What is Cancer ?

What Is Cancer ?

By Professor Serge Jurasunas

This is a good question since the disease today has already reached an alarming proportion. Who doesn't have a friend or relative diagnosed with cancer, who is either sick or dying? It causes pain and suffering and despite the repeated expectation by medicine to cure cancer it is a complete failure, even for many oncology doctors who have yet to find an answer or somewhere else to turn?

First of all, cancer is not a new disease, since the earliest known description of a tumor appears in several Egyptian papyri , discovered late in the 19th century. Two of them are well known, the Ebers  medical papyrus (Herbs and Incantations)  and the Edwin Smith papyrus (Surgical document from the  16-17 Dynasties) were written around 1600 BC and are believed to date from sources as early as 2500 BC.

The word cancer was originally coined by Hippocrates who referred to the tumor by calling it Karkinos or crab in the Greek language, meaning a swelling masse that can penetrate into tissue. Later on, the Roman encyclopaedist Celsus, in De Medicina, translated Karkinos into the Latin word cancer. Today just to hear, “You have cancer,” creates a state of fear among people.

So what is cancer? Answer: A local disease, a cellular disease or also a whole disease? Cancer is a multi-factorial disease but particularly a cellular disease caused by a number of aggressive exogenous and endogenous factors and a deficient defense and cellular mechanism that sometimes come with hereditary risk. The more people you have in your family with cancer, the higher is the risk to develop a cancer or tumor. Today new lines of research show that Cancer is a disease of the cell cycle and failure of checkpoint and of apoptosis, called natural programmed cell death. Before a cell divides the DNA is checked to make sure it has replicated correctly. If the DNA does not copy itself correctly, or cells divide incorrectly then a gene mutation can occur. Abnormal cells are promptly eliminated by this mechanism that is activated by the P53 tumor suppressor gene. One particularity of cancer cells is their refusal to die, thus escaping from apoptosis because of the failure of the tumor suppressor genes controlling cell cycle and apoptosis. P53 mutation occurs in more than 50% of all cancer and appears necessary in many types of cancer. Not only does P53 mutation impair the destruction of abnormal/cancer cells but also acquires as we say oncogenic properties that activate tumor growth and invasion.

What Can Cause Mutation?

Answer: Radiation, tobacco, pollutants, insecticides, chemicals, viruses and bacteria. There are four important letters that make up the entire 3 billion letter genetic code and they are Adenine,Thymine, Guanine, Cysteine or ATGC. Any change or error in the position of the four letters lead to DNA mutation (P53 mutation) and starts to disrupt the cell cycle. Radiation, excessive oxidative stress can damage the DNA components and conducts to mutations.

How Does a Cancer Start?

Answer: Damaged cells not destroyed continue to divide, accumulate mutations, become less differentiated and do not respond anymore to cell signaling pathways. They then become independent and turn into cancer cells that start to proliferate, build more blood vessels for growth, utilizing degradation enzymes to expand and invade surrounding tissues. Some cancer cells detach from the primary tumor through loss of adhesion and penetrate into the blood or lymphatic circulation, what we call metastasis (meaning I am here but not here anymore) and establish secondary tumors at other locations in the body such as the liver, lung, brain and bones, depending on the type of cancer. After a period of dormancy cancer cells awaken and try to form a new tumor after a lapse of time from 6 months to 6-10 years and even more. I even have a case of breast cancer with a recurrence to the lungs, bones and brain after 15 years of dormancy. It depends on the dormancy state and the capacity of the cancer cells to build new blood vessel called angiogenesis, apoptotic failure and also immune defense failure.

Development of Cancer over Time

Cancer metastasis prevention is totally neglected by oncology. Metastasis is becoming a danger and responsible for 90% of cancer mortality. Today's hallmark of cancer is reportorial, representing the essential factors of cancer development and growth which includes P53 failure, angiogenesis, activation of oncogenes, failure of the immune defense, hypoxia and oxidative stress. Without tumor suppressor failure, activated oncogenes and especially tumor vascularization cancer is not possible.

The immune system, particularly the Natural Killer cells (NK-cells) play a crucial role in our defense against cancer but of course only are activated when cancer cells are circulating or to attack a tumor. They are known as our first line of defense against cancer. However we know that patients with cancer have a reduced N.K cell activity functioning only from 10-50% in comparison of a healthy person. Oncology continues to neglect this, however recently some limited articles are speaking about a new revolutionary treatment called 'Immuno-Oncology' to improve the standard treatment, which fact is what my colleagues and I have already been doing for the past several decades. Other new attractive future treatments are pointing to reactivating the apoptotic genes like the P53 tumor suppressor gene which I personally had already worked on for the past 10 years.

