By: David Servanschreiber Md Phd

Genes account for at most 15% of cancers. What matters most in prevention or getting the most of treatments is not our genetic makeup but the biology we create within our body to support our natural defenses against tumor growth.


The Genetic Fallacy Most of us live with the false belief that cancer is a genetic Russian roulette. As one in three of us will die of cancer, the odds are indeed as bad -- worse actually -- than those of that dreadful game. But it is NOT genetic. A large Scandinavian study of identical twins (who share exactly the same genes) found that in the majority of cases they did not share the risk for cancer. In fact, the authors concluded, in the New England Journal of Medicine, that "inherited genetic factors make a minor contribution to susceptibility to most types of [cancers]. This finding indicates that the environment has the principal role in causing common cancers."

A New Approach to Cancer: Changing the Terrain When it comes to treating cancer, there is no alternative to conventional treatments: surgery, chemotherapy, radiotherapy, immunotherapy or, soon, molecular genetics.

However, these treatments target the tumor much like an army wages war: focusing all of its efforts on destroying the cancerous cells. Yet, it's as important to change the environment that supports the growth new cancer cells as it is to continue to pound them with targeted attacks.

We all need to learn to change the "terrain" -- our biology -- to make it as inhospitable as possible to cancer growth. As much for prevention as to increase the benefits of treatments.

The new model of cancer that has emerged from the last 10 years of research moves us away from genetics and squarely into the life-style factors that we can control.

Indeed, another New England Journal of Medicine study showed that people who were adopted at birth have the cancer risk of their adoptive parents rather than that of the parents who gave them their genes. At most, genetic factors contribute 15% to our cancer risk. What matters for 85% of cancers is what we do -- or do not do enough of -- with our life.

Since we all carry cancer cells in us, what determines whether we do develop cancer is to a large extent the balance between factors that promote cancer, and factors that help resist cancer.

Common promoters of cancer are:

* Cigarette smoke and more than two alcoholic beverages per day * Refined sugar and white flour * Omega-6 fatty acids and trans-fats (corn, soybean, sunflower and safflower oils, hydrogenated and partially hydrogenated vegetable oils) * A variety of chemical agents present in some foods and household products (parabens, phthalates, PVCs, pesticdes and herbicides) * Complete lack of physical activity * Responses to stress that lead to feelings of helplessness and persistent despair rather than a sense that one can help oneself or count on the support of others

Factors that slow down the growth of cancer are:

* Several phytochemicals contained in some fruits and some vegetables, some herbs and spices. * Omega-3 fatty acids (fatty fish, canola and flaxseed oil, flaxseeds, walnuts, some green vegetables) * Physical activity (at least 30 minutes of walking six times a week) * The ability to manage stress so as to avoid helplessness (emotional management through meditation or yoga or good psychotherapy) or benefiting from the support of intimate relationships, or both.

Knowing that genetics are only a minor contribution to cancer helps us realize how much is in our power to help our body be a stronger partner in nourishing life and resisting cancer.

David Servan-Schreiber, MD, PhD, is a clinical professor of psychiatry at the University of Pittsburgh School of Medicine and cofounder of the Center for Integrative Medicine. He lives in Pittsburgh, Pennsylvania, and Paris, France. He has been a cancer survivor for 16 years, and is the author of the International Best-Seller Anticancer: A New Way of Life, coming from Viking September 2008.

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One of the causes of cancer is abnormal genes. Cancer causing genes are called oncogenes and genes that prevent cancer are called tumor suppressor genes. Cancers can occur when the normal genes are not functioning normally. Genes, as you know, are the blueprints to the body. They tell a cell what it will be and what it will do. We could not function if the process did not run well. There is a system in place that is designed to keep good genes running and suppress bad genes. This process is called epigenetics.

Epigenetic changes are modifications to the genome that are heritable during cell division but do not involve a change in DNA sequence. Expression of genes is not regulated by the DNA sequence, which is the same in every cell, but by epigenetic marking and packaging. This process regulates chromatin structure through DNA methylation, histone variants, post-translational modifications, nucleosome positioning factors or chromatin loop and domain organization.

How can this cause cancer? Well, if a tumor suppressor gene is abnormally turned off, or an oncogene is turned on, then cancer (carcinogenesis) can occur. One key is a chemical change to the DNA called methylation. First, we need to define the process to make it clearer.

