Note: In this book, 15 cancer doctors share the details of their treatment protocols and answer difficult questions about cancer. Each physician is given their own chapter. The page you are viewing contains sample material; to read the rest of the book, you can place your order for the book from the publisher, Amazon, or Barnes & Noble. You can also buy the Kindle Edition.

EXCERPTED FROM Dr. Burzynski’s Chapter: Two things must be done in order to control abnormal genes. First, the genes which cause cancer cells to grow in the body, called oncogenes, must be turned off. Second, the genes which fight cancer, called tumor-suppressor genes, must be turned on. In order to accomplish these goals, molecular switches must be used. As an analogy, consider a switchboard that has different switches for turning on and off a piece of machinery. You can turn off certain switches to make the machinery stop, and turn on other switches to turn it back on.

The human body has similar molecular switches, some of which turn off oncogenes, and others which turn on tumor-suppressor genes. These switches are called antineoplastons, which are naturally occurring peptides and amino acid derivatives in the blood and urine that the human body naturally uses to control cancer growth. They comprise a biochemical defense system that controls cancer without destroying normal cells. The name “antineoplastons” comes from their function in controlling neoplastic or cancerous cells: i.e., anti-neoplastic cell agents.

Hence, treating cancer involves using biochemically synthesized antineoplastons that will both turn off the activity of the genes which cause cancer and turn on the activity of genes which suppress cancer.

Since the function of antineoplastons is to bring gene activity to a normal level, they affect only abnormal genes in the body. They turn off the genes which are hyperactive and turn on the genes which are inactive. They do nothing in normal cells, because the activity of a normal cell doesn’t need to be affected. As an analogy, suppose that you need to adjust the temperature in various rooms of your house. You turn up the thermostat in the rooms that are too cold, and you turn it down in the rooms that are too warm. The too-hot and too-cold rooms represent the body’s abnormal cells, and the thermostat represents the antineoplastons, which either turn up the temperature or turn it down (or turn off hyperactive genes and turn on silent genes). The room where the temperature is normal represents the normal cell that isn’t affected by antineoplastons.

How I Discovered Antineoplastons

I discovered antineoplastons a long time ago, in 1967, when I was a medical student. In addition to being a medical doctor, I am also a chemist. Through my research as a chemist, I discovered that cancer patients had a deficiency of certain peptides in their blood; peptides which we all have and which protect our bodies against cancer. I isolated these peptides and tested them together with scientists at the MD Anderson Cancer Center and learned that many of them would kill malignant cancer cells, but not harm normal cells.  After isolating the peptides, I characterized their chemical structure and reproduced them synthetically (in the typical manner that all pharmaceutical agents are developed for use on cancer patients). Thus began my work with antineoplastons.

Using Antineoplastons and Gene-Targeted Therapy to Treat Cancer

At my clinic, my fellow doctors and I have been given permission by the FDA to use antineoplastons mostly in clinical trials. The antineoplastons we use in these trials affect approximately 100 different genes which have been instrumental in the formation of patients’ cancers. I have discovered that if I can turn off around 100 genes which are causing a cancer to grow, then I can stop the growth of that cancer, or even eliminate it. To achieve this in our patients, we must determine the proper combination of genes for each one. 

The entire world is moving in the direction of gene-targeted therapy for cancer treatment by creating its own gene-targeted therapies. However, the current gene targeted therapies on the market are quite primitive: most, like Avastin, only work by affecting a single gene. So while these therapies can work for awhile, they are insufficient for treating cancer because cancer has a gene-signaling network of thousands of genes (on average 2,400) and will eventually overcome the effects of any therapy that is targeted to affect only one of its genes. At our clinic, we are really a decade or two ahead of others who use gene-targeted therapy because our medications (antineoplastons) work on close to 100 different genes and are comprised of naturally-occurring chemicals that don’t harm the patient’s body, unlike other gene-targeted therapies which often have adverse effects upon normal cells.

If doctors use a therapy that works on just one gene (the targeted gene is typically called the “driver” oncogene), then it’s possible for their patients’ tumors to shrink. Unfortunately, those tumors will eventually find a way to subvert that gene. Also, there are about twelve main gene signaling pathways in cancer (gene signaling is part of a complex system of communication that governs cellular activity and which coordinates cell action), which means that, in order for gene therapy to work, doctors must influence not only single genes, but their entire pathways, which are also comprised of numerous genes. And that’s still not the end of the story! In addition to this challenge, they must get rid of their patients’ malignant stem cells, which multiply and produce new cancer cells. Further complicating matters is the fact that these malignant stem cells are practically immortal. So treatment requires finding special combinations of antineoplastons that will also influence the gene signaling pathways and kill malignant stem cells without harming normal stem cells. Once doctors are able to do this, then their patients can be cured.

At our clinic, we have antineoplastic medications that address all of these areas. Nevertheless, every one of our patients is different, and because cancer can alter its DNA, we are always working with a moving target. Currently, scientists have discovered that there can be up to 3,152 different abnormal genes in cancer, and that count will increase over the next year or two as they continue to discover new genes. My average patient has approximately 80 of these, so there are a tremendous number of abnormal gene combinations which can result in a patient. Since every patient has a unique genomic signature, we can’t use the same treatment for everybody.

It’s important to emphasize that although patients may be diagnosed with the same type of cancer, the abnormal genes which cause their cancers will be different. We have to identify the particular genetic signature of each one of our patients and then put together the best combination of medications that will neutralize their cancer-causing genes.

[End Excerpt]

Buy the book to read the rest of this chapter. The following are additional sections contained in this chapter:

  • What Cancer Is, What Causes It, and How to Treat It
  • Treatment Process
  • Types of Antineoplastic and Gene-Targeted Medications
  • Use of Antineoplastons for Other Diseases
  • Dietary and Supplement Recommendations
  • Preventing Cancer with Supplements
  • Detoxification
  • Treatment Outcomes
  • Training Other Doctors to Use Antineoplastons
  • Improving Cancer Care
  • The Problem with Conventional Oncology
  • When to Use Conventional Medicine to Treat Cancer
  • Side Effects of Gene-Targeted Therapies
  • Other Factors That Affect Patients’ Healing
  • How Family and Friends Can Support Their Loved Ones with Cancer
  • Roadblocks to Healing
  • Insurance Coverage for Treatments
  • The Politics of Cancer Treatment in the United States and My Battle with the FDA
  • The Future of Cancer Treatment 
  • Last Words
  • Useful Websites
  • Last Words

Buy the book to finish reading this chapter.


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