The current belief in medical research holds that
cancer begins with a genetic mutation, in simple terms: with injured
genes. However, the huge effort and billions of dollars invested
by the National Institute of Health (NIH), private foundations, and
pharmaceutical companies in searching for injured, that is, mutated genes in cancer has
produced few discoveries and little benefits to the public. The reason for
this limited success is very simple. The genes in
the tumors of most cancer patients are not injured, they are completely healthy.
Hunting for Genetic Mutations and Cancer
A little background:
1. What is a gene? A gene is a creature that produces a protein, like a
football player who produces yards during games.
2. What are proteins? Proteins are the major building blocks of cells,
yards in our example.
3. What is a mutated gene? A mutated gene is an injured player. Very rarely a
mutation is beneficial to the organism (X-Men, Evolution, Lance
Armstrong?). In all other cases, the mutation is damaging the gene. Think
of the effect of a serious knee injury on our football player.
The current belief in medical research holds that most cancers are caused by exposure to carcinogens, and that carcinogens
begin the cancer process by injuring certain genes. This belief is so ingrained that the National Human Genome Research Institute (NHGRI), an institute at the NIH, recently stated that "all cancers are based on genetic mutations in body cells." Moreover, a search on PubMed, the search engine for scientific papers in life science, with the keywords "Mutation" AND "cancer" produced 86,490 papers and 12,238 reviews. Mutation hunting is also a big business. Look at the NIH budget allocated to discoveries of genetic mutations, the number of biotech companies chasing genetic mutations, the magnitude of the licensing agreements between biotech and pharmaceutical companies aimed to utilize newly discovered genetic mutations, and the number of stories in the media on genetic mutations and their so-called "link" to disease. However, this huge effort and billions of dollars has produced few discoveries and little benefits to the public.
And the public starts to react
to the continuing failure of the injured gene dogma. Examine the
level of tax payers funds allocated to the National Cancer Institute (NCI)
Until 2003, the public and
their representatives believed in the promise of the injured gene dogma,
and increased the NCI budget (note the green lines). But in 2003, the
public and Congress lost faith and started to cut back. Look at the
NCI budgets from 2004 to 2007, what a vote of no confidence in mainstream
The reason for this limited success
of the injured gene idea is simple.
The cause of most cancers is not a mutated gene.
The story of the BRCA1 gene is a typical example of mutation hunting.
The Mystery of BRCA1
Genes, in general, produce proteins, which are the building blocks of cells. The concentration of proteins is tightly regulated. A mutated or
injured gene produces an abnormal concentration of its protein, which may lead to disease. In 1994, Mark Skolnick, PhD, discovered the BRCA1 gene (BRCA1 is short for BReast CAncer
1). Following the discovery, scientists observed a low level of the BRCA1
protein in breast cancer tissues. This observation created a lot of excitement. At the time, scientists believed that they were on the verge of finding the cause of breast cancer. The reasoning was that breast cancer patients must have a mutated BRCA1 gene, which would explain the decreased production of the protein, and the
development of tumors.
In the United States, 180,000 cases of breast cancer are diagnosed each year. However, the BRCA1 gene is mutated in less than
5% of these cases.
In more than 95% of
breast cancer patients the gene is not mutated, the gene is not injured,
no scars, no limited motion, nothing.
So here is the mystery. If the gene is not mutated in the great majority
of the breast cancer patients, why are the tumors showing low levels of
the BRCA1 protein? The BRCA1 gene is not unique. Many normal (perfect
shape, non-mutated) genes exhibit a mysterious abnormal (increased or
decreased) production of proteins in cancer.
These observations prompted Dr. Raxit J. Jariwalla to conclude in his European Journal of Cancer paper
that "genetic alteration is not the initiating event of cancer." (Jariwalla RJ. Microcompetition and the origin of cancer. Eur
J Cancer. 2005 Jan;41(1):15-9)
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?
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
The infection with the latent virus is starving many genes, and as a result, it
is causing the development of many major 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
effect of the gene starvation caused by the latent viruses residing in
the adipocytes (or fat cells) of obese people, 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 major diseases.
This discovery was first described by Dr. Hanan Polansky in his highly
acclaimed "purple" book,
entitled "Microcompetition with Foreign DNA and the Origin of Chronic Disease."
The book was published by The Center for the Biology of Chronic Disease (more
on the book, including reviews of leading scientists, see on the
publisher's website at:
Dr. Hanan Polansky's highly acclaimed "purple"
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 latent virus that starves our genes.
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
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 many major 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 the major 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 the major diseases. The idea that viruses are the cause of some major 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 the treatment of many major diseases. 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 major 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 major 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 the major diseases. 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 the major diseases. 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
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.
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) requesting 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, or CBCD (see
http://www.cbcd.net/) Rochester, NY
The CBCD is a 501(c)3 not-for-profit organization that specializes in researching the biology of chronic disease.
"The biology of chronic disease" means the original disruption that causes the disease, and the sequence of events that
lead from the original disruption to the development of clinical symptoms. The CBCD hopes 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.
© 2013 All rights reserved