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A diet high in inorganic phosphates, which are found in a variety of processed foods-including meats, cheeses, beverages, and bakery products-can increase the risk and spread of lung cancer, according to a new study.
Washington, Dec 30 : A diet high in inorganic phosphates, which are found in a variety of processed foods-including meats, cheeses, beverages, and bakery products-can increase the risk and spread of
lung cancer, according to a new study.
The study, using a mouse model, indicated that inorganic phosphates might speed growth of
lung cancer tumours, and even contribute to the development of those tumours in individuals predisposed to the disease.
Conducted by Myung-Haing Cho, D.V.M., Ph.D., and his colleagues at Seoul National University, the study also suggested that dietary regulation of inorganic phosphates might play an important role in
lung cancer treatment.
"Our study indicates that increased intake of inorganic phosphates strongly stimulates
lung cancer development in mice, and suggests that dietary regulation of inorganic phosphates may be critical for lung cancer treatment as well as prevention," said Cho.
The study revealed that high levels of inorganic phosphates can stimulate non-small cell
lung cancer (NSCLC) pathways.
Lung cancer is a disease of uncontrolled cell proliferation in lung tissue, and disruption of signaling pathways in those tissues can confer a normal cell with malignant properties. Deregulation of only a small set of pathways can confer a normal cell with malignant properties, and these pathways are regulated in response to nutrient availability and, consequently, cell proliferation and growth," explained Cho.
He added: "Phosphate is an essential nutrient to living organisms, and can activate some signals. This study demonstrates that high intake of inorganic phosphates may strongly stimulate
lung cancer development by altering those (signaling) pathways."
For the study, the researcher analysed
lung cancer-model mice for four weeks.
The mice were randomly assigned to receive a diet of either 0.5 or 1.0 percent phosphate, a range roughly equivalent to modern human diets.
After four-weeks, the lung tissue was analysed to determine the effects of the inorganic phosphates on tumours.
"Our results clearly demonstrated that the diet higher in inorganic phosphates caused an increase in the size of the tumours and stimulated growth of the tumours," said Cho.
"The results of this study suggest that dietary regulation of inorganic phosphates has a place in
lung cancer treatment, and our eventual goal is to collect sufficient information to accurately assess the risk of these phosphates," he said.
The study has been published in the January issue of the American Journal of Respiratory and Critical Care Medicine.

A study on almost 24,000 Japanese women recently published in the British Journal of Cancer has found that lack of sleep can greatly increase the risk of breast cancer, with women who slept 6 hours or less every night having a significantly higher risk.Breast Cancer StatisticsBreast cancer is the most common cancer to hit women worldwide. In Japan, when age-standardized to the world population, the incidence rate was 28.3 per 100,000 in 1991, and rose to 39.5 in 2001.In the United States in 2004, the disease hit more than 185,000 women and over 1,800 men, with almost 41,000 women and 362 men dying from it that year. In that year, after non-melanoma skin cancer, breast cancer was the next highest cancer killer of American women. It was also their fifth highest killer overall.Next up, over to Canada, where, among the women, breast cancer is the most common type of cancer to strike. According to Canadian Cancer Society estimates, about 22,400 women will be diagnosed with the disease this year, with about 5,300 dying from it.With such grim statistics, every little thing which can be done to prevent and combat the disease becomes all the more critical.Details of StudyThe Ohsaki National Health Insurance (NHI) Cohort Study started in 1994 and involved 28,515 women in northeastern Japan. The questionnaire used included information on sleep duration and other lifestyle habits.Participants who had withdrawn from the NHI study before follow-up, had a history of cancer, did not provide information on their sleep duration, and who reported having slept for less than 4 hours or more than 12 hours every night were omitted. This left the data for 23,995 women to be analyzed. An 8-year period, from 1995 to 2003, was used, during which 143 women were hit with breast cancer.Findings of StudyThe women who slept 7 hours each night was used as the reference group. It was then found that women who slept 6 hours or less each night had a 62% higher risk of getting breast cancer. On the other hand, those who slept 9 hours or more every night had a 28% lower risk of getting the disease.It would follow, then, that those who slept 6 hours or less every night had 2.25 times the risk of getting breast cancer when compared to those who slept 9 hours or more each night.The results remained largely consistent even when participants who were diagnosed with breast cancer within 3 years from the start of the study were excluded, or when the data was analyzed by age and menopausal status.Previous StudiesThe findings of this study validates the findings of two previous prospective cohort studies relating breast cancer and sleep duration (Verkasalo et al, 2005, Wu et al, 2008). Those two studies had also shown a significant decrease in breast cancer risk for those who slept the longest.It must be noted, though, that another such study (Pinheiro et al, 2006) did not find any such association. The study team pointed out, however, that that study had looked at residential nurses, who underwent rotating-shift work and had varying sleep timings. The findings of that study thus might not be applicable to the general population.Strengths and Limitations of StudyAccording to the study team, their research had a couple of strong points. Firstly, it used study subjects from the general population, thus allowing for overall generalization of its findings. In addition, it used the Miyagi Prefectural Cancer Registry, which the study team said is “one of the earliest and most accurate population-based cancer registries in Japan”.There were also, however, several limitations. Firstly, self-reported sleep data was used, and assessment was also only carried out once. In addition, and probably very significantly, no information on sleep quality, sleep timing, use of sleep medication, or presence of sleep disorders were available. These factors, of course, are very important as they can directly or indirectly affect cancer risk.Further, the researchers added that they had no information with regard to rotating-shift work or night work, but they felt that would not have affected their findings greatly as more than half of the study subjects were housewives, farmers or retired.The Sleep Duration – Breast Cancer LinkWhy is breast cancer risk linked to sleep duration? The answer could lie in melatonin, which is secreted during night sleep. When a person sleeps fewer hours, less melatonin is secreted, and lower levels of the chemical had previously been associated with increased breast cancer risk.In addition, melatonin may possess an inhibitory effect on gonadal function, which includes synthetizing and secreting sex hormones. It had also been found to have an antiproliferative effect on breast cancer cells.The Bottom LineIf the findings from this study are indeed accurate, then there is an immense difference in breast cancer risk between sleeping 4 to 6 hours every night, and just sleeping 1 to 3 hours more each night. In fact, it is more than likely that the protective effects of sufficient sleep also extend to other forms of cancer. 7 hours of sleep a night may thus be a good number to aim for.Hopefully, in time to come, further research will reveal more information relating sleep and disease risk, with sleep quality and sleep timing being two of the main possibilities.Main SourceSleep duration and the risk of breast cancer: the Ohsaki Cohort Study (

