| LE: We talked about cancer genes. What about “tumor suppressor
genes”? How do they relate to cancer?
Burzynski: Tumor suppressor genes normally cause proteins to be
made that provoke apoptosis—a process that naturally destroys
cancer cells. This goes on all the time in healthy tissue. In cancer
cells, tumor suppressor genes are shut down; they don’t work.
The idea is to reactivate them.
LE: The p53 gene is an important tumor suppressor gene, isn’t
it?
Burzynski: Yes, and it is of great interest to us because it’s
not working in about 70% of white Americans with brain tumors.
In Japanese patients, it doesn’t work in 50-60%. One of the
antineoplastons reactivates p53.
 |
| Stanislaw
Burzynski, MD, PhD |
LE: What causes the gene to shut down?
Burzynski: First, abnormal methylation and mutation of the gene
itself, and antineoplastons reverse this. Also, three important
enzymes relate to how cancer cells multiply. All three involve
methylation. We’ve discovered that in normal cells, the enzymes
stick together briefly, and then come apart. In cancer cells, they
stick together and make the cells keep replicating. It’s
as though a switch is stuck in the “on” position. At
least three of our antineoplastons make the enzymes disassociate.
When the enzymes are normalized, the cancer cells undergo apoptosis,
or cell death.
LE: So some antineoplastons appear to be able to restore the normal
function of important genes without toxicity?
Burzynski: Yes, from what we know so far. The 3,000-gene microarray
that we’ve just done is going to give us more information
in this regard.
LE: As if methylation and cancer weren’t complicated enough,
your latest publication concerns some new research on DNA structures
known as histones and their role in cancer.
Burzynski: Yes, this also has to do with normalizing
the behavior of cancer cells. “Histone deacetylase inhibitors” are
a new class of drugs being tested for cancer. Some of the antineoplastons
are natural histone deacetylase inhibitors. Acetylation is a process
related to methylation. Both affect how genes behave. One affects
the other, so it’s important to address both processes. When
cancer cells are treated with drugs that modulate both, you get
a better response.
LE: We understand that four antineoplastons are undergoing clinical
trials under FDA supervision for a variety of cancers, including
brain stem glioma, childhood cerebral astrocytoma, malignant lymphoma,
colon cancer, melanoma, prostate cancer, breast cancer, and others.
Burzynski: There are 76 studies in all.
LE: Brain cancer is your special interest, but do you treat other
types of cancer?
Burzynski: Yes, we do.
LE: When you administer the antineoplastons, the patient wears
a pump that constantly delivers the treatment. Why is it done this
way?
Burzynski: The treatment has to be given gradually because the
cancer cells are dying. There is something called “tumor
lysis syndrome,” where the patient can get sick from the
dying cells. We’ve found that if the treatment is given over
a period of two to eight months, the tumor disappears more quickly
and safely.
LE: Are the antineoplastons made synthetically? In other words,
once you isolate the natural substance from the body, you then
create it in a laboratory?
Burzynski: That’s correct.
LE: Could antineoplastons possibly have other uses? Aging is another
phenomenon that involves abnormal methylation. Could antineoplastons
be used to reverse aging as well?
Burzynski: Yes. We’ve noticed that people who get antineoplastons
for cancer treatment receive other benefits as well—for example,
they are resistant to common viral infections. Their blood cholesterol
is normalized and they are less susceptible to breast cancer and
enlargement of the prostate. Their skin is healthier, they are
less depressed, and they have more energy.
LE: One final question. If you were able to isolate and synthesize
every antineoplaston made by the entire body, could you theoretically
cure every type of cancer there is?
Burzynski: Possibly.
LE: And more, right?
Burzynski: And more.
| Antineoplastons Show Promise
in Preliminary Studies
Most cancer patients who receive
antineoplaston therapy have failed conventional therapy.
Many are in advanced stages of the disease and have
undertaken other therapies, making it difficult to
determine how well antineoplastons work compared to
other treatments. The most dramatic results seen so
far are in people with brain cancer.
