Unlocking the Mystery of AntineoplastonsMay 2004
By Terri Mitchell
|LE Magazine May 2004|
|Unlocking the Mystery of Antineoplastons
A Natural Anticancer Agent
By Terri Mitchell
When Dr. Stanislaw Burzynski began searching in the 1960s for factors that would stop cancer, he had no idea he would discover one of the twenty-first century’s most exciting anticancer treatments. He also had no idea it would take 40 years to isolate a few peptides from the human body.
The Origin of Peptides
Medical practitioners in ancient Egypt, Greece, India, and Rome predicted the existence of what are now called peptides. These ancient healers believed healthy people had substances in their bodies that could be taken out and put into sick people to cure them. These mysterious factors are among other phenomena that have been demonstrated but not identified for eons. We now know some of these substances by names like antibodies, cytokines (produced by immune cells), and vitamins. These factors maintain organ function and curtail threats such as bacteria, but it is reasonable to suspect that the human body manufactures other compounds that might target cancer.
In the late 1800s, the Polish researcher Stanislaus Bondzynski discovered natural “bioactive peptides” in the body, but did not realize that they could stop the growth of cancer. Although published in scientific journals of the time, his findings were ignored by all but a few. Today, however, bioactive peptides are a big-ticket item for drug companies searching for new sources of profits. Peptides such as insulin and growth hormone have changed the face of medicine.
Subsequent research found that Dr. Burzynski’s antineoplastons could be divided into two groups: those with broad-spectrum activity against cancer, and those with effects against certain types of cancer. Dr. Burzynski continued to refine and test the factors throughout the 1970s. Finally, it was proven beyond a doubt that the factors did in fact stop cancer growth, both in vitro and in vivo. But Dr. Burzynski was unable to determine exactly how they worked.
Meanwhile, another medical researcher, Dr. Ming Liau, had been investigating abnormalities in cancer cells that allow them to keep multiplying. Dr. Liau discovered that cancer cells have abnormal versions of enzymes involved in cell growth. These enzymes relate to “methylation,” a simple biochemical reaction with enormous implications for cancer patients because of its relationship to cancer cell growth. Dr. Liau discovered that methylation-related enzymes in cancer cells switch the reaction into permanent “overdrive” so that cancer cells constantly replicate.
Dr. Liau joined Dr. Burzynski’s group and began testing whether antineoplastons could affect this process. He discovered that some antineoplastons stop runaway cell growth and cause the cells to revert to normal behavior. This ability of cancer cells to “normalize” is an exciting phenomenon in cancer research. Only a few things are known to provoke it, including vitamin A derivatives, hormones, vitamin D3, and emodin (found in grape vines and other plants).
Methylation and Cancer
Dr. Burzynski continued to isolate antineoplastons from healthy people and synthesize them for use in people with cancer. He knew that cancer patients actually have the factors but for some reason excrete them, and that if patients stopped excreting the factors when treated with antineoplastons, they would likely respond to treatment. Above all, Dr. Burzynski knew that the factors work with very little toxicity, selectively targeting cancer cells while leaving healthy cells alone.
Aside from knowing that some antineoplastons affect methylation enzymes, however, Dr. Burzynski still was not sure how they worked. Nevertheless, he noted that one antineoplaston attaches to DNA like some types of cancer drugs, while another was structurally related to phenylbutyrate, a natural fatty acid that can stop cancer through a process known as “acetylation.” Acetylation is similar to methylation in its ability to control the activation and deactivation of genes, which is critical to the study of cancer. Today, acetylation is a hot topic in both cancer and longevity research.
To date, Dr. Burzynski has isolated and synthesized 20 different antineoplastons from humans and several others from animals. His “third generation” of antineoplastons has 1,000 times more activity than the first ones he isolated, allowing fewer to be given but with much greater effect.
While Dr. Burzynski continues to look for new anticancer factors, finding them is slow, painstaking work, and many such factors may be needed for each type of cancer. Hundreds of antineoplastons may wait undiscovered. Finding, isolating, and synthesizing each one may take a long time. Yet, as the mysterious workings of antineoplastons continue to be revealed, Dr. Burzynski plunges forward with the enthusiasm of a young student on the brink of a great discovery.
Life Extension caught up with Dr. Burzynski at his clinic in Houston, where he specializes in treating glioma, a form of brain cancer.
LE: You’re very excited about some new research that’s coming out. Tell us about it.
Burzynski: We are about to learn the results of a DNA microarray we did to see what one of the antineoplastons does to 3,000 genes of glioblastoma brain tumor cells.
LE: What is a microarray?
Burzynski: Essentially, it’s a test that enables us to take a close look at a lot of genes in a short period of time.
LE: Why is this important?
Burzynski: By looking at the DNA of the cancer cell, we can see which genes are abnormal, and how antineoplaston treatment may reverse these abnormalities.
LE: Give us an example of what you’re looking for.
Burzynski: In about 30-40% of all cancers, an oncogene, or cancer gene, known as “ras” is activated. When activated, ras allows a protein to stick to the cell and send an abnormal signal. If we can deactivate ras, we can slow down cancer. The microarray will tell us which antineoplastons can shut this gene down.
LE: Why is ras activated in cancer cells but not in normal cells?
Burzynski: Abnormal methylation or mutation of the ras gene causes abnormal activation. If we can normalize methylation or inhibit protein produced by the gene, we can deactivate the gene and interfere with cancer’s ability to replicate and spread.
LE: Can antineoplastons normalize DNA methylation?
Burzynski: Yes. Antineoplastons normalize DNA methylation and deactivate ras oncogene protein, making a gene behave normally.
LE: Does the treatment affect normal cells?
Burzynski: No, this is why antineoplastons are a nontoxic treatment. They affect only abnormal cells. Another example of the ras gene being abnormally activated is the “elephant man” (John Merrick). The abnormal growths on his head and body were probably benign tumors caused by a defect in the gene that inhibits ras. In effect, the elephant man may have been suffering from methylation abnormalities, among other things.
LE: The most hopeful and exciting thing about methylation research as it relates to cancer is that abnormal methylation can be reversed—it can be made normal again—which means that nonfunctional genes can be made to function again.
Burzynski: That is correct.