Back in 1973 the evidence about the dangers of talc prompted the FDA to think about steps to reduce the level of the asbestos-like fibers in cosmetic talc. The dangers are that talc is related to asbestos – a known carcinogen – and that the presence of talc particles is linked to tumors. However, the FDA did not regulate cosmetic talc even after 1993 when the National Toxicology Program reported that cosmetic talc, which had no fibers, was the cause of tumors in animals.Talc is a soft green-gray colored mineral produced from rocks and processed into a powder. Pure talc mineral is a hydrous magnesium silicate. Some trace minerals are removed in processing but very small fibers remain which are similar to those that occur in asbestos.Most talc is formed from altered dolomite or magnesite when there is excess dissolved silica. A number of minerals associated with talc include: tremolite, serpentine, anthophyllite, magnesite, mica and chlorite. Note that there are six minerals are defined as asbestos and two of these are also talc – tremolite and anthophyllite.Commercial talc may contain impurities and contaminates such as asbestos and crystalline silica. In fact asbestos may occur in talc.Talc is used in diverse industries and for a wide variety of purposes. It is commonly used in cosmetics and body powders, including those for babies. It has hydrophobic surface properties helping to keep skin dry.In the paper industry, talc is used as a filler which enhances the quality of the paper for printing and appearance of opacity. It is used in ceramic tiles, and in paints and coatings. Did you know that the dust on some chewing gums contains talc? Talc is also used in in flea and tick powder, deodorants, chalk and crayons, textiles and soap.Now we have another study (published in the Cancer Epidemiology, Biomarkers and Prevention journal) that shows that women who use talcum powder around their genital areas are 40% more likely to develop ovarian cancer. The study led by Dr Maggie Gates of Harvard Medical School analyzed 3,000 women. The risk of ovarian cancer for those who used talcum powder once a week was found to be 36%, while those using it every day the risk went up to 41%.In a recent separate incident a group of doctors at the Harvard Medical School found talc particles in the pelvis of a woman diagnosed with ovarian cancer. She had used talcum powder every day for around 30 years.In 1982 in Cancer magazine the conclusions from a study recommend that the lifetime use of talcum powder increases the risk of ovarian cancer by more than three times. Consequently, various cancer organizations warn against the use of talcum powder. For many people this warning is a bit late.Talc also causes poisoning due to accidental exposure. The website (see link below) state that from the early 1980’s accidental inhalation of talc (baby powder) has caused the death or serious illness of several thousands infants.Talc is used in some medications such as some antiacids and in some antiseptics. So the question is is talc dangerous when used as medications? Actually there are so many questions we need to ask. What guidelines should be available and what regulations exist that protect people? Why do so many children suffer needlessly because of lack of care demonstrated by authorities? Why weren’t women protected against the use of talcum powder 30 years ago?Over and over again when there is a choice about caring for our fellow human beings and about earning profits, selfishness wins. And the authorities lack the care and the compassion required to serve us well.Reference:

After decades of attempting to fight AIDS with experimental vaccines and drugs, scientists have recently discovered how several natural substances could be powerful weapons against the disease. For example, in mid-November, UCLA AIDS researchers published research concluding that the herb astragalus contains a substance with the potential to possibly replace the side-effect plagued HAART (highly active antiretroviral therapy) currently used to treat AIDS patients. Penn State immunologists say they’ve documented how a micronutrient could help battle AIDS. Their findings, just published in the Journal of Biological Chemistry, show how selenium could dramatically put the brakes on the replication of HIV, the virus that causes AIDS.Selenium is needed by the body to maintain normal metabolism. It’s also increasingly being studied for its anti-cancer properties. Although other nutrients usually bind to proteins, selenium actually becomes incorporated into proteins, forming what are called selenoproteins. These selenium-containing proteins are believed to slow the spread of infections. However, when HIV infects a person, the virus manages to degrade selenoproteins, probably due to a protein, dubbed Tat, produced by the HIV virus. In particular, Tat seems to target a selenoprotein known as TR1.But there may be a way to get around this degradation of selenoproteins -- supplementation with selenium. "Since HIV targets the selenoproteins, we thought that the logical way to deal with the virus is to increase the expression of such proteins in the body," K. Sandeep Prabhu, assistant professor of immunology and molecular toxicology at Penn State, said in a statement to the press.To test their idea, the scientists isolated blood cells from human volunteers who did not have HIV. Then they infected those cells with the virus and added a form of selenium called sodium selenite to the cell culture.The result? The added selenium inhibited the replication of HIV at least 10-fold, in comparison to cell cultures with no added selenium. The scientists also selectively reduced the production pf the selenoprotein TRI. When there was less selenium-containing protein,HIV replication soared 3.5 times. Bottom line: The research confirms that an increase in selenium in cells zaps replication of HIV while a reduction in the amount of selenium-containing TR1 protein gives the virus a boost."We have found that increasing the expression of proteins that contain selenium negatively affects the replication of HIV. Once we fully understand the function of these selenium proteins, it will give us a handle to come up with more effective drugs," said Dr. Prabhu in the prepared statement for the media.Two more new studies offer additional evidence that selenium may impact the immune system. German scientists from St. Josefs-Hospital in Wiesbaden recently published a study in the Swedish medical journal Acta Oncologica that suggests the micronutrient could help prevent prostate cancer and prostate enlargement. The researchers found that whole blood selenium levels were significantly lower in all men tested who had prostate cancer or benign prostate hypertrophy (which can cause difficulty with urination) and concluded, “our findings may support the recommendation of selenium supplementation” to help prostate health. What’s more, a study just published in the journal Molecular Nutrition and Food Research suggests enzymes that contain selenium have anti-oxidative and anti-inflammatory effects that could make them important in preventing prostate and colorectal cancers.Too much selenium in can cause a condition called selenosis, resulting in loss of hair, nail problems, nausea, irritability, fatigue, and mild nerve damage. However, selenium toxicity is extremely rare. A lack of selenium may, in fact, be far more common and potentially more dangerous to health. According to the National Institutes of Health, people age 14 and older should take in about 44 micrograms of selenium a day. Good sources of the micronutrient include Brazil nuts, eggs, brown rice, whole wheat bread and pasta, walnuts and oatmeal.

The director of the University of Pittsburgh Cancer Institutes and the Cancer Centers at the University of Pittsburgh Medical Center has issued a warning to all 3,000 faculty and staff under his supervision, warning them to limit cellular phone use in order to avoid adverse health effects."Recently I have become aware of the growing body of literature linking long-term cell phone use to possible adverse health effects including cancer," the memo from Dr. Ronald Herberman reads. "Although the evidence is still controversial, I am convinced that there are sufficient data to warrant issuing an advisory to share some precautionary advice on cell phone use."Herberman advises keeping mobile phone conversations as short as possible and using headsets, text messages or speaker phone settings to keep the phone away from the head. He also warns that children should only you cellular phones in emergencies, because their still-developing organs "are the most likely to be sensitive to any possible effects of exposure."The doctor noted that similar warnings have been issued by the governments of several European countries, and that Toronto's public health agency has called on children to avoid using the phones.Herberman is believed to be the first director of a U.S. cancer center to issue such a warning.Among the studies referenced by the memo is a still-ongoing study of cell phone users in 13 European countries. Preliminary data suggest that long-term users are significantly more likely to develop brain tumors, especially on the side of the head with the phone is most often held. Similar results have been found in other long-term studies."From a public health perspective, it makes sense to limit risks," said Dr. Dan Wartenberg of the University of Medicine and Dentistry of New Jersey.Along with Herberman and roughly 20 other international experts, Wartenberg has signed a letter calling for precautions on cell phone use, and for manufacturers to make phones "with the lowest possible risk" and to "encourage consumers to use their devices in a way that is most compatible with preserving their health."Sources for this story include:

