiating effects. IMPATH
Laboratories, cited earlier in this protocol, can ascertain
immuno-histochemistries which will ascertain RAS and p53 status. -
Determining thrombotic risk factors. In
patients affected with different tumors, disorders concerning blood clotting
are frequently observed. The biological processes leading to coagulation are
probably involved in the mechanisms of metastasis. About 50 percent of all
cancer patients, and up to 95 percent of those with metastatic disease, show
some abnormalities-a pre-thrombic state-in the coagulation-fibrinolytic
system. Thromboembolic complications are seen in up to 11 percent of cancer
patients, and hemorrhage occurs in about 10 percent. Thromboembolism and
hemorrhage, as a whole, are the second most common cause of death after
infection. In
a recently published study, subclinical changes in the
coagulation-fibrinolytic system were frequently detected in lung cancer
patients. Five conventional and one new test of blood coagulation-that is,
platelet count (P), prothrombin time (PT), partial thromboplastin time (PTT),
fibrinogen (F) and D-Dimer of fibrin (DD)-were prospectively recorded in a
series of 286 patients with new primary lung cancer. A pre-thrombotic state
(depicted by a prolongation of PT, PTT and increase of D-Dimer of fibrin) was
significantly associated with an adverse outcome. Anticoagulant
treatment of cancer patients, particularly those with lung cancer, has been
reported to improve survival. These interesting though preliminary results of
controlled trials lent some support to the argument that activation of blood
coagulation plays a role in the natural history of tumor growth. Recently,
two studies compared the effectiveness of standard heparin with low molecular
weight heparin (LMWH) in the treatment of deep vein thrombosis (DVT). In both
studies, mortality rates were lower in the patients randomized to LMWH. The analysis
of these deaths reveals a striking difference in cancer-related mortality. Cancer-related
mortality of patients treated with standard heparin was 31 percent, versus
only 11 percent among those treated with low molecular weight heparin. This
difference cannot solely be attributed to thrombotic or bleeding events.
Because large numbers of cancer patients were included in the studies, it
seems unlikely that ones with more advanced tumors were present in the
standard heparin group. Although it is also possible that standard heparin
increases cancer mortality, such an adverse effect has not been reported.
These considerations suggest that low molecular weight heparin might exert an
inhibitory effect on tumor growth that is not apparent with standard heparin.
The evidence of lowered cancer mortality in patients on LMWH has renewed
interest in these agents as antineoplastic drugs. If your oncologist will not
test for thrombotic risk factors, contact the Life Extension Foundation at
1-800-544-4440 or order OnLine. -
Assessing immune function. In
order to assess the effectiveness of immune-boosting therapies, a complete immune cell subset test could be performed bimonthly in
order to measure CD4 (T-helper) total count, CD4/CD8 (T-helper to
T-suppressor) ratio, and NK (natural killer cell) activity. CD4
T-cells have been shown to differentiate into TH1 or TH2 cells, with different
cytokine profiles and functions. TH1 cells produce interleukin-2 and gamma
interferon, activate macrophages, and cause delayed type hypersensitivity
reactions, whereas TH2 cells produce interluken-4, interluken-5 and
interluken-10, cause eosinophilia, and are more specialized in providing B
cell (antibody) help for immunoglobin production. The differential
development of these immune system subjects is a major determinant of the
outcome of physiological as well as pathological immune responses to cancer. One
of the soluble factors secreted by monocytes, interleuken-12, is a major
cause of differentiation of T cells towards the TH1 type, while suppressing
TH2 cytokine development. The capacity of interleukin-12 to stimulate growth
and gamma interferon production in T cells and NK cells is probably the main
reason for its TH1-inducing capacity. Another product of activated monocytes,
prostaglandin E2, has been shown to be an important regulatory factor in
inducing TH2 responses. PGE2 affects T helper responses opposite to
interleukin-12: the synthesis of TH1 cytokines (interleukin-2 and gamma
interferon) is much more sensitive to inhibition by PGE2 than TH2 cytokine
production (IL-4, IL-5, IL-10). Because TH1 and TH2 cytokines negatively
cross-regulate each other's production, the selective inhibition of TH1
cytokines by PGE2 could result in dominant TH2 responses. These findings
provide opportunities to treat patients with dominant TH2 responses by
selectively inhibiting synthesis of PGE2 during therapy, as this would
increase interleukin-12 production and cause a shift toward TH1 cytokine
production. Many
human tumors, including gastric, colon, estrogen receptor-negative breast,
prostate and lung produce more prostaglandin E2 than their associated normal
tissues. The mechanisms and implications are not fully understood, but PGE2
may act as a tumor promotor in tumor angiogenesis, in cachexia (wasting
syndrome) and in the suppression of immune function. Prostaglandins
are synthesized from arachidonic acid by the enzyme cyclo-oxygenase. There
are two isoforms of cyclooxygenases: Cox-1 is expressed constitutively in
most tissues and helps maintain gastric mucosal integrity; Cox-2 is inducible
and is associated with cellular growth and differentiation. In a recently
published study, PGE2 was shown, for the first time, to up-regulate the MRNA
levels of its own synthesizing enzyme, Cox-2, in four human cells lines. In
this regard, it is conceivable that cells continuously sustain their growth
in part by using extra cellular PGE2 that they themselves produce and release
to up-regulate the expressions of Cox-2 and possibly other growth related
genes. Elevated Cox-2 expression may make cancer cells resistant to
apoptosis. Inhibition of excess activity with Cox-2 specific non-steroidal
anti-inflammatory drugs might restore the cell's ability to die by apoptosis
and so cause tumor regression. Super
aspirins that selectively inhibit Cox-2 are being developed by several drug
companies to try and avoid the side effects of NSAIDS. The currently
commercially available NSAIDS are nonselective Cox inhibitors and are
associated with peptic ulceration in the stomach. Nimesulide is a novel NSAID
that is one hundred times more selective for Cox-2 than for Cox-1. In a
recently published study, patients received either nimesulide or aspirin for
14 days. PGE2 formation fell markedly in the nimesulide treated patients,
whereas aspirin had no effect. In contrast, nimesulide had no significant
effect on Thromboxane B2 which was suppressed by aspirin. Nimesulide
suppressed Cox-2 in vivo with no detectable effect on platelet Cox-1. Nimesulide
has been commercially available throughout most of the rest of the world for
more than 10 years. It has not been licensed by the FDA for use in the United
States. The Life Extension Foundation has identified sources that will ship
nimesulide to Americans for personal use. There
are several thousand studies that substantiate the anti-cancer potential of
the nutrients listed in this Cancer Treatment protocol. Please refer to the
References section for additional studies. Product availability: You can order Life Extension Mix , Life Extension Herbal Mix, selenium complex, Thymex, DHEA, Melatonin, Vitamin-A emulsified drops, Vitamin-d3, Mega Soy Extract, Green Tea caps, Coenzyme Q10, Garlic, Vitamin-C, Phyto-Food, carnitine, Acetyl-L-Carnitine and modified citrus pectin by calling 1-800-544-4440 or
order OnLine. Ask for
the names of companies that will ship nimesulide and other cancer drugs to
Americans for personal use. For
some forms of cancer, you may be able to get in a free program utilizing
experimental cancer therapies sponsored by the National Cancer Institute. For
information about experimental cancer therapies, call 1-800-4-CANCER. Make
sure you do not enroll in a study where you may be part of a placebo group or
where the potential toxicity of the drug may kill you before the cancer does. Become a of the Foundation Created: Saturday, September 27, 1997 Updated: 11/28/98 |