DNA contains four bases: adenine, guanine, cytosine, thymidine, but there is a fifth base methylated cytosine. DNA methyl-transferase (DNMT) produces methyl-cytosine where cytosines precede guanine (CpG). The CpG areas are not symmetric but clustered in CpG islands located at promoter regions. The promoter region is the region at the beginning of a gene and it controls the start of gene transcription. If the promoter is off, then the gene never is expressed.

Abnormal methylation in cancer has been known for 20 years. Hypo-methylated areas turn on normally silent areas such as virally inserted genes or inactive X-linked genes. Hyper-methylated areas silence tumor suppresser genes.

We know that cancers have abnormal levels of methylation and we know foods can help prevent cancers. Is there a link between foods and epigenetics? Yes!

The study of food nutrients and their effect on disease through epigenetics is known as nutrigenomics. This is a growing field, in fact, it is exploding. A Google search for the term nutrigenomics produces 127,000 entries.

Epidemiologic studies suggest there are bad foods and good foods. BAD: red meat, processed meat, grilled meat, dairy, animal fat, partially hydrogenated fats. Good: Fish, fruits, vegetables, tree nuts, omega-3 fatty acids, whole grains.

You can study the epigenetic effects of bad or good foods. I'm going to talk about some of the cancer preventing foods and how their mechanisms include epigenetic effects.

Foods with epigenetic effects include green tea, cruciferous vegetables, and grapes. Usually we hear about antioxidants and foods. Antioxidants are important but there are beneficial substances in foods called polyphenols which can affect genes. Of the polyphenols, different forms exist but flavonoids are the most highly cited for health benefits and are found in a variety of vegetables and fruits. Types of flavonoids include flavanols in tea, isothiocyanate in cruciferous vegetables, anthocyanidins in grapes and berries, flavonone in citrus fruits, flavonols in onions, isoflavones (genistein) in soy.

All tea contains polyphenols, but the highest levels are in green and white tea. Green tea has been well studied and appears to have anti-cancer benefits. In China, green tea drinkers are 50% less likely to develop gastric or esophageal cancer (Carcin 2002; 23 (9): 1497), and 2 cups daily added to topical tea extract reversed oral leukoplakia (J. Nutri Biochem 2001; 12 (7): 404).

Green tea has powerful antioxidant effects but it also helps to balance normal methylation in DNA. In fact, one study in esophageal cancer cells demonstrated that EGCG from green tea is able to turn on tumor suppressor genes that had been chemically silenced by methylation (Cancer Research 2003;63:7563).

Cruciferous vegetables include broccoli, cauliflower, kale, Bok choi and their anti-cancer effects have been demonstrated in epidemiologic studies. These powerful vegetables not only induce enzymes that break down carcinogens but they also inhibit DNA methylation allowing tumor suppressor genes to thrive. Inhibiting abnormal methylation also helps cruciferous vegetables to inhibit the cancer causing action of tobacco smoke by preventing the formation of nitrosamine-DNA adducts.

Grapes, which contain reserveratrol, are excellent for heart health and they have anti-cancer activity. Grapes work by preventing the formation or initiation and promotion of cancers. They don't have methylating actions as discussed above but they work by modulation histones.

Histones are the chief protein component of the DNA chain (chromatin). They act as spools for the DNA to wind around which then shortens the length of the DNA to 30,000 times shorter than an unwrapped strand. This process not only allows the long DNA chain to fit into a cell but also plays a role in gene expression because how the genes are wound affects which are exposed and available for turning on or off. Rolling the spool a different way would expose other genes and change their expression.

Histones are modified after translation by acetylation, methylation, phosphorylation, ubiquitination. The changes occur at lysine residues (except for phosphorylation of serine or threonine). When the histone is acetylated the charge is changed and the histone loosens its grip on the DNA strand and the DNA unwinds, exposing the genes to be transcribed, or repaired.

When histone tails (H3,H4) are acetylated, genes are transcribed, when they are deacetylated, genes are turned off. Histone deacetylases work to maintain deacetylated sites.

Resveratrol, found in grapes, activates Sirtuins; SirT1 (Sir2 proteins). There are at least 7 Sir2-like proteins and they are histone deacetylators. Sirtuins are induced in animals during starvation states. They seem to have a life preservation effect. Interestingly, when an animal is starved, it can live longer. When the calorie intake of rodents was decreased by 40% in rodents, they actually lived 50% longer and appear to have fewer chronic diseases. The same benefit occurs when rodents when they are given resveratrol in their diet.