Like to eat meat? Consider this unappetizing truth: When you gulp down a nice juicy steak or hamburger, you are contributing to tumor-fueling inflammation in your body.In fact, eating a diet rich in red meat has long been linked to a host of ills including an increased risk of several types of cancer. But what is it about meat consumption that could impact cancer growth? Now scientists at the University of California, San Diego School of Medicine, have found a mechanism that explains how eating red meat, as well as milk, could spur the growth of malignancies. The new study, headed by Ajit Varki, M.D., suggests that inflammation resulting from a molecule introduced through eating these foods could make cancer grow. The research is set for upcoming publication in the Proceedings of the National Academy of Sciences (PNAS).Dr.Varki, UC San Diego School of Medicine distinguished professor of medicine and cellular and molecular medicine and co-director of the UCSD Glycobiology Research and Training Center, and his research team studied a non-human glycan, or sugar molecule, known as N-glycolylneuraminic acid (Neu5Gc). Although this molecule is not produced naturally in the human body, it’s incorporated into human tissues if you eat red meat. The body then develops antibodies against Neu5Gc – and this immune response could potentially trigger a low-grade chronic inflammation, spurring the growth of cancer. In a statement prepared for the media, Dr. Varki explained it has been recognized by scientists for some time that chronic inflammation can stimulate cancer progression."We've shown that tumor tissues contain much more Neu5Gc than is usually found in normal human tissues. We therefore surmised that Neu5Gc must somehow benefit tumors,” Dr. Varki said in the press statement. So the scientists came up with this hypothesis: The fact that Neu5Gc accumulates in human tumors despite circulating anti-Neu5Gc antibodies suggests a low-grade, chronic inflammation has developed, and caused the tumor to grow. To test this idea, the researchers worked with specially bred mice. The animals lacked the Neu5Gc molecule , just as humans do before they eat red meat and the molecule is absorbed into their bodies, and they had tumors.Anti-Neu5Gc antibodies were given to half of the mice . In those animals, the antibodies induced inflammation and their cancers started growing faster. In the control group comprised of mice that were not treated with antibodies, their tumor growth was far less aggressive.Building on previous research that has shown that humans who take non-steroidal anti-inflammatory drugs (commonly known as NSAIDs) have a reduced risk of cancer, the researchers tried giving NSAIDs to the mice with cancerous tumors fueled by anti-Neu5Gc antibodies. The result? The anti-inflammatory treatment blocked the effect of the Neu5Gc antibodies and the tumors became smaller."Taken together, our data indicate that chronic inflammation results from interaction of Neu5Gc accumulated in our bodies from eating red meat with the antibodies that circulate as an immune response to this non-human molecule – and this may contribute to cancer risk," Varki said in the media statement.For anyone interested in reducing inflammation through natural, non-drug methods, here are seven top strategies to incorporate into your lifestyle:1. Stop eating meat and dairy products.2. Concentrate on a Mediterranean flavored style of eating with lots of fruits, vegetables, whole grains , olive oils and nuts. Research has shown these foods lower inflammation levels.3. Don’t smoke and avoid those who do – second hand smoke can contribute to inflammation.4. Know your oils. Avoid all inflammation-causing trans-fats, hydrogenated and partially hydrogenated oils as well as saturated animal fats. Instead, add inflammation-fighting omega-3 oils like flaxseed, canola and walnut oil to your diet.5. Lose weight if you need to. Research has shown that a waist that measures over 40 inches in a man or over 35 inches in a woman is a sign of probable high inflammation.6. Don’t skimp on sleep. Previous studies have concluded less than six hours of sleep can result in inflammation .7. De-stress. Try yoga, meditation, walking and other forms of exercise. Staying continually stressed out means your body is releasing excess, inflammation-promoting stress hormones . Schedule a minimum of 20 minutes a day to let your worries go.

It’s amazing that more than 2000 years ago we realized many universal truths, and we did it without the scientific method. One person who really knew what he was talking about was Hippocrates, who said “Let food be thy medicine and medicine be thy food”.We lost our common sense for awhile and fell in love with a disease establishment that claimed science was on its side. Apparently we are now coming to earth again in a new age where science and sense meet. Scientists are now explaining the finer points of the truth Hippocrates was trying to tell us -- nature has provided us with all the tools we need to stay healthy. An example of this type of research is a study published in the January, 2008 edition of Frontiers in Bioscience that deals with the importance of regulation of the cell cycle in prevention of cancer.What is the cell cycle?The growth and maintenance of plants, animals and humans is the result of an ordered series of events which constitute the cell cycle. During this cycle, chromosomes are duplicated and one copy of each duplicated chromosome is transferred from the mother cell to the daughter cell. Proper regulation of this cycle is essential for the normal development of multi-cellular organisms. If control of this cycle is lost for any reason, cancer or other degenerative diseases may be the result.Successful cell replication depends on two critical processes: the replication of DNA, and mitosis -- the nuclear division of the daughter cell from the mother cell. The master controllers of these processes are protein kinases that regulate the proteins involved in this DNA replication and mitosis.The researchFor this study, scientists reviewed the sequence of events that regulate cell cycle progression with an eye towards the check points and mechanisms that cells employ to insure DNA stability during this cell cycle even in the face of genotoxic stress.They noted that key transitions in the cell cycle are regulated by the activities of the various protein kinase complexes composed of cyclin and cyclin-dependent kinase (CDK) molecules. These cyclins are CDK binding partners which are required for kinase activity and are intimately linked to the cell cycle stage. CDK activity can be controlled by other mechanisms, such as the addition of a phosphate group, resulting in deregulation of the cell cycle. This is the process that leads to cancer.Although diets rich in fruits and vegetables are increasingly being recommended for the prevention of cancer, their active ingredients and mechanisms of action have not been well understood. This research presents evidence that dietary agents identified from fruits and vegetables can act to modulate the effects of deregulated cell cycle checkpoints. It is through this mechanism that cancer may be prevented by dietary choice.Compounds from fruits and vegetables that appeared particularly noteworthy were apigenin (celery, parsley), curcumin (turmeric), epigallocatechin-3-gallate (green tea), resveratrol (red grapes, peanuts and berries), genistein (soybeans), and silymarin (milk thistle).

