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?
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).
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.