So, if a genetic alteration (also called genetic mutation or genetic injury) is not the initiating event of most cancers, what is the initiating event?

The Discovery

A virus is a collection of genes. To replicate, some viruses settle in the nucleus of the host cell and use the cell machinery to replicate. What is the effect of the presence of a virus in the nucleus?

Like all athletes, a gene needs energy. When a virus enters the nucleolus it starts to consume the energy in the nucleus.  The result? A starved athlete, and a decrease in yardage during games.  In terms of the BRCA1 gene, the virus consumes the energy.  The BRCA1 gene is starved.  The production of the BRCA1 protein is decreased, and the breast tissue starts to develop tumors. (See a more technical description in the European Journal of Cancer paper and at http://www.cbcd.net/microcompetition.pdf.)

The infection with the latent virus is starving many genes, and as a result, it is causing the development of many chronic diseases. This sequence of events easily explains why people who suffer from obesity are also more likely to suffer from diabetes, heart disease, and cancer. It also tells you that obesity is not a cause of cancer, another common misconception, but rather another result of the starved genes, and why a recent large scale study found that a low-fat diet does not protect against breast cancer. It also explains another surprising observation that male pattern baldness is associated with heart disease and prostate cancer. In general, this sequence of events easily explains the numerous observations indicating a co-existence or co-morbidity of some chronic diseases.

This discovery was first described by Dr. Hanan Polansky in his book, Microcompetition with Foreign DNA and the Origin of Chronic Disease, published by The Center for the Biology of Chronic Disease (about the book see http://www.cbcd.net/book.htm).

In his European Journal of Cancer, Dr. Raxit J. Jariwalla reports an interesting observation on the microcompetition discovery: "The key point of the theory is that the competing DNA sequences do not bind each other but compete for binding to a limiting transcription complex. In the example cited, the viral DNA and BRCA1 do not bind each other but compete for binding to the limiting GABP*p300/cbp transcription complex. It is interesting that when explaining observations reported in the literature, biologist tend to rely on the traditional physicochemical philosophy which centers on binding/non-binding events, or physical contact between molecules. In contrast, microcompetition with foreign DNA, which in essence is a reallocation of a rare resource, seem to draw on economic rather than physicochemical principles."

To summarize: Most cancers begin with a starved gene not an injured (mutated) gene.

What about carcinogens and cancer? Take a person who harbors a latent infection. The higher the number viruses present in the nucleus, the more starved is the BRCA1 gene, and the larger the decrease in the concentration of the BRCA1 protein. What determines the number of viruses present in the nucleus? Among other things, exposure to carcinogens. More exposure to carcinogens leads to more copies of the virus, less BRCA1 protein, and a higher risk of cancer.

Reaction of the Scientific Community

What is the scientific community saying about Dr. Polansky's discovery?

Since publication, the book has been reviewed by many peer-reviewed journals: Cell Cycle; Archives of Virology; Infection, Genetics and Evolution; Developmental & Comparative Immunology; Archives of Dermatological Research; American Journal of Diabetes; Experimental Dermatology; Genetic and Molecular Research; Internet Journal of Infectious Diseases; Neuroimmunomodulation; Immunogenetics; Veterinary and Human Toxicology; Viral Immunology; The Journal of Experimental Therapeutics and Oncology; and Perspectives in Biology and Medicine.

The author was also invited to present seminars on his discovery at several leading universities around the world.

The following is a selection of highlights from a few reviews (the full text is posted, with permission from the journals, on the publisher’s website at http://www.cbcd.net/journals.htm. The website also includes excerpts from the book at http://www.cbcd.net/book.htm):

Naumova EN. Book review. Arch Virol. 2004 Jun;149(6):1257-8.
“No student of biomedical sciences could ignore the appearance of a new theory offering explanations for the origin of chronic diseases. Systematic testing and better understanding of a framework outlined by such a theory may lead to a paradigm shift in scientific view on the nature of ‘health’ as well as causality of ‘disease’. To be honest, it took me three attempts to read this book. The first attempt resulted in frustration and confusion. The unusual writing style, complex terminology, and volume of information was daunting. I put the book aside, but the seeds of curiosity had been planted, and intriguing ideas took root. They began to grow, and soon I was forced to return to my reading. My second attempt was far more productive but nevertheless challenging. I went through all seven chapters of technical notes. It was a slow process, not because of the numerous mathematical equations (which were straightforward and well-supported) but because I found myself repeatedly distracted by independent thoughts and ideas triggered by the content of the book. I would read a sentence or two and immediately attach my own observations to the proposed frame, and test the fit; I was amazed by the serendipities. My third attempt was joyous; the book served its purpose - it made me think differently! What had first seemed like cumbersome technical notations became transparent when I connected them to the work I perform daily. I also realized that the area of my research interest - mathematical modeling of disease temporality - would benefit greatly by applying many fruitful ideas presented in Dr. Polansky’s book. I believe that Dr. Polansky’s book will catalyze the scientific learning process, promote interdisciplinary cross-fertilization, stimulate development of treatment strategies and drug discovery, and leave the reader inspired.”