Can you eat the foods you love occasionally without compromising your health? A new study shows that adding certain compounds to your diet can protect you from the harmful effects of acrylamides found in many of American’s favorite foods.Acrylamides are cancer causing agents created when foods are grilled, fried, baked or roasted. They are a byproduct of cooking starchy foods at high temperatures. Acrylamides are found in the highest levels in foods that become browned in the cooking process such as french fries, potato chips, and grilled meats and vegetables that have grill marks on them. Toasted bread and cereals, and baked foods such as sweet potatoes and browned meats also contain substantial amounts, as does dried fruit.The danger of acrylamides was first revealed in 2002, when researchers found that women who consumed 40 micrograms or more of acrylamides each day had twice the risk of endometrial and ovarian cancer risk of women who ate substantially smaller amounts. This would be the amount of acrylamides contained in a small portion of potatoe chips. The FDA has been slow to acknowledge the threat of acrylamides. Food manufacturers have not been required to publish data on the levels of acrylamides in their products.Research reveals the way for consumers to protect themselvesAs published in the July 15, 2008 edition of the Journal of Agriculture and Food Chemistry, researchers found that three dietary constituents, tea polyphenols, resveratrol, and diallyl trisulfide, inhibit damage to DNA from acrylamides at levels typically found in human exposure. Results of analysis of the compounds with accelerator mass spectrometry demonstrated that all three significantly inhibited the formation of acrylamide damage to liver DNA, whereas tea polyphenols and diallyl trisulfide reduced DNA damage to protamines and hemoglobin as well.Further biochemical studies showed that acrylamides could significantly inactivate creatine kinase and glutathione S-transferase and deplete glutathione. When the inhibitors were treated with acrylamide, all of them could effectively recover the activities of creatine kinase. In addition, tea polyphenols and diallyl trisulfide could increase glutathione S-transferase at a remarkably high level. Creatine kinase is an enzyme essential in biochemical reactions and energy generation. Glutathione S-transferase is a family of enzymes that play key roles in the detoxification of substances such as carcinogens, drugs, and byproducts of oxidative stress.Acrylamides are formed when carbohydrate containing foods are baked, fried or roasted. They have been shown to cause cancer in animals exposed to high doses, as well as nerve damage. Acrylamides are not added to foods but occur naturally in the cooking process. Because of this, information on them is not required on food labels.Any starchy food cooked at high temperatures will contain acrylamides. Potatoes that are fried may be the worst offenders, with potato chips fried to a golden brown containing the highest levels. Boiled or mashed potatoes will contain acrylamides as will cooked sweet potatoes. It can also be found in toasted or roasted cereal grains and bread products -- again with the highest levels contained in those baked to a golden brown, and corn roasted on a grill, or popped in oil. Pretzels are promoted as healthy snacks, but that golden brown color is your tip that they contain high levels of acrylamides. Coffee creates acrylamides during its roasting.Acrylamides were discovered by Swedish scientists in 2002, and made headlines across America when they were first reported. Since then, there has been little interest by the FDA to keep people abreast of the dangers of eating acrylamide containing foods. The method by which acrylamides form in food remains unknown.What we do know from this study is that by taking steps to protect ourselves from acrylamides, we don’t have to be boorish sticks when we go out with our friends. We can eat foods containing acrylamides without suffering their effects if we also make sure we are fortified with tea polyphenols, resveratrol and diallyl trisulfide.Numerous studies have demonstrated the anti-cancer properties of tea polyphenols, with recent studies adding gastric, esophageal and skin cancers to the list of those inhibited by polyphenols from tea consumed in high amounts. Another study showed ovarian cancer risk reduced by 46 percent in women drinking 2 cups of tea daily. Researchers have found tea polyphenols to lower cholesterol levels, prevent blood clots, and help prevent heart disease. All types of tea contain polyphenols, with green and white tea having the highest levels due to their minimal processing.Resveratrol is turning out to be so good for us that red wine may end up on the superfood list. It is found in the skin of red or purple grapes, and in peanut products that contain the skins, such as Spanish peanuts. Resveratrol has also been shown to help prevent cardiovascular disease and cancer. A glass of tea or red wine during a meal containing foods that have produced acrylamides will offer you protection.Diallyl trisulfide is a compound found in garlic that has been roasted, smashed or otherwise processed. Shown particularly effective in the prevention and treatment of prostate cancer, this compound is also a potent immune system booster.All three of these compounds are extremely effective antioxidants.If you plan to be eating foods that contain acrylamides, you can protect yourself by having supplements of theses compounds on hand. Each offers an array of other health benefits.

Will the stress in your life cause you to develop cancer? The answer to this question may depend on what you eat according to a study published in the August, 2008 edition of the International Journal of Oncology.Researchers examined the possible growth promoting effects of the stress-associated hormone norepinephrine on immortalized human pancreatic duct epithelial cells. The results suggested that norepinephrine can increase proliferation of these cells. They then evaluated the ability of norepinephrine to induce interleukin-6, and vascular endothelial growth factor, both believed to promote cancer of pancreatic duct epithelial cells. They found that norepinephrine can indeed increase the interleukin-6 and vascular endothelial growth factor in the cells.Based on theses results, the researchers performed further testing to see if dietary agents sulforaphane and resveratrol can inhibit norepinephrine-mediated increases in cell proliferation. Results indicated that sulforaphane but not resveratrol inhibits the norepinephrine-mediated increases in cell proliferation. Sulforaphane also inhibited norepinephrine-mediated increase of the interleukin-6 levels of the cells.We are living through an extremely stressful period of history. Hundreds of studies have documented how stress impacts our immune systems and ability to fight off invading organisms. This study goes a long way toward documenting the link between stress and cancer. The implications for further research are huge.Inhibiting norepinephrine is no small feat. Norepinephrine is a neurotransmitter that is similar to adrenaline. These hormones act together to produce heart rate and blood pressure increases among other biochemical actions to launch us into our natural defense mode, described as fight or flight. Chronic high levels of stress result in chronic high levels of norepinephrine and adrenaline.Sulforaphane is a compound that can be obtained by eating cruciferous vegetables such as Brussels sprouts, broccoli, cabbage, cauliflower, bok choy, kale, collards, kohlrabi, mustard, turnip, radish, rocket, and watercress.The compound’s anticancer activity is thought to be related to the induction of phase-II enzymes such as quinone reductase and glutathione S-transferase, and the enhanced transcription of tumor suppressor proteins.Sulforaphane is particularly abundant in broccoli sprouts. Researchers at Johns Hopkins University School of Medicine have been dedicated in their efforts to provide us with a broccoli sprout that guarantees a consistent level of sulforaphane. According to Johns Hopkins, eating just one ounce of their broccoli sprouts provides as much sulforaphane as more than a pound of cooked broccoli. Their product, called Brocco Sprouts, is available at many traditional supermarkets.If eating healthy amounts of cruciferous vegetables does not appeal to you, try adding broccoli sprouts to a sandwich or salad. Broccoli sprouts don’t have to be eaten daily to provide their full effect. A one ounce serving is good for three days worth of full spectrum antioxidant protection from sulforaphane comparable to the best antioxidant supplements on the market. A box of sprouts contains four of these servings and retails for about 4 dollars.Juicing is another good way to consume cruciferous vegetables, particularly if you have digestive difficulties. You can add cruciferous vegetables to your vegetable juice recipes. One large stalk of broccoli makes only about an inch of power packed juice in a glass, so it doesn’t have a huge impact on the taste of the recipe.Supplements of broccoli sprouts are available at health food stores and online health retailers such as Vitacost or Lucky Vitamin. The best known is called Broccoliv. Vitacost has a less costly house brand.

Smoking strongly increases a person's risk of developing bladder cancer - a risk that the majority of the population seems to be unaware of, according to a new analysis conducted by researchers from the University of Michigan Comprehensive Cancer Center."The general public understands that cigarette smoking can lead to lung cancer, but very few people understand that it also can lead to bladder cancer," study co-author James E. Montie said.The researchers compiled data from all studies in the MEDLINE database that had been conducted on the connection between bladder cancer and smoking between 1975 and 2007. The correlation between smoking behavior and bladder cancer risk, they found, was strong. For example, one study found that a person's risk of developing bladder cancer goes down by 40 percent within the first four years of quitting smoking.Yet the general population remains unaware of this connection, the researchers also found, as are patients who have been diagnosed with bladder cancer. Only 22 percent of bladder cancer patients surveyed knew that smoking increases the risk of developing the disease."A big gap exists between patient knowledge and their actual risk," co-author Seth A. Strope said. "Our study suggests that physicians must do a much better job of communicating the risk to our patients, and directing them toward smoking cessation programs."Bladder cancer is one of the most expensive forms of cancer to treat. In the United States, it is the fourth most common cancer in men in the ninth most common in women, with more than 47,000 new cases diagnosed in men and 16,000 in women each year. The higher prevalence in men is believed to be due to the fact that male sex hormones play a role in the development of the disease.Other than smoking, risk factors include being African-American or Hispanic and having a family history of the cancer. Exposure to secondhand smoke is also a suspected risk factor.

