Major Breakthrough In The Understanding Of Cancer

Hunting for Genetic Mutations and Cancer

The current paradigm in medical analysis holds that the result in of most cancers is a genetic mutation. For instance, according to the National Human Genome Analysis Institute (NHGRI), an institute at the NIH, “all cancers are based on genetic mutations in body cells.” In truth, mutation hunting is large business. Just look at the NIH price range allocated to discoveries of genetic mutations, the quantity of biotech businesses chasing genetic mutations, the magnitude of the licensing agreements amongst biotech and pharmaceutical firms aimed to utilize newly found genetic mutations, and the number of stories in the media on genetic mutations and their so-named “link” to disease. However, this large work and billions of dollars has made handful of discoveries and little rewards to the public. The reason for this limited achievement is easy. The result in of cancer is not a genetic mutation.

The story of the BRCA1 gene is a typical instance of mutation hunting.

The Mystery of BRCA1

Genes, in common, create proteins, which are the constructing blocks of cells. The concentration of the protein is tightly regulated. A mutated gene produces an abnormal concentration of its protein, which might lead to disease. In 1994, Mark Skolnick, PhD, discovered the BRCA1 gene (BRCA1 is short for BReast CAncer 1). Following the discovery, scientists observed an abnormally low level of the BRCA1 protein in breast cancer tissues. The BRCA1 protein is a cell cycle suppressor, which implies that the protein prevents cell replication. This observation developed a lot of excitement. At the time, scientists believed that they had been on the verge of locating the result in of breast cancer. The reasoning was that breast cancer patients have to have a mutated BRCA1 gene, which would explain the decreased production of the protein, and the excessive replication of breast cancer cells in tumors.

In the United States, 180,000 circumstances of breast cancer are diagnosed each and every year. However, the BRCA1 gene is mutated in much less than 5% of these instances. In far more than 95% of breast cancer patients the gene is not mutated.

So here is the mystery. If the gene is not mutated in the wonderful majority of the breast cancer patients, why are the tumors showing low levels of the BRCA1 protein? Right now, this is one particular of the largest mysteries in cancer investigation.

The BRCA1 gene is not unique. A lot of normal (non-mutated) genes exhibit a mysterious abnormal (increased or decreased) production of proteins in cancer. Moreover, research also report abnormal gene expression of normal genes in other illnesses, such as atherosclerosis, obesity, osteoarthritis, variety II diabetes, alopecia, variety I diabetes, numerous sclerosis, asthma, lupus, thyroiditis, inflammatory bowel illness, rheumatoid arthritis, psoriasis, atopic dermatitis, and graft versus host illness.

According to Dr. Raxit J. Jariwalla in his paper published in the European Journal of Cancer (Jariwalla RJ. Microcompetition and the origin of cancer. Eur J Cancer. 2005 Jan41(1):15-9): “The prevalent view of the nature of cancer holds that it is a complex genetic process resulting from the progressive accumulation of mutations in certain cellular genes, such as proto-oncogenes or tumor-suppressor genes, leading to perturbations in processes involving signal transduction, cell cycle regulation, and/or apoptosis. Genetic instability in tumors has been known for decades, even so, the role of genomic instability in causing and advertising tumor growth remains controversial. Additionally, even though many studies report abnormal gene expression in cancer cells, typically, no mutations or chemical modifications are observed around the locus of the dysregulated gene(s), suggesting that a genetic alteration is not the initiating event of cancer“.

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 a viral gene on the production of cellular proteins?

Feel of a gene as an assembly line of a protein. Like all assembly lines, the gene has two components, a conveyor (the gene coding section), and a control panel (the gene promoter/enhancer). Imagine a cellular shop that assembles a product called BRCA1. 1 of the several buttons on the manage panel is called N-box. Pressing the button increases production. Nevertheless, only a modest quantity of operators (called transcription aspects), these who pass a unique certification (known as the p300 test), have permission to press this button. What occurs when a virus opens a shop across the street from the cellular shop (known as latent infection) to create its viral items? The manage panel in the viral shop also has an N-box button. To start off production, the virus begins to employ away some of the certified operators. What is the effect of this “hiring away” on the number of obtainable BRCA1 units? The number decreases. Furthermore, the lower becomes apparent even before the virus begins production (the “hiring away” is what creates the impact, not the viral proteins). The viral assembly line competes with the BRCA1 assembly line for the certified operators, and by hiring them away prevents the cellular shop from creating the optimum, or “healthful” quantity of BRCA1 units. The lower quantity of BRCA1 units leads to excessive cell replication and breast cancer. (See a more technical description in a recent paper published in the European Journal of Cancer.)