Pouliot M. Book review. Cell Cycle. 2004 Apr;3(4): 519-20.
“First, I would like to congratulate the author for putting together such an insightful theory and impressive collection of supporting evidence, and most importantly, for being able to delineate functional links between seemingly distinct sets of observations. This is a well-organized, highly rigorous presented theory. The concept of microcompetition will change our approach in the study of chronic diseases and will furthermore give scientists a higher level of understanding in biology. Presentation of this concept undoubtedly provides a new set of opportunities for attacking chronic diseases. The idea that viruses are the cause of chronic diseases is not new, but the underlying mechanism, the evidence put forward, the molecular observations, the analyses, and conclusions certainly are. They lead the way to new approaches in chronic disease treatment. In my opinion, this book could be of great use to fundamental researchers. Investigators of specific areas will find well-presented concepts that transform our way of thinking about chronic diseases, and about the implication of viruses in biology and health in general. This work will eventually also have an impact on medical research and drug discovery, although realistically not in the near future; these areas not being typical bearers of new ideas. This is a very good theory, one that makes a lot of sense, and one that helps a lot in terms of trying to identify possible causes for chronic diseases. Time will tell, but regardless of being proved right or wrong, this theory has the merit of changing our current way of thinking, and this is probably the greatest contribution a new theory can bring.”

Kulski JK. Book review. Infect Genet Evol. 2004 Jun;4(2):171.
“Having worked previously in a variety of research disciplines such as on the enzymology of phosphatases, endocrine regulation of reproductive biology and lactation, viruses and cancer, comparative genomics, immunogenetics and autoimmunity, I very much enjoyed the multidisciplinary aspects of the book. Hanan Polansky has connected the dots from various disciplines and revealed a compelling and unifying theory for the origin of chronic disease. His theory is well-supported by the reinterpretation of a considerable amount of published data. I particularly liked the way a number of different gene products, such as TF, CD18 and GABP, were used to integrate the different findings of cellular and molecular biology into a logical explanation of chronic disease. I found this book to be a fascinating read and I expect it will help me to reassess and resynthesize some of my own ideas and concepts about the origins of psoriasis, rheumatoid arthritis and atherosclerosis. All together, the book adds clarity to a highly complex subject even though it may require some rereading and follow-up studies to fully benefit from this thought-provoking and ultimately essential account of the origin of chronic disease.”

Pickrell JA. Book review. Vet Hum Toxicol. 2004 Feb;46(2):106.
“When discussing instruction in higher education with professional colleagues, we think-but are not sure-that we know what will be required of tomorrow’s professional students. In reading this book, there arises a growing certainty, that tomorrow this theory’s knowledge will be required of today’s professional students. There is the sense that this book needs to be read, because we could learn valuable lessons and gain valuable perspectives. Enjoyment was irrelevant (and virtually nonexistent); however, it was nearly impossible to put it down! If most serious students try hard to understand Polansky’s theory, we will view health and environmental sciences in a whole new way. If most researches whose work involves chronic diseases read this and work to understand it, we’ll involuntarily begin to view and perhaps reshape our work through Dr. Polansky’s lenses. It is hard to see how much this theory will reshape our lives. On the chance that we may be seeing, inexactly, the face of future medicine, we should read the 543 pages of ‘Microcompetition with Foreign DNA and the Origin of Chronic Diseases,’ by H Polansky.”

You can find more reviews and the biographies of the scientists reacting to Dr. Polansky's discovery on the publisher's website at http://www.cbcd.net/.

Hope for Cure and Protection

Why is the discovery of the starved genes such great news? We are incredibly lucky that 95% of the cases start with starved genes, not injured genes. Today, we don't know how to fix injured genes. But we do know how to feed starved genes, at least in principle. If the National Cancer Institute will allocate a tiny fraction of its budget to develop the starved gene idea, we can be on our way towards a cure.

Summary

The significance of Dr. Polansky's discovery cannot be overstated. For the first time, we can start to feel a little better about cancer. With his discovery, pharmaceutical and biotech companies can now start to design medications that will target the cause of cancer rather than its symptoms, and therefore, cure the sick and protect the healthy from this deadly disease.

Want to help?

Send a letter to the Director of the National Cancer Institute (NCI), or to the Director of the National Institute of Health (NIH) demanding that they allocate funds for further research on the starved gene discovery. Without your letter, it might take years until the conservative NIH will respond to the discovery. 

John S. Boyd, Ph.D.
The Center for the Biology of Chronic Disease (see http://www.cbcd.net/) Rochester, NY

We are a 501(c)3 not-for-profit organization that specializes in researching the biology of chronic disease. By "the biology of chronic disease" we mean the original disruption that causes the disease, and the sequence of events that lead from the original disruption to the development of clinical symptoms. We hope that once the biology is clear, pharmaceutical and biotech companies will be able to formulate drugs that reverse the effects of the disruption, and therefore cure the disease, or even block the original disruption, and therefore prevent the disease from developing in healthy individuals.