Saw palmetto may be a man’s best friend. It's the primary herb helping men maintain prostate health that’s very popular throughout Europe for its ability to relieve symptoms associated with benign prostatic hyperplasia (BPH), otherwise known as enlargement of the prostate. In the U.S. where pharmaceuticals are the standard of care for prostate problems, saw palmetto is gaining popularity following several recent studies showing it provides relief from short-term urinary symptoms and other symptoms of BPH, as well as relief from inflammation of the prostate and cell proliferation. It also promotes hair growth in men with thinning hair or baldness. It provides these benefits safely, naturally and with no noted side effects.Saw palmetto, botanically known as Serenoa repens or as sabal palm in Europe, is a magnificent palm tree that grows naturally in Florida, Georgia and Mississippi. The therapeutic compound comes from the berries of the plant. Historical use of the herb can be traced in the Americas to the Mayans who used it as a tonic and to the Seminoles who took it as an expectorant and antiseptic.Saw Palmetto prevents conversion of testosterone to DHTThe herb possesses several mechanisms of action, with the primary action relating to prostate health being its ability to inhibit the 5-alpha reductase enzyme which converts testosterone, the male sex hormone, to a more potent metabolite, dihydrotestosterone (DHT). In addition, it blocks receptor sites on cell membranes required for cells to absorb DHT. An excess of DHT is believed one of the primary causes of prostate problems as well as the cause of male baldness.Recent research documents the health benefits of saw palmettoIn a study reported in the Journal of Urology, men with BPH obtained significant short-term symptom relief with saw palmetto. Ninety-two men between the ages of 49 and 75 with lower urinary tract symptoms were divided into two groups, one treated with two soft gels of saw palmetto, and the other treated with a placebo. Both groups were treated for a twelve week period. Maximum urinary flow was significantly higher in the treatment group compared to the placebo group, and urinary resistance was significantly lower. Yet mean prostate volume was comparable in the two groups.The American Family Physician journal reported a diagnosic and management review of BHP. They found that through its ability to inhibit 5-alpha reductase, saw palmetto as well as rye grass pollen extract, and pygeum relieved symptoms such as urinary hesitancy, weak stream, nocturia, incontinence, and recurrent urinary tract infections.A review of literature published in Archivio Italiano di Andrologia found that saw palmetto, lycopene and selenium, the three most widely used compounds in treatment of the prostate, have a common feature which may be a dual activity on proliferative disorders as well as on inflammatory conditions at the level of the prostate gland.A study reported in Anticancer Research investigated the effect of an extract of saw palmetto on hormone sensitive and insensitive prostate and breast cancer cells, and urinary bladder, colon and lung cancer cells in order to assess its growth inhibitory abilities. They found that saw palmetto extract induced a dose-dependent anti-proliferative effect on all the human malignant cells tested.Saw Palmetto reduces male pattern hair lossMale hair loss can often be attributed to the conversion of testosterone to DHT promoted by the 5-alpha reductase enzyme. DHT causes hair thinning by shrinking the follicles in the scalp, which results over a period of time in the follicles being far too small for hair to grow, resulting in baldness.The link between DHT and hair loss has been well established, with numerous clinical studies and surveys concluding that this hormone can be directly linked as a cause of as many as 95% of all cases of hair loss. The studies have shown that this condition is genetically linked, with excessive production of DHT being passed from generation to generation. It is this condition that is targeted by pharmaceutical products such as propecia (finasteride), and rogaine (minoxidil).While the testosterone to DHT conversion creates hair loss on the head, it also promotes the growth of hair in places where it is not wanted. By preventing this hormonal conversion, saw palmetto is showing in research to be effective in the treatment of male hair loss. It is able to get the hair off men’s backs and back on their heads. Some studies have shown it to be as effective as Propecia and Rogaine. This aspect of saw palmetto was discovered by people using it for prostate issues who started reporting the regrowth of hair on their heads.Shampoos and lotions containing saw palmetto are available at health food stores and on line. Saw Palmetto is available as a supplement. The dosage amount for men is 300 to 500 mg. per day. Saw palmetto has been shown in research to be non-toxic and safe for extended use.Saw Palmetto is not the only herb able to influence prostate healthSeveral other herbs and plant compounds are potentially useful in maintaining prostate health, including pygeum, nettle, beta sitosterol, and carotenoids such as lycopene. Health of the prostate gland is heavily influenced by the overall health of the body. It’s hard to find a sick prostate gland in a body otherwise possessing excellent health. Following the basics for general health will go along way in promoting prostate health.Pygeum is an African plum tree found in tropical Africa. An extract from the bark of pygeum has been used in Europe as a prevention and treatment of prostate disorders including BPH. More recently in the U.S. pygeum has been marketed along side saw palmetto for prostate health and cancer prevention and treatment.An interesting study reported in Endocrine tested the anti-cancer potential of pygeum in vitro and in vivo. In tissue culture, pygeum extract inhibited the growth of cancerous cells, induced appropriate programmed cell death and altered cell kinetics, down regulated ER-alpha and PKC-alpha protein, and demonstrated the ability to bind with estrogen and androgen receptors. Mice fed with pygeum showed a significant reduction in prostate cancer incidence of 35% compared to controls. Researchers concluded pygeum is a useful supplement for men at high risk of developing prostate cancer.

Eating raw cruciferous vegetables can reduce the risk of bladder cancer, according to studies conducted by researchers from the Roswell Park Cancer Institute.The cruciferous vegetable family includes broccoli, cabbage, cauliflower, arugula, Brussels sprouts, collard greens, daikon, garden cress, horseradish, kale, kohlrabi, mustard, radish, rape (canola), rapini, rutabaga, tatsoi, turnip, wasabi and watercress.In one study, Roswell Park researchers found that the risk of bladder cancer in rats decreased as the amount of freeze-dried broccoli sprout extract in their diets increased. In another study, people who ate as little as three servings of cruciferous vegetables per month had a 40 percent lower risk of bladder cancer than those who ate less. No benefit was found, however, in those who ate the vegetables cooked.Much of the vegetables' cancer-fighting effect is attributed naturally occurring plant compounds known as isothiocyanates. Isothiocyanates have been linked to decreased risk of both cancerous and noncancerous tumors, and at least one variety has been observed to induce cell death even in chemotherapy-resistant cancer lines.Cooking can destroy 60 to 90 percent of a meal's isothiocyanate content.Isothiocyanates and other components of cruciferous vegetables are believed to help regulate an enzyme response that helps the body protect itself against cancer. In addition to bladder cancer, cruciferous vegetables and their chemical components have been found to protect against cancers of the breast, cervix, colon, endometrium, liver and lung."When they are eaten raw, they induce a kind of enzyme that may detoxify carcinogens," said Roswell Park's James Marshall. A press release from the institute cited the case of Katie Herdlein, who boosted her intake of fruits and vegetables to help her get through chemotherapy.