The Mechanism of Cancer

The mechanism of cancer is very complex since it takes an average of about 7-14 years for tumor to reach the clinical stage of 1cm, but grows faster for every additional cm. This means that we have a mechanism of cancer going on but we don't know its happening, then patients are often diagnosed at a later stage already having developed multiple metastases to the bones, liver and even the lungs. Why? Because the initiation of cancer and metastases invasion is asymptomatic since the process of initiation, growth and development is done in silence. Cancer cells first start to multiply and divide so as to make 2 cancer cells, then 4,8, then 16,32,64, and then exponentially to 128, 256 onward. Just realize that three quarters of the existence of a tumor remains undiscovered before the clinical stage. But one other important complexity of a malignant tumor is that within the same tumor, cancer cells may be differentiated from each other. Some cancer cells may have a high index of mutation while others have a different growth speed cycle (10-20-30 hours) and thus divide differently. Other cancer cells may even enter in the GO dormant phase of the cell cycle, do not divide anymore and are protected from destruction by chemotherapy drugs which target cancer cells only when they divide quickly. The cancer cells with slow division are not sensitive to chemotherapy even in the same tumor. This is why chemotherapy is inefficient on lung cancer since these cancer cells divide very slowly.

During dormancy in the GO phase cancer cells active their repair mechanism and become more resistant when they reenter the cycle sometime after not been destroyed by chemotherapy. This is why during chemotherapy cancer cells can spread even faster. Instead of improving patients get worse. This is what happens after a remission where many cancer cells enter into dormancy and then restart their cycle after few months or a few years to form a new tumor. However it has been shown that breast cancer recurrence for instance is associated with an immune deficiency, where often there is a failure or mutation of the P53 gene, mostly from bad dietary style and oxidative stress. Therefore some cancer cells may respond to apoptosis stimuli and be destroyed but others are more resistant, do not respond to chemotherapy and continue to divide. After being damaged they accumulate more mutations and become even more aggressive. This is more less the molecular basis of cancer that of course needs more details to explain, since a myriad of genes (oncogenes) is associates with certain cancers, cancer stage or metastasis cancer when they are activated, but you can view some of my lectures such as, “How to Understand and Treat Cancer from a Molecular Basis” or “Integrative Cancer”, both available on Slideshare, www.slideshare.net/sheldonstein .

Often it makes a difference between a tumor diagnosed with no metastases or a tumor already with multiple metastases. These genes or oncogenes can be targeted using dietary active compounds such as Transforming Growth Factor Beta (TGF.B), involved in many cellular processes including cell growth, cell differentiation and apoptosis, but when upregulated may to the contrary inhibit apoptosis and immune response and associate with metastasis invasion. C-Myc is an oncogene that normally plays a role in cell cycle progression and apoptosis but is often overexpressed or mutated in many cancers associated with metastasis and disease recurrence. The P53 tumor suppressor gene is part of a network that involves the function of many genes like TGF-B, Ras, Pten, C-Myc, while the mutation of P53 disrupts the other genes that start to be overexpressed, which is why we say that mutant P53 has a oncogenic function and not only associated with a failure of apoptosis.

One other example is the inhibition of apoptosis by survivin, a new inhibitor of apoptosis that is overexpressed in many cancers such breast and prostate that increases survival in cancer cells. Usually survivin expression is detected only in cancer tissue but not in healthy tissue and therefore is considered as a cancer Biomarker. The percentage of survivin-positive patients (and level of proteins) within the same tumor series is variable, ranging from 30-100%. This reflects the genetic heterogeneity of individual tumors and complexity of the disease, showing that each patient is an individual and therefore needs personalized treatment. In my clinic I can observe in similar types of breast cancer or prostate cancer the same overexpressed survivin proteins from a middle to very high level which in this case is an unfavorable marker of disease progression. We have also detected very early prostate cancer in patients with a high level of survivin proteins in their blood and treated them successfully without undergoing surgery and chemotherapy. We have also detected a very high level of survivin in breast disease recurrence along with a poor response to chemotherapy. Over the years we have accumulated enough experience with a variety of dietary active compounds to reduce or totally eliminate survivin activity and thus increase apoptosis and destruction of cancer cells by chemotherapy. I have offered many other examples in some of my lectures available on slideshare.

But of course there is another hypothesis or set of causative factors that associates with cancers such as mitochondrial and ATP energy failure, along with the breakdown of the cellular respiration caused by mitochondrial component damage and mtDNA mutation from an excess of endogenous free radicals and pollutants. ATP energy is essential for all cellular functions including cell differentiation, apoptosis and even to activate the immune system. Cell division and differentiation is 60% controlled by three DNA genomes and remaining 40% is controlled by the mitochondrial genome that drives the early cell division and differentiation cell performance. Meaning the decreasing ATP energy from a cancer phenotype means less differentiation as well as abnormal cells turning more and more into cancer cells. So it may be reasonable to say that cellular DNA mutation may be a secondary result of the primary process of mitochondrial dysfunction. It's important also to remember that apoptosis is driven by the mitochondria and not by the cell itself that only triggers the signal through the P53 gene, which in turn activates the pro-apoptotic gene Bax. Bax penetrates the mitochondria through the membrane and activates an enzyme called Cytochrome C, that's also released through the pore of the membrane in the Cytosol activating the apoptosis mechanism by further activating a family of proteins called Caspases. Survivin the IAP (Inhibitor of apoptosis) that I described above inhibits Caspases activity and counters the death of cancer cells by apoptosis. Therefore the membrane of mitochondria also plays a crucial role in the mechanism of apoptosis.

