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The current paradigm in curative investigate holds that the cause of most cancers is a genetic mutation. For instance, according to the National Human Genome investigate create (Nhgri), an create at the Nih, "all cancers are based on genetic mutations in body cells." In fact, mutation hunting is big business. Just look at the Nih allocation allocated to discoveries of genetic mutations, the amount of biotech fellowships chasing genetic mutations, the magnitude of the licensing agreements in the middle of biotech and pharmaceutical fellowships aimed to apply newly discovered genetic mutations, and the amount of stories in the media on genetic mutations and their so-called "link" to disease. However, this huge endeavor and billions of dollars has produced few discoveries and little benefits to the public. The fancy for this little success is simple. The cause of cancer is not a genetic mutation.
The story of the Brca1 gene is a typical example of mutation hunting.
The mystery of Brca1
Genes, in general, furnish proteins, which are the building blocks of cells. The concentration of the protein is tightly regulated. A mutated 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 an abnormally low level of the Brca1 protein in breast cancer tissues. The Brca1 protein is a cell cycle suppressor, which means that the protein prevents cell replication. This consideration created a lot of excitement. At the time, scientists believed that they were on the verge of looking the cause of breast cancer. The mental was that breast cancer patients must have a mutated Brca1 gene, which would clarify the decreased production of the protein, and the inordinate replication of breast cancer cells in 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.
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? Today, this is one of the biggest mysteries in cancer research.
The Brca1 gene is not unique. Many normal (non-mutated) genes exhibit a mysterious abnormal (increased or decreased) production of proteins in cancer. Moreover, studies also article abnormal gene expression of normal genes in other diseases, such as atherosclerosis, obesity, osteoarthritis, type Ii diabetes, alopecia, type I diabetes, multiple sclerosis, asthma, lupus, thyroiditis, inflammatory bowel disease, rheumatoid arthritis, psoriasis, atopic dermatitis, and graft versus host disease.
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 Jan;41(1):15-9): "The prevalent view of the nature of cancer holds that it is a complicated genetic process resulting from the progressive accumulation of mutations in definite cellular genes, such as proto-oncogenes or tumor-suppressor genes, important to perturbations in processes consuming signal transduction, cell cycle regulation, and/or apoptosis. Genetic instability in tumors has been known for decades, however, the role of genomic instability in causing and promoting tumor growth remains controversial. Furthermore, although many studies article abnormal gene expression in cancer cells, often, 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 resolve in the nucleus of the host cell and use the cell machinery to replicate. What is the ensue of a viral gene on the production of cellular proteins?
Think of a gene as an assembly line of a protein. Like all assembly lines, the gene has two parts, a conveyor (the gene coding section), and a control panel (the gene promoter/enhancer). Imagine a cellular shop that assembles a goods called Brca1. One of the many buttons on the control panel is called N-box. Pressing the button increases production. However, only a small amount of operators (called transcription factors), those who pass a extra certification (called the p300 test), have permission to press this button. What happens when a virus opens a shop across the road from the cellular shop (called latent infection) to furnish its viral products? The control panel in the viral shop also has an N-box button. To start production, the virus begins to hire away some of the certified operators. What is the ensue of this "hiring away" on the amount of available Brca1 units? The amount decreases. Moreover, the decrease becomes apparent even before the virus starts production (the "hiring away" is what creates the effect, 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 producing the optimum, or "healthy" amount of Brca1 units. The lower amount of Brca1 units leads to inordinate cell replication and breast cancer. (See a more technical article 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 result, the development of other lasting diseases. This sequence of events easily explains why people who suffer from obesity are also more likely to suffer from diabetes, cancer, and heart disease, and why a recent large scale study found that a low-fat diet does not safe against breast cancer. It also explains someone else surprising consideration that male pattern baldness is related 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 lasting diseases.
This discovery was first described by Dr. Hanan Polansky in his book, Microcompetition with Foreign Dna and the Origin of lasting Disease, published by The town for the Biology of lasting Disease.
In his European Journal of Cancer, Dr. Raxit J. Jariwalla reports an consuming consideration on the microcompetition discovery: "The key point of the theory is that the contentious 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 consuming that when explaining observations reported in the literature, biologist tend to rely on the primary physicochemical religious doctrine which centers on binding/non-binding events, or bodily touch in the middle of 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: the cause of cancer, and other lasting diseases, is not a genetic mutation, it is a reallocation of scarce genetic resources caused by the presence of latent viral Dna sequences (or other types of foreign Dna).
Reaction of the Scientific Community
What is the scientific community saying about Dr. Polansky's discovery?
Consider what the notable heart surgeon and "Living Legend," Michael E. DeBakey, said about the discovery, "The theory basal the basic conception concerning the origin of lasting diseases presented by Dr. Polansky is most interesting, easily consuming ... Maybe a symposium could be held to provide a forum for added discussions and critiques of this consuming theory."
Elena N. Naumova, PhD, associate Professor, branch of family rehabilitation and community Health, Tufts University School of Medicine, said, "Dr. Polansky's work compellingly demonstrates a framework that could bring together researchers from distinct fields. His proposed theory will work its magic by clarifying ambiguous definitions, identifying similarities and differences in discrete biological processes, and discovering new pathways ... I believe that Dr. Polansky's book will catalyze the scientific studying process, promote interdisciplinary cross-fertilization, stimulate development of rehabilitation strategies and drug discovery, and leave the reader inspired."
Sivasubramanian Baskar, PhD, Senior Scientist from the National Cancer Institute, Nih, said, "At first, I wish to congratulate Dr. Hanan Polansky for his scientific bravery to take such a unique, novel arrival to added stimulate our comprehension of the origin and establishment of lasting diseases. The religious doctrine underscored is an exquisite one ... The remarkable correlation in the middle of theoretical predictions and observed in vivo effects seems to bring us a step closer to a deeper comprehension of such complicated biologic processes."
Marc Pouliot, PhD, Assistant Professor, branch of Anatomy and Physiology, Faculty of Medicine, Université Laval, Canada, said, "The conception of microcompetition will turn our arrival in the study of lasting diseases and will furthermore give scientists a higher level of comprehension in biology. Presentation of this conception easily provides a new set of opportunities for attacking lasting diseases ... They lead the way to new approaches in lasting disease treatment."
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 endeavor to provide a unifying basis for lasting diseases. His theories are stimulating and offer a basis for experimental testing and possible treatment."
Michael J. Gonzalez, PhD, Professor, curative Sciences, University of Puerto Rico, said, "I know this book will profoundly impact curative research, drug discovery, as well as natural therapies. I also believe it will advantage the scientific community and community in normal by providing added means of rehabilitation for conditions in which only palliative care is available."
You can find more reactions and the biographies the scientists reacting to Dr. Polansky's discovery on the publisher's website at http://www.cbcd.net/.
Hope for Cure and Protection
The significance of Dr. Polansky's discovery cannot be overstated. For the first time, we can start to feel a little great about these diseases. With his discovery, pharmaceutical and biotech fellowships can now start to create medications that will target the cause of the disease rather than its symptoms, and therefore, cure the sick and safe the healthy from these deadly diseases.
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