According to a combined analysis of previous studies, adjuvant (post-surgery) treatment with an aromatase inhibitor results in fewer recurrences than treatment with tamoxifen (Nolvadex®) among postmenopausal women with early, hormone receptor-positive breast cancer. These results were presented at the 2008 annual San Antonio Breast Cancer Symposium (SABCS).
Each year more than 180,000 U.S. women are diagnosed with breast cancer. Many of these breast cancers will be hormone receptor-positive, meaning that they are stimulated to grow by the circulating female hormones estrogen and/or progesterone.
Treatment of hormone receptor-positive breast cancer often involves hormonal therapies that suppress or block the action of estrogen. These therapies include tamoxifen as well as agents known as aromatase inhibitors. Tamoxifen acts by blocking estrogen receptors, whereas aromatase inhibitors suppress the production of estrogen in postmenopausal women.
Several large trials comparing aromatase inhibitors to tamoxifen have established the efficacy and safety of aromatase inhibitors for the treatment of hormone receptor-positive breast cancers among postmenopausal women. Follow-up of these trials continues.
To further explore the effects of aromatase inhibitors, researchers affiliated with the Aromatase Inhibitors Overview Group conducted a combined analysis of previous studies, including the following six randomized trials:
Arimidex, Tamoxifen, Alone or in Combination (ATAC)
Breast International Group (BIG) 1-98/International Breast Cancer Study Group (IBCSG) 18-98
Austrian Breast and Colorectal Cancer Study Group (ABCSG)
German Austrian Breast Cancer Group (GABG)/Arimidex-Nolvadex (ARNO)
Intergroup Exemestane Study (IES)/BIG 2-97
Italian Tamoxifen Anastrozole (ITA)
Some of these studies compared five years of treatment with an aromatase inhibitor to five years of treatment with tamoxifen, and others evaluated the effect of switching to an aromatase inhibitor after two to three years of tamoxifen.
The aromatase inhibitors that were evaluated were Femara® (letrozole), Arimidex® (anastrozole), and Aromasin® (exemestane).
In the studies that compared five years of tamoxifen to five years of an aromatase inhibitor, the following results were reported:
Over the course of five years, 9.6% of women treated with an aromatase inhibitor experienced a cancer recurrence compared with 12.6% of women treated with tamoxifen.
There was no statistically significant difference in survival between the two groups.
In the studies that evaluated a switch from tamoxifen to an aromatase inhibitor, the following results were reported:
Over the course of six years, 12.6% of women who switched to an aromatase inhibitor experienced a cancer recurrence compared with 16.1% of women who remained on tamoxifen.
Women who switched to an aromatase inhibitor also had modestly improved survival compared with women who remained on tamoxifen.
The researchers concluded that these results provide clear evidence that aromatase inhibitors significantly reduce recurrences in early, hormone receptor-positive, postmenopausal breast cancer. There was also some evidence that switching to an aromatase inhibitor after two to three years of tamoxifen improved survival compared with continued treatment with tamoxifen. The duration of follow-up in these studies is still somewhat short, however; longer follow-up may provide additional information about effects on survival.
Reference: Ingle J, et al. Aromatase inhibitors versus tamoxifen as adjuvant therapy for postmenopausal women with estrogen receptor positive breast cancer: meta-analysis of randomized trials of monotherapy and switching strategies. San Antonio Breast Cancer Symposium. December 10-14, 2008. Abstract 12.

Cancer Research UK scientists have discovered for the first time that stem cells could be the root cause of bowel cancer, according to a study published in Nature* today (Wednesday).
Scientists at Cancer Research UK's
Beatson Institute for Cancer Research in Glasgow, Cardiff University and the Hubrecht Institute in the Netherlands – isolated stem cells in the bowels of mice and 'knocked out' a gene called APC from them. These damaged stem cells then rapidly started to multiply out of control and to form tumours.
Bowel cancer** is the third most common cancer in the UK affecting more than 36,500 people each year. This research could pave the way for new treatments to target damaged stem cells and quench their ‘ignition’ of the disease.
A stem cell is one that, when it divides, produces two 'daughter' cells. One remains a stem cell, while the other multiplies into the sorts of cells required by its organ to keep it functioning. Previously scientists could not be sure if the cancer causing faults occurred directly to stem cells, or whether ‘daughter’ cells were the route cause of the tumour. This study provides extremely strong evidence to suggest that most bowel cancers start from stem cells.
Study author Dr Owen Sansom, from Cancer Research UK's Beatson Institute, said: "When we studied the effect of blocking the APC gene in the 'parents' – or stem cells – the results were striking and the cells started to transform within days. It was clear the 'ignition point' for the disease was to be found in the stem cells. Using the same experiment, the daughter cells also developed into tumours, but not nearly as often as the stem cells changed. We are now looking to understand how we can use these results to seek out and destroy stem cells that are lacking the APC gene."
Lead author Professor Hans Clevers, from the Hubrecht Institute said: "We are very excited by these findings but we need to establish whether the stem cells behave the same way in human cancers as they do in mice – and this will form the basis of the next stage of our research. We only looked at the APC gene to understand its onset of bowel cancer – it’s likely that other genes also play a role in the progression of the disease."
Dr Lesley Walker, Cancer Research UK's director of cancer information said: "As in most cancers, the cell that the cancer originates from has remained elusive in bowel cancer. So this work is a big leap forward in our understanding of the origins of the disease.
"Bowel cancer is one of the most common forms of cancer so anything that adds to our understanding of the disease is very important work."

The National Institute for Health Research Health Technology Assessment (NIHR HTA) programme has commissioned a study to assess the feasibility of a lung cancer screening programme in the UK.
The NHS currently has established national screening programmes for breast cancer, cervical cancer and bowel cancer.
Experts now want to know whether a programme using computerised tomography (CT) to scan high-risk people - such as ex-smokers - would be beneficial in the UK.
We await the results of this important study with interest. - Professor Tim Eisen, Cancer Research UK
Lead researcher Professor John Field, director of the Roy Castle Lung Cancer Research Programme at the University of Liverpool, revealed that the number of lung cancer deaths has fallen in recent years thanks to a decline in smoking and greater public awareness.
"However, there is a large ex-smoking population who remain at high risk of developing lung cancer," he noted.
"Screening to detect the disease before patients develop any symptoms is a method that urgently requires evaluation as surgical resection at an early stage of the disease remains the only realistic option for a cure."
If the feasibility study suggests a lung cancer screening programme might be effective, a pilot study would then be conducted followed by a large-scale clinical trial.
"Only then would evidence be available to show whether a National Lung Cancer Screening Programme should be considered," said Professor Field.
He added: "We are delighted that the HTA has decided to invest in this first stage, which will help inform whether it is feasible to conduct a full trial."
Professor Tim Eisen, Cancer Research UK clinician and chair of the National Cancer Research Institute's lung cancer clinical studies group, said: "We know that most people - around 80 per cent - who get lung cancer only find out about it once the cancer has gone past the point where it can be cured.
"This trial aims to assess the proportion of people who are diagnosed at a time when it can still be successfully treated. We await the results of this important study with interest."

New research moves us one step closer to personalised breast cancer treatment

The research shows that women who have a duplication of chromosome 17 in their tumour will benefit from anthracycline drugs, while others can be spared the side-effects of the treatment. This group of chemotherapy drugs includes epirubicin which has already been shown to improve women's survival by a third.
This research is important as both the chemotherapy drugs and the test are already available, so a change in clinical practice could happen in the very near future.
The results of the British study are being presented at the San Antonio Breast Cancer Symposium today.Professor John Bartlett, a Cancer Research UK funded scientist from the University of Edinburgh, said: "We were looking for markers to help decide when to give women this type of chemotherapy using a test that is already part of patients' treatment.
"From previous trials we know that women who are treated with these drugs do better and are less likely to relapse. But, unless we know the drugs will be of benefit, we don’t want to give them to everyone because of the unpleasant side effects."
The researchers took small sections of tumours from over 2,500 women who had taken part in one of a number of studies, including the UK NEAT (National Epriubicin Adjuvant Trial)*. They tested the tumours to identify which markers could predict whether the chemotherapy treatment would be successful.
The results of the trial provide evidence that the marker – a duplication of Chromosome 17 – could be used to predict which women will benefit from chemotherapy and could go on to be introduced as a routine test in treatment**.
Professor Bartlett said: "This study gives us a key in the door to personalised chemotherapy treatment. Until now we haven't been able to predict which women are likely to benefit from this type of chemotherapy.
"We are now close to being able to use this new marker in the clinic to select appropriate therapies in early breast cancer."
Kate Law, director of clinical trials at Cancer Research UK, said: "These results are really encouraging and have the potential to change the way we treat women with breast cancer.