Cancer is a Disease of the Cellular Cycle

Thus cancer is both a disease of the cellular cycle but also of mitochondrial failure. See my articles,“Mitochondria and Cancer” and “The Clinical Evidence of Cellular Respiration to Target Cancer”, both available online. Consider further that the auto-intoxication and inflammation of the Extra Cellular Matrix is associated with tumorigenesis. A state of auto-intoxication and high oxidative stress triggers a chronic inflammation that modifies the fluid consistency of the ECM, causing an edema that leads to a total blockage of nearly all the exchange procedures between the body and the epithelial cells and pushes an abnormal cell with a genetic instability to become a cancer cell. In my new book, “ Health and Disease Begin in the Colon”, is not only about the colon but includes many other interesting chapters associated with cancer where I fully describe how auto-intoxication of the ECM can lead to cancer.

Today we know that the micro-environment plays a key role in tumor growth. We know that cancer cells are not isolated but are influenced by the condition of the micro-environment, even when tumor needs blood vessels in order to grow and expand. The tumor uses growth factors available in the micro-environment to attract blood vessels. In another one of my lectures, “The Biological Approach to Breast Cancer”, I present the relationship between the tumor and the micro-environment. Furthermore, inflammation of surrounding tissue in turn stimulates the further growth of a cancerous tumor which is associated with bad ground and bad inflammatory foods. We need to understand dietary style and detoxifying the body, especially the colon may be a key protection against cancer. Diet accounts for 30-40% of cancers. Industrial food is associated with higher cancer risk and will even rise in the future. Pollution and environmental toxins are also largely implicated, especially insecticides which are associated with breast and brain cancers. Scientists in the USA found a footprint of insecticides on the P53 gene located in chromosome 17 of the cell, which offers more proof of the implication of insecticides in causing cancer. We can discuss more about molecular medicine and a cell's DNA, but further ask, what makes a good cell? This depends on our food, our oxygen supply circulating in the blood, having blood free of toxins, pollutants and bacteria, which also depends on having a good immune system. So we need a clean colon and to prevent auto-intoxication of the colon. This is also an important step that we often forget about that I describe in my book. You'll never find a cancer patient especially in women without intestinal dysfunction and chronic constipation or patients not having nutritional deficiency and intoxicated blood.

Cell Cycle and Cancer

Excess industrial foods, toxins and stress reduce the activity of the immune system which is supposed to protect us from cancer. In the year 1900, 1 person out of 100 developed the risk of cancer, but today we have reached 1 person out of 3, while soon 1 in 2 will develop a cancer. While enormous progress has been done in the discovery of new mechanisms such the cell cycle, tumor suppressor genes, hundreds of recent articles focusing on new attractive treatments, it's still only in the theoretical phase and not yet a clinical application since the cornerstone of medicine is only concentrated on research and development for new treatments of chemotherapy with hundreds of millions of dollars invested, but in return for billions of dollars of profit.

Little research has been done on the preventive and therapeutic value of food against cancer, yet we know that many foods and dietary compounds can change genetic expression such as in brain and prostate cancer, where cruciferous vegetables, selenium, zinc, flax seed, vitamin D and chlorella extract offer increased protection against cancer or may be used together with conventional therapy for better results. We have to learn how to influence our internal landscape and not open the door to cancer.

Today a new science called Epigenetics suggests that many cancers may not be caused solely by mutations in genes but by changes in how the genes function. They can work faster or more slowly. Environmental toxins are mostly implicated in Epigenetic change, particularly the example of the P53 that I mentioned with a footprint of insecticides. The gene is shut down not only by mutation but they do not produce P53 protein. This is what I have often observed from the testing I have done on my cancer patients. Some have a totally inactive P53 without P53 protein, while others harbor mutated P53. The epigenetic transformation can be transmitted through several generations and with no surprise this new generation is much more vulnerable. Suppressed or mutated P53 is transmitted to our descendants who are already born with a deficient or mutated P53, already on the way to cancer. We need more attention from pediatric doctors caring for our children. This disease can also arise much later especially if we keep our bad life style where their parents think they are healthy or have healthy children. However this interaction between genes and the environment can also affect a number of susceptible persons, while others remain unaffected.

However my book gives all the details about the theory of cancer, about Epigenetics and the environment, how food can modulate our genes, the role of the P53 tumor suppressor gene and also about mitochondria and their implication in cancer. It especially offers the reader full details about diet, about food, juice combinations and especially about how to detoxify the body and the colon, so you can be more healthy and have a better chance to prevent cancer.

www.sergejurasunas.com

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