Resveratrol deacetylates histones causing tighter packing of the chromatin and a lower level of transcription of DNA. This silencing of the DNA is thought to be the mechanism of life prolongation, heart health, and its beneficial actions to prevent cancers. This is why grapes or red wine is beneficial to your health. How much red wine should you drink? No one knows for sure, but any beneficial effects might be negated after two glasses a day because of the alcohol. I wouldn't advise drinking more than this until more is known. The data is very promising, but more research is needed.

Our knowledge of disease expanded in the genomic era due to the human genome project but the study of genes is not enough. Epigenetics is a very important and complicated concept that helps explain how genes are turned on or off. As more studies are completed we will be able to unlock the mechanisms to diseases and produce new therapies that could turn off bad genes and turn on good genes. More importantly, these studies will demonstrate how foods affect your genes and can prevent or reverse diseases or cancers. Nutrigenomics, the study of how food chemicals (nutrients) affect genes, is a growing field and promises to change the way we look at and eat our meals. Some of the most beneficial foods include green tea, cruciferous vegetables and grapes, but don't stop there. The more fruits and vegetables the better when it comes to your health.

Robert Avery MD, is a practicing oncologist in the St. Louis area. He has a keen interest not only in cancer care and therapy but also nutrition and how is helps prevent cancer. He is owner of Citrine Sun, an online company dedicated to helping cancer patients through every stage of their illness through education and natural supplements. An interesting newsletter and information about helpful supplements are available at his website, http://www.citrinesun.com Contact Dr. Avery through his email, AskDrAvery@citrinesun.com

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By Jane Patrick

In a statement released by the National Institutes of Health, a team made up of National Human Genome Research Institute and National Institutes of Health scientists have announced that through an effort to map the genomic changes found in lung cancer, they have discovered a gene alteration that had not been connected to any type of cancer.

"This view of the lung cancer genome is unprecedented, both in its breadth and depth," said senior author Matthew Meyerson, M.D., Ph.D., a senior associate member of the Broad Institute of MIT and Harvard in Cambridge, Mass., and an associate professor at Dana-Farber Cancer Institute and Harvard Medical School in Boston. "It lays an essential foundation, and has already pinpointed an important gene that controls the growth of lung cells. This information offers crucial inroads to the biology of lung cancer and will help shape new strategies for cancer diagnosis and therapy."

Over one million individuals die each year from lung cancer. 150,000 of those are in the U.S. Lung cancer is the leading cause of cancer death in the U.S., and it kills more women than breast cancer. A fact that very few women realize due to the publicity of breast cancer. Lung cancer is not as well publicized, and because of the smoking issue attached to it, many do not like to talk about it. Lung adenocarcinoma, which is the lung cancer that is diagnosed most frequently, was the focus of the study.

The researchers discovered 57 genomic changes that happen often in lung cancer patients. Over 40 of the changes are connected to genes never before associated with lung adenocarcinoma. With more research scientists should be able to identify the genes. At the moment the scientists are just happy about the possibility that the discovery could lead to more ways of stopping the cancer.

"This outstanding work clearly demonstrates the value of comprehensive approaches for exploring the genomic underpinnings of cancer. The impacts of these findings extend far beyond lung cancer and indicate that many more important cancer-related genes still await our discovery," NHGRI Director Francis S. Collins, M.D., Ph.D. "Now, we must forge ahead and apply this strategy as quickly as possible to other common types of cancer."

During the study, one of the genes discovered to be associated was found to actually influence growth of cancer in cells. This discovery could lead to certain types of medication that could affect many types of cancers.The study group is laying the ground work for larger scale cancer projects that might be started in the future, including The Cancer Genome Atlas.

Study Identifies Novel Gene Alterations in Lung Cancer, National Institute of Health

Jane Patrick, Lung Cancer Still Kills More Than Breast Cancer, Associated Content

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By: Radoslaw Pilarski

The demise of cells by programmed cell death referred to as apoptosis, a Greek word that means “dropping off“ or “falling off“ as in leaves from a tree, has been recently a topic of intense interest in biomedical sciences. Apoptosis is a well-defined sequence of morphological changes of cells that shrink and condense and then fragment, releasing small membrane-bound apoptotic bodies, which are phagocytosed by other cells. Importantly, the intracellular constituents are not released into the extracellular milieu where they might have deleterious effects on neighboring cells. On the contrary, cells that die in response to tissue damage or other reasons exhibit very different morphological changes generally called necrosis. The cells that undergo this process swell and burst, releasing their intracellular contents, which can damage surrounding cells and often cause inflammation. Apoptosis refers to a particular morphology in which a chromatin condenses or coalesces to a heterochromatin in one or more masses in the nucleus. It usually settles along still-intact nuclear membrane referred to as margination of the chromatin. One of the essential functions of apoptosis is the elimination of cells in which DNA damages, faulty proliferation or improper adhesion to extracellular matrix that cannot be repaired. In cancer cells, the mechanism of apoptosis induction is broken. Therefore, more and more ideas and hypotheses for selective inducing apoptosis in cancer cells are tested in a growing number of laboratories all over the world. The subject of programmed cell death has been recently discussed in almost 80 000 publications. As it is known, cell apoptosis may be induced by various stress factors (e.g. hypoxia, expression of oncogenes, mutations, DNA damages). On the other hand, apoptosis may be induced via internal or external signals, for instance proteins. Some of such endogenous and exogenous proapoptotic proteins have been found and described. Their genes may be used in modern anticancer therapies.