* Publisher: Jones and Bartlett Publishers

* Number Of Pages: 552

* Publication Date: 2007-12-28

* ISBN-10 / ASIN: 0763755621

Product Description:

Completely revised and updated for 2008, this practical handbook is an up-to-date guide to all aspects of cancer chemotherapy. The book provides a comprehensive, easy to use catalogue of over 100 drugs-both on- and off-label-commonly used in cancer treatment. A section on Common Chemotherapy Regimens provides a quick reference to management of specific cancers, arranged alphabetically.
no password

Product Description:

This book discusses the principles and practice of breast cancer management within the context of multidisciplinary team working and places emphasis on pragmatism. The text provides a comprehensive and contemporary account of the subject and should permit the reader to develop a firm understanding of the disease from epidemiology, genetics and screening, to pathology, diagnosis, treatment, and prevention. This in turn will enable healthcare personnel to deliver a high quality and up-to-date service to breast cancer sufferers.
PDF 6.1 MB
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By Manfred Schwab

* Publisher: Springer

* Number Of Pages: 3235

* Publication Date: 2008-10

* ISBN-10 / ASIN: 3540368477

Product Description

:The Encyclopedia of Cancer provides rapid access to focused information on all topics of cancer research for clinicians, research scientists and advanced students. Given the overwhelming success of the first edition, which appeared in 2001, and fast development in the different fields of cancer research, it has been decided to publish a second fully revised and expanded edition, following the principal concept of the first edition that has proven so successful.Recent developments are seeing a dynamic merging of basic and clinical science, with translational research increasingly becoming a new paradigm in cancer research. The merging of different basic and clinical science disciplines towards the common goal of fighting against cancer has long ago called for the establishment of a comprehensive reference source both as a tool to close the language gap between clinical and basic science investigators and as a platform of information for students and informed laymen alike.While the First Edition featured scholarly contributions from approximately 300 scientists/clinicians in one Volume, the Second Edition includes more than 1.000 contributors in 4 Volumes with an A-Z format of more than 7.000 entries. It provides definitions of common acronyms and short definitions of related terms and processes in the form of keyword entries. In addition, there are detailed essays, which provide comprehensive information on syndromes, genes and molecules, and processes and methods. Each essay is well-structured, with extensive cross-referencing between all entries.A panel of Field Editors, each an eminent international expert for the corresponding field, will ensure the presentation of timely and authoritative Encyclopedia entries. These new traits will meet the expectance that a wide community has towards a cancer reference works.The Encyclopedia of Cancer will be accessible both in print and online, and this information source will be of value to both the clinical and basic scientific community as well as to the public.

PDF 49.8 MB




Researchers recommend that at least 15 lymph nodes be removed and examined in patients with early gastric or pancreatic cancers. These results were recently published in the Archives of Surgery.
For accurate staging, or determination of extent of spread of gastric and pancreatic cancers, surgeons remove lymph nodes near the cancer. The lymph nodes are examined under a microscope to assess whether the cancer has spread to the lymph nodes, and if so, the extent of spread. Because treatment options are determined by the stage of the disease, an accurate assessment of spread to lymph nodes (nodal metastases) is imperative for optimal therapeutic choices.
Medical institutions that treat a high volume of patients with this disease or institutions affiliated with the National Comprehensive Cancer Network (NCCN) or National Cancer Institute (NCI), which follow strict guidelines, often tend to remove a larger number of lymph nodes during surgery than community centers or centers that treat a lower volume of patients with these diseases. It is currently not clear whether the removal of more nodes is associated with improved outcomes; however, patients treated at NCCN or NCI-designated centers or treated at medical centers that experience a high volume of these patients tend to have improved outcomes.
To further explore the possibility that the removal of more lymph nodes is associated with improved outcomes for patients diagnosed with gastric or pancreatic cancers, researchers evaluated outcomes among patients with gastric and pancreatic cancers who were treated at either high-volume or community medical centers (lower-volume centers). Included was data from the National Cancer Data Base from 2003-2004, which included more than 4,000 patients.
Patients undergoing surgery at National Comprehensive Cancer Network (NCCN) or National Cancer Institute (NCI)-designated institutions had more lymph nodes removed and examined than those treated at a community medical center.
Patients undergoing surgery at medical centers treating high volumes of patients with either gastric or pancreatic cancers also had more lymph nodes removed than those undergoing treatment at medical centers treating low volumes of these patients.
The researchers concluded that NCCN and NCI-designated centers and medical centers that treat a high volume of patients with pancreatic and gastric cancers tend to surgically remove more lymph nodes than community centers or medical centers that treat a low volume of patients with these diseases. The authors state: “Examination of at least 15 lymph nodes is an appropriate quality surveillance measure for gastric and pancreatic cancer because it is a feasible, achievable, and modifiable factor that is associated with improved outcomes.”
Patients diagnosed with gastric or pancreatic cancers may wish to speak with their physician regarding the status of the center at which they are receiving surgery. They may also wish to discuss their individual risks and benefits of greater removal of lymph nodes at the time of surgery.
Reference: Bilimoria K, Talamonti M, Wayne J, et al. Effect of hospital type and volume on lymph node evaluation for gastric and pancreatic cancer. Archives of Surgery. 2008;143:671-678

According to the results of a Phase II clinical trial, the addition of the investigational drug EndoTAG™-1 to chemotherapy with Gemzar® (gemcitabine) may improve survival among patients with inoperable pancreatic cancer. These results were presented at the 33rd Congress of the European Society for Medical Oncology (ESMO).
Pancreatic cancer has one of the highest mortality rates of all cancers. It accounts for approximately 2% of all newly diagnosed cancers in the United States each year but 5% of all cancer deaths. Pancreatic cancer is often called a “silent killer” because its symptoms are usually not recognizable until it has advanced and spread outside the pancreas. As a result the majority of pancreatic cancers are not diagnosed until they have reached advanced stages and are considered incurable.
Chemotherapy is a common treatment for advanced pancreatic cancer. However, due to the poor long-term survival achieved with chemotherapy alone, researchers continue to evaluate novel ways to improve outcomes for these patients.
EndoTAG™-1 is an investigational drug that is intended to “starve” cancer by destroying blood vessels that supply the tumor. It binds to cells that line new blood vessels and then releases the chemotherapy drug paclitaxel.
To evaluate EndoTAG™-1 in the treatment of pancreatic cancer, researchers conducted a Phase II clinical trial among 200 patients with inoperable, locally advanced or metastatic pancreatic cancer. In addition to treatment with the chemotherapy drug Gemzar® (gemcitabine), patients were assigned to receive one of three doses of EndoTAG™-1 or a placebo.
12-month survival was 17% among patients treated with Gemzar alone. Among patients treated with both Gemzar and EndoTAG™-1, survival was 22% among patients treated with the low dose of EndoTAG™-1, 36% among patients treated with the medium dose of EndoTAG™-1, and 33% among patients treated with the high dose of EndoTAG™-1.
During the latter part of the study, patients who responded to EndoTAG™-1 had the opportunity to continue treatment with EndoTAG™-1 for a longer period of time. Among these patients 12-month survival was 25% among patients treated with the low dose of EndoTAG™-1, 52% among patients treated with medium dose of EndoTAG™-1, and 40% among patients treated with the high dose of EndoTAG™-1.
This study suggests that EndoTAG™-1 may improve survival among patients with inoperable pancreatic cancer. Dr. Mathias Löhr, the principal investigator on the study, noted that “These study data demonstrate a noticeably higher efficacy from EndoTAG™-1 treatment compared to currently available treatments for pancreatic cancer.” These results will need to be confirmed in other studies.
Patients with pancreatic cancer may wish to discuss with their physician the risks and benefits of participating in a clinical trial further evaluating this or other promising therapeutic approaches. Two sources of information about ongoing clinical trials are the National Cancer Institute ( and
Reference: MediGene press release. MediGene reports positive 12-month survival data for EndoTAG™-1 from Phase II pancreatic cancer study. Available at: (Accessed September 17, 2008).