Glioblastoma multiforme is a type of brain cancer that
responds poorly to standard therapy. With conventional
treatment, survival time is six to nine months; untreated,
the survival time is approximately four months. The percentage
of people having a partial response to chemotherapy has
been reported to be just under 5%.
 |
Abnormal MRI (magnetic
resonance imaging)
scan of a brain showing glioblastoma, a malignant tumor formed by uncontrolled
proliferation of glial cells. Glial cells,
or neuroglia, are small nerve cells that support the central
nervous system. Transverse cross section. |
In a trial of 80 people who had recurrent or persistent
tumors after conventional treatment and who were then
treated with antineoplastons, 15 responded with a complete
or partial response; 24 were stable, meaning they had
a less-than-50% reduction in tumor with no progression;
and 41 saw their disease progress. The median survival
time was 15 months. Of those who responded, five have
survived more than seven years, with two of the five
surviving more than 10 years. Interestingly, in some
cases, it appears that antineoplastons take over a year
to show effects.
Dr. Burzynski recently reported on the progress of
a phase II study on people with recurrent diffuse intrinsic
brain stem glioma, another difficult-to-treat cancer.
Of those receiving antineoplastons, two had a complete
response (the cancer is completely gone, without steroids),
three had a partial response (the tumor regressed at
least 50%), three stabilized (less than 50% reduction,
but no progression), and two saw their disease progress.
Two have been tumor-free for over five years since diagnosis,
and two more have survived four and five years, respectively.1
In another study of people with high-grade glioma,
antineoplastons produced a complete or partial response
in 36%, stabilized the disease (less than 50% reduction
in tumor size but no progression) in 35%, and resulted
in no change (disease progression) in 29%. By comparison,
a recent phase II study using thalidomide and a new FDA-approved
chemotherapy drug called Temodar® produced a complete
or partial response in 21% of the patients, stabilized
the disease in 14%, and resulted in disease progression
in 65%.
The use of antineoplastons to treat breast cancer has
not been as successful as hoped. Dr. Burzynski believes
this is because the antineoplastons currently in use
target the p53 tumor suppressor gene, a gene not frequently
associated with this type of cancer.
Using antineoplastons along with traditional therapy
is an idea that has recently caught on. In a study published
in Cancer Letters, researchers report that women with
breast cancer excrete antineoplaston A-10 at high rates.2 This correlates with destruction of blood cells known
as neutrophils. Antineoplaston A-10 reverses this trend
and may be useful in restoring neutrophil levels and
immunity in breast cancer patients.
Recurrence is another area in which antineoplastons
are proving successful. Japanese researchers treating
10 liver cancer patients with antineoplaston AS2-1 increased
the time to recurrence up to 16 months, compared to five
months in those not receiving it. AS2-1 worked better
in stage I patients than in stage IV patients.3
In a separate report, a 72-year-old man with colon
cancer and 14 metastases to the liver was treated with
surgery and microwave ablation to the liver masses. He
then received antineoplastons to prevent recurrence.
At one year, the liver cancer had returned and he again
underwent microwave treatment. At four years, liver cancer
had also returned, and he again received microwave treatment.
After that, the cancer disappeared and has not returned.
He is still alive, more than eight years later.4
For more information on Dr. Burzynski, his clinic,
and his research, visit his website (www.cancermed.com).
For information on cancer trials, including trials on
antineoplastons, visit the National Institutes of Health
website (http://clinicaltrials.gov).
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1. Burzynski SR, Lewy
RI, Weaver RA, et al. Phase II study of antineoplaston A10 and AS2-1
in patients with recurrent diffuse intrinsic brain stem glioma: a preliminary
report. Drugs R D. 2003;4(2):91-101.
2. Badria F, Mabed M, El-Awadi M, Abou- Zeid L, Al-Nashar E, Hawas
S. Immune modulatory potentials of antineoplaston A- 10 in breast
cancer patients. Cancer Lett. 2000 Aug 31;157(1):57-63.
3. Tsuda H, Sata M, Kumabe T, Uchida M, Hara H. The preventive effect
of antineo- plaston AS2-1 on HCC recurrence. Oncol Rep. 2003 Mar-Apr;10(2):391-7.
4. Ogata Y, Tsuda H, Matono K, et al. Long-
term survival following treatment with
antineoplastons for colon cancer with unre- sectable multiple liver
metastases: report of a case. Surg Today. 2003;33(6):448-53. |