For example, introducing into cancer cells proapoptotic genes as Bax, Bcl-X5 or E2F-1 significantly increases induction of apoptosis. Some clinical trials concern therapeutic application of a 121-amino acids apoptin originated from chicken anemia virus (CAV). Recent data suggest that apoptosis induced by this protein involves caspases, a family of cysteinyl aspartate-specific proteinases. In vitro results show that apoptin is very active against cancer cells without inducing toxicity to normal cells. This tumor-specific effect may be explained by the nuclear localization of the protein in tumor cells required for its action. Moreover, apoptin is equally active, such as p53-mutant, Bcl-2-overexpressing or BCR-ABL-expressing tumor cells. Other investigations showed that E4orf4 induces apoptosis in cancer cells by linking with 2A (PP2A) phosphatase. Unfortunately, induction of apoptosis by introducing genes encoding proapoptotic proteins has been little known.

One possible mechanism is associated with destruction of mitochondrial membranes and, in consequence, disturbing electrons transport, oxidative phosphorylation and ATP synthesis. Finally, the cell dies but the death is slightly different than that during typical apoptosis induced by caspases due to prolonged time of this process.

Proapoptotic proteins cannot be directly introduced to cancer cells because there are no specific receptors. They are transported through membranes in complexes by special fusion proteins called ligands. Other method is introducing them as genes by vectors and this approach has been already successfully applied. Clinical trials are presently underway to test efficiency of new apoptosis-triggering drugs. A large number of adenoviral agents are being constructed, including replication-incompetent and replication-selective oncolytic adenoviruses. One of them is ONYX-015, a replication-competent virus genetically engineered to selectively replicate in and lyse p53-deficient cancer cells. Other agent, INGN 201, was shown to deliver a p53 expression.

Preclinical studies in human cell lines and animals with head and neck cancers have shown that the p53 gene is transcribed and translated into p53 protein. Respectively, 5% and 58% of patients receiving three intratumoral injections of INGN 201 in conjunction with radiation therapy for over 6 weeks were shown to have achieved complete and partial responses. Other example may be a gene encoding the proapoptotic Vpr protein that was successfully transferred into cancer cells by the HIV-1 virion. These agents are introduced by intravascular infusion or intratumoral or epitumoral injections. An example of a target therapy against cancer is an intravenous administration of liposomal form of tretinoin (ATRA). Treatment of acute promyelocytic leukemia (APL) with ATRA alone or in combination with chemotherapy results in an almost complete remission rate as high as 85% to 95%.

Other proapoptotic anticancer therapeutics is Genasense developed by the Genta Company. Genasense is a phosphothioate oligonucleotide consisting of 18 modified DNA bases. First, the single-stranded DNA molecule must be incorporated into a cancer cell and then target the mRNA by having a complementary sequence to it.

This drug inhibits the production of a protein known as Bcl-2 that is widely expressed in many types of cancer. This up-regulation of Bcl-2 blocks the release of cytochrome C from the mitochondria thereby preventing apoptosis. Furthermore, Bcl-2 appears to be a major contributor to both inherent and acquired resistance to current anticancer treatments. By inhibiting production of Bcl-2, Genasense enables the cancer cells to be killed by apoptosis when treated with current state of the art therapy. Interesting apoptosis-inducing drug is Velcade jointly developed by NCI and Millenium Pharmaceuticals. Activity of Velcade is mainly associated with reversible inhibition of the proteasome and building up many proteins including BAX. In the normal cells, the BAX protein induces apoptosis by blocking the activity of Bcl-2. When BAX level increases, BAX inhibition of Bcl-2 also increases and the cells undergo apoptosis. Non-clinical studies have demonstrated that cancer cells are more sensitive to the effects of the proteasome inhibition than normal cells.