Preoperative radiation nearly doubles the survival rate for patients with operable pancreatic cancer, according to the results of a study published in the November 15, 2008 issue of the International Journal of Radiation Oncology Biology Physics.
The pancreas is an organ that is surrounded by the stomach, small intestine, bile ducts (tubes that connect the liver to the small intestine), gallbladder, liver, and spleen. The pancreas helps the body to break down food and also produces hormones, such as insulin, to regulate the body’s storage and use of food.
Pancreatic cancer has one of the highest mortality rates of all cancers. It accounts for approximately 2% of all newly diagnosed cancers in the United States each year but 5% of all cancer deaths. Pancreatic cancer is often called a “silent killer” because its symptoms are usually not recognizable until it has advanced and spread outside the pancreas. As a result the majority of pancreatic cancers are not diagnosed until they have reached advanced stages and are considered incurable.
If pancreatic cancer has not spread to surrounding or distant organs, it is usually considered operable. Historically, patients have been treated with surgery followed by chemotherapy and/or radiation to destroy any micrometastases (cancer cells that have spread outside the pancreas). New research indicates, however, that neoadjuvant radiation therapy (radiation delivered prior to surgery) might offer greater benefit to patients because it can potentially shrink the tumor prior to surgery, thereby ensuring a better chance of removal. Furthermore, because pancreatic surgery is so invasive, many patients are in no condition to undergo radiation treatment after surgery, so neoadjuvant treatment allows them to receive radiation that they might not receive otherwise.
Researchers from the Weill Cornell Medical College used data from the Surveillance, Epidemiology, and End Results (SEER) registry database to perform a retrospective analysis on patients who had surgically resected (removed) pancreatic cancer between 1994 and 2003. The researchers compared the overall survival rates among patients who received neoadjuvant radiation, adjuvant radiation, or no radiation. Patients who received neoadjuvant radiation survived 23 months, compared with 12 months for patients who did not receive radiation and 17 months for those who received adjuvant radiation (following surgery).
The researchers concluded that neoadjuvant radiation therapy offers a significant benefit over surgery alone or surgery with adjuvant radiation therapy in treating pancreatic cancer. Research will likely be ongoing to further explore these findings.

An international research team has identified two genetic variations that appear to increase a person's risk of developing lung cancer by up to 60 percent, they reported on Sunday.
In April the same researchers identified another
gene that raised lung cancer risk and they said their latest finding was relevant for both smokers and non-smokers.
"We are looking at differences in the
DNA that makes you more or less likely to develop lung cancer," said Paul Brennan, a cancer epidemiologist at the World Health Organisation's International Agency for Research on Cancer.
"The idea is if you can identify genes then that might indicate why people develop lung cancer."
Lung cancer is the leading cause of cancer death in men and the second leading cause of cancer death among women worldwide, according to the American Cancer Society, with about 975,000 men and 376,000 women forecast to die annually.
Smoking is the leading
risk factor but increasingly scientists are looking to genetics to help explain why some long-time smokers never develop the disease and why some non-smokers do.
The study published in the journal Nature Genetics included researchers from 18 countries who analyzed genetic
mutations in more than 15,000 people -- 6,000 with lung cancer and 9,000 without the disease.
The researchers discovered a region on the fifth
chromosome containing two genes -- TERT and CRR9 -- where they believe variations can boost the likelihood of lung cancer by as much as 60 percent.
"We are looking at versions of genes that everybody has," Brennan said in a telephone interview.
Not much is known about CRR9 but pinpointing the TERT gene is promising because it activates an
enzyme called telomerase which is key to aging and cancer, Brennan said.
Cancer is caused by defects in DNA, the basic genetic material. All chromosomes, which carry the DNA, also have little caps on each end called telomeres.
Each time a
cell divides, these telomeres become a little more frayed. When they are too worn out, the cell dies.
But when cells become cancerous, they produce telomerase, which can renew the telomeres and lets the cells reproduce out of control, eventually to form a tumor.
So implicating the TERT gene in a specific cancer can help lead to a better understanding of how cancer develops and boost the design of new drugs to stop tumors, Brennan added.
"The principle is there," he said. "If one can identify what goes wrong, it may be possible to identify targeted drugs." (Reporting by Michael Kahn; Editing by Maggie Fox and Matthew Jones)

NEW YORK DEC 02, 2008 (Reuters Health) - Carriers of certain haplotypes of the BRCA1 gene, which plays a central role in the DNA repair system, do not appear to respond to platinum-based chemotherapy for non-small-cell lung cancer, Korean researchers report in the Journal of Clinical Oncology published online ahead of print.
"Results from this study," senior investigator Dr. Jeong-Seon Ryu told Reuters Health, "show that lung cancer patients with two copies of AACC of
BRCA1 do not benefit from platinum doublets -- gemcitabine/platinum, docetaxel/platinum or paclitaxel/platinum -- that are standard regimens worldwide for locally advanced or metastatic non-small-cell lung cancer."
Dr. Ryu of Inha University Hospital, Inchon, and colleagues came to this conclusion after studying the relationship of 4 tagging single-nucleotide BRCA1 polymorphisms and their haplotypes on the outcome of treatment in 300 patients. The five haplotypes studied were AACC, AACA, GCTC, GATC and AATC.
Median survival was 13 months and the researchers did not find any significant associations between any of the tagging polymorphisms and overall survival.
However, patients with two copies of the AACC (wild type) haplotype had significantly shorter survival than those with one or no copy (8.47 versus 14.57 months). This continued to be true after adjustment for factors including weight loss and second-line treatment (hazard ratio, 2.097).
This effect on survival was seen in patient with squamous cell
carcinoma but not in those with adenocarcinomas.
"Therefore," concluded Dr. Ryu, "this result suggests that a new strategy is needed for these patients, especially in squamous cell carcinoma."

US and Israeli scientists have found evidence that a family history of brain cancer may increase a person's chances of developing the disease.
Researchers at the University of Utah and Tel Aviv University analysed the medical records of nearly 1,500 people from Utah and tracked back for between three and ten generations of family members.
Their findings are published in the journal
They found that a family history of brain tumours - including the aggressive glioblastoma - increases a person's likelihood of developing the disease, sometimes as much as fourfold.
Dr Deborah Blumenthal, co-director of Tel Aviv University's Neuro-oncology Service and an affiliate associate professor at the University of Utah Huntsman Cancer Institute, said that the study is unique as it was able to track genealogy records back so far.
She recommended that people with a family history of brain cancer should report this to their family doctor at routine medical checks.
"Until now, brain tumours were not thought to be an inheritable disease," said Dr Blumenthal. "A few earlier studies did find an increased risk in immediate relatives, but in such cases it is hard to distinguish between the effects of a shared environment and heredity."
However, Dr Blumenthal emphasised that the risks of having a hereditary brain tumour are still "very low" as the majority of primary brain tumours are not inheritable.
Less than five per cent of rare primary brain tumours are hereditary and the risk of inheriting genes that may increase the risk of a brain tumour is therefore low.
She explained: "Reporting to your family doctor that brain cancer runs in the family just gives a more comprehensive picture of your medical history. It may provide doctors and family members with useful information."
The researchers now hope to use blood and tissue samples from high-risk families to try to identify genes associated with brain tumours so that, in future, it may be possible to screen people with a family history of the disease and identify those whose genes place them at greater risk

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