The infection with the latent virus causes abnormal production of other genes, and as a outcome, the development of other chronic diseases. This sequence of events effortlessly explains why individuals who suffer from obesity are also far more likely to suffer from diabetes, cancer, and heart illness, and why a current massive scale study identified that a low-fat diet does not safeguard against breast cancer. It also explains yet another surprising observation that male pattern baldness is linked with heart disease and prostate cancer. In general, this sequence of events simply explains the many observations indicating a co-existence or co-morbidity of some chronic illnesses.

This discovery was first described by Dr. Hanan Polansky in his book, Microcompetition with Foreign DNA and the Origin of Chronic Illness, published by The Center for the Biology of Chronic Disease.

In his European Journal of Cancer, Dr. Raxit J. Jariwalla reports an exciting observation on the microcompetition discovery: “The important point of the theory is that the competing DNA sequences do not bind each and every other but compete for binding to a limiting transcription complex. In the instance cited, the viral DNA and BRCA1 do not bind every single other but compete for binding to the limiting GABP*p300/cbp transcription complex. It is intriguing 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 get in touch with between molecules. In contrast, microcompetition with foreign DNA, which in essence is a reallocation of a rare resource, appear to draw on financial rather than physicochemical principles.”

To summarize: the result in of cancer, and other chronic diseases, is not a genetic mutation, it is a reallocation of scarce genetic resources brought on by the presence of latent viral DNA sequences (or other kinds of foreign DNA).

Reaction of the Scientific Community

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

Think about what the well-known heart surgeon and “Living Legend,” Michael E. DeBakey, said about the discovery, “The theory underlying the simple concept regarding the origin of chronic diseases presented by Dr. Polansky is most intriguing, indeed fascinating … Possibly a symposium could be held to provide a forum for additional discussions and critiques of this fascinating theory.”

Elena N. Naumova, PhD, Associate Professor, Division of Family Medicine and Community Health, Tufts University School of Medicine, stated, “Dr. Polansky’s operate compellingly demonstrates a framework that could bring together researchers from different fields. His proposed theory will function its magic by clarifying ambiguous definitions, identifying similarities and differences in a variety of biological processes, and discovering new pathways … I think that Dr. Polansky’s book will catalyze the scientific studying procedure, promote interdisciplinary cross-fertilization, stimulate improvement of treatment methods and drug discovery, and leave the reader inspired.”

Sivasubramanian Baskar, PhD, Senior Scientist from the National Cancer Institute, NIH, said, “At very first, I wish to congratulate Dr. Hanan Polansky for his scientific bravery to take such a unique, novel approach to further stimulate our understanding of the origin and establishment of chronic illnesses. The philosophy underscored is an outstanding 1 … The remarkable correlation among theoretical predictions and observed in vivo effects appears to bring us a step closer to a deeper understanding of such complex biologic processes.”

Marc Pouliot, PhD, Assistant Professor, Department of Anatomy and Physiology, Faculty of Medicine, Université Laval, Canada, mentioned, “The concept of microcompetition will adjust our strategy in the study of chronic diseases and will moreover give scientists a higher level of understanding in biology. Presentation of this idea undoubtedly offers a new set of opportunities for attacking chronic illnesses … They lead the way to new approaches in chronic disease remedy.”

Howard A. Young, PhD, Section Head, Cellular and Molecular Immunology Section, Laboratory of Experimental Immunology, National Cancer Institute, NIH, said, “In summary, Dr. Polansky is to be applauded for his try to give a unifying basis for chronic illnesses. His theories are stimulating and supply a basis for experimental testing and achievable remedy.”

Michael J. Gonzalez, PhD, Professor, Medical Sciences, University of Puerto Rico, mentioned, “I know this book will profoundly influence medical investigation, drug discovery, as nicely as natural therapies. I also believe it will benefit the scientific community and society in common by providing further implies of treatment for circumstances in which only palliative care is offered.”

You can locate much more reactions and the biographies the scientists reacting to Dr. Polansky’s discovery on the publisher’s site at

Hope for Remedy and Protection

The significance of Dr. Polansky’s discovery can not be overstated. For the initial time, we can begin to really feel a tiny far better about these illnesses. With his discovery, pharmaceutical and biotech businesses can now begin to style medicines that will target the result in of the illness rather than its symptoms, and for that reason, remedy the sick and defend the healthful from these deadly illnesses.