Selected references

Adachi, S.L.L., Carson, D.A., Nakahata, T., 2004. Apoptosis induced by molecular targeting therapy in hematological malignancies. Acta Haematologica 111, 107-123.
Ferreira, C.G., Epping, M., Kruyt. F.A.E., Giaccone, G., 2002. Apoptosis: Target of Cancer Therapy. Clinical Cancer Research 8, 2024-2034.
Ghobrial, I.M., Witzig, T.E., Adjei, A.A., 2005. Targeting Apoptosis Pathways in Cancer Therapy. CA: A Cancer Journal for Clinicians 55, 178-194.
Hengartner, M.O., 2000. The biochemistry of apoptosis. Nature 407, 770-776.
Lowe, S.W., Lin, A.W., 2000. Apoptosis in cancer. Carcinogenesis 21, 485-495.
Tamm, I., Dorken, B., Hartmann G., 2001. Antisense therapy in oncology: new hope for an old idea? Lancet 358, 489-197.
Tamm, I., Schriever, F., Dorken, B., 2001. Apoptosis: implications of basic research for clinical oncology. Lancet Oncology 2, 33-42.

About the Author:

Radoslaw Pilarski is a PhD candidate working in Institute of Bioorganic Chemistry (Polish Academy of Sciences, Poznan, Poland). mLingua providing professional language translations to and from all major Western and Asian languages, software localization and web site translation service. Please visit http://mlingua.pl for further information. Translated by www.mLingua.pl

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by: Bo Carpenter

It's a fact that every day, cells in your body divide, grow and die. Most of the time they do it in an orderly manner. But sometimes they grow out of control. This type of cell growth forms a mass or lump called a tumor. Tumors can either benign or malignant.

Benign tumors are not cancerous. But left untreated, some can pose a health risk, so they are often removed. When these tumors are removed, they typically do not reappear. Most importantly, the cells of a benign tumor do not spread to other parts of the body or invade nearby tissue.

Malignant tumors are made of abnormal cells. Malignant tumor cells can invade nearby tissue and spread to other parts of the body. A malignant tumor that develops in the breast is called breast cancer.

To continue growing, malignant breast tumors need to be fed. They get nourishment by developing new blood vessels in a process called angiogenesis. The new blood vessels supply the tumor with nutrients that promote growth. As the malignant breast tumor grows, it can expand into nearby tissue. This process is called invasion. Cells can also break away from the primary, or main, tumor and spread to other parts of the body. The cells spread by traveling through the blood stream and lymphatic system. This process is called metastasis.

When malignant breast cells appear in a new location, they begin to divide and grow out of control again as they create another tumor. Even though the new tumor is growing in another part of the body, it is still called breast cancer. The most common locations of breast cancer metastases are the lymph nodes, liver, brain, bones and lungs.

There are genes that control the way our cells divide and grow. When these genes don't work like they should, a genetic error, or mutation, has occurred. Mutations may be inherited or spontaneous. Inherited mutations are ones you were born with — an abnormal gene that one of your parents passed on to you at birth. Inherited mutations of specific genes, such as the BRCAI and BRCA2 genes, increase a woman’s risk of developing breast cancer.

Spontaneous mutations can occur within your body during your lifetime. The actual cause or causes of mutations still remains unknown. Researchers have identified two types of genes that are important to cell growth. Errors in these genes turn normal cells into cancerous ones.

You need to be aware that cells may be growing out of control before any symptoms of the disease appear. That is why breast screening to find any early changes is so important. The sooner a problem is found, the better a your chance is for survival.

Experts recommend that women 40 years and older have a mammogram every year. If you have a history of breast cancer in your family, talk with your doctor about risk assessment, when to start getting mammograms and how often to have them. If your mother or sister had breast cancer before menopause, you may need to start getting mammograms and yearly clinical breast exams before age 40. It is important for all women to have clinical breast exams done by a health care provider at least every three years starting at age 20 and every year after age 40 and to do breast self-exams once every month starting by age 20.

PANDORA is pleased to announce its support of Susan G. Komen For The Cure. For 2007, a guaranteed minimum contribution of $25,000 and a portion of the sales from the pink ribbon charm will go to the organization.

For each pink ribbon charm sold, PANDORA will donate a percentage of the proceeds to Susan G. Komen For The Cure to help eradicate breast cancer through research, education, screening, and treatment.

Lewis Jewelers is proud to carry the full line of Pandora Jewelry. For more information, contact Lewis Jewelers at 877-88-LEWIS or visit www.pandorabraceletsusa.com .

source:searchwarp.com/

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