Showing posts with label Cancer. Show all posts

Cancer Treatment Targets Tumor Blood Supply In Patients

A clinical trial has for the first time proven that an antibody called J591 specifically targets an antigen found in high amounts on both prostate tumors and on blood vessels of all solid tumors, according to a study by medical researchers at NewYork-Presbyterian Hospital/Weill Cornell Medical Center in New York City.

Since the prostate-specific membrane antigen (PSMA) exists only on tumors and not other tissues, J591 armed with a drug or radiation offers a way to selectively target cancer while leaving healthy tissues unharmed, thereby resulting in very low levels of toxicity and fewer side effects for patients.

While the study, published in the Feb. 10 issue of the Journal of Clinical Oncology, was designed to prove that J591 could exclusively target tumors (it did not try to reduce tumor size), researchers now have a vehicle for selectively transporting drugs or a radioactive isotope to destroy the blood vessels that feed tumors, thereby cutting off the cancer's blood supply.

"This was a proof-of-principle study designed purely to confirm that we could successfully target tumor vasculature without targeting normal tissue," said the study's senior author, Dr. Neil H. Bander, a urological cancer specialist at the medical center and the Bernard and Josephine Chaus Professor of Urological Oncology at Weill Cornell Medical College. "Now that we have confirmed specific and accurate targeting, in subsequent studies we will arm the J591 antibody with drugs or radioactivity, and then we will assess tumor response. We are already using such armed antibodies in patients with prostate cancer and have been able to show significant anti-tumor activity."

The research team used a radioactive tracer, attached to the antibody, to follow J591's progress throughout the body. The trial involved 27 cancer patients with a wide range of solid tumors -- including kidney, bladder, lung, breast, colorectal, pancreatic and skin. All patients had widespread disease that had failed conventional treatments.

PSMA has been an attractive target for cancer drug development because it is not only present in high amounts in prostate cancers but it also is the only known molecular target that is present on tumor blood vessels but not on normal blood vessels.

Other researchers are developing drugs that indirectly starve tumors of blood by reducing the growth of new blood vessels. But, such therapies are less effective against more advanced tumors with established blood vessels. By directly targeting tumor blood vessels, however, J591 treatments could destroy the tumor's blood supply and shrink even advanced tumors.

"In the future, we envision a multipronged attack on the tumor -- for example, combining therapies aimed directly at the malignant cells, along with therapies to both directly kill the tumor's blood supply as well as prevent it from regrowing," Bander said.

This work was supported by the U.S. National Institutes of Health, U.S. Department of the Army, Cancer Research Institute, David H. Koch Foundation, Robert McCooey Cancer Research Fund, Laurent and Alberta Gerschel Foundation, Yablans Family Foundation and BZL Biologics Inc. Bander is a consultant to -- and owns stock in -- BZL Biologics, which has licensed the PSMA antibodies from Cornell.

Co-researchers, all medical doctors, include Matthew Milowsky, David Nanus, Lale Kostakoglu, Shankar Vallabhajosula and Stanley Goldsmith of NewYork-Presbyterian Hospital/Weill Cornell Medical Center and Jeffrey Ross and Christine Sheehan of Albany Medical Center.

Chemotherapy-Resistant Cancer Stem Cell Could Be 'Achilles' Heel' of Cancer

Scientists at Mount Sinai School of Medicine have discovered a subpopulation of cells that display cancer stem cell properties and resistance to chemotherapy, and participate in tumor progression. This breakthrough could lead to the development of new tests for early cancer diagnosis, prognostic tests, and innovative therapeutic strategies, as reported in Cancer Cell.

Resistance to chemotherapy is a frequent and devastating phenomenon that occurs in cancer patients during certain treatments. Unfortunately, tumors that initially respond to chemotherapy eventually become resistant to it, contributing to tumor progression and death. The study reveals that these new cancer "stem" cells, which have not been differentiated into more specific cell types, are capable of multiplying despite being exposed to chemotherapy, while differentiated cells die.

Led by Carlos Cordon-Cardo, MD, PhD, Chair of Pathology, and Josep Domingo-Domenech, MD, PhD, Assistant Professor of Pathology at Mount Sinai, the research team generated cellular models of drug resistance by treating prostate tumor cell lines with increasing doses of the common chemotherapy drugs, including docetaxel. They identified a cell population expressing markers of embryonic development. In addition, these cells displayed cancer stem cell functions, including the capacity to initiate tumor cell growth. Next, the team evaluated human tissue samples of prostate cancer and found that patients with more aggressive or metastatic tumors had more of these cancer "stem" cells.

"This is the first time these so-called cancer stem cells of prostate have been identified as the basis for drug resistance and tumor progression, indicating that they are cancer's 'Achilles Heel,'" said Dr. Cordon-Cardo. "These findings are the culmination of more than six years of innovative research, which has led to the successful unveiling of cancer characteristics that are critical to understanding how the disease works and progresses."

The study also defines a new therapeutic strategy for patients with prostate cancer, consisting of a combination of standard chemotherapy and two pharmacological agents that inhibit key signaling pathways associated with embryonic development and cell differentiation. Results showed that chemotherapy eliminated differentiated tumor cells, whereas the signaling pathway inhibitors selectively depleted the cancer stem cell population. Some of these inhibitors are already in clinical trials, and some are FDA-approved.

"By targeting these newly identified cancer 'stem' cells, we are attacking the foundation of tumor growth, rather than treating the symptoms of it," said Dr. Domingo-Domenech. "The novel discovery of this cell population could lead to the development of new tests for early cancer diagnosis, prognostic tests, and innovative therapeutic strategies."

Ongoing studies suggest that this new cell type exist in other tumor types such as breast cancer, colon cancer, bladder cancer and lung cancer. Dr. Cordon-Cardo's team is studying these disease areas to determine the presence and impact of these cancer cells.

Potential Biomarker for Cancer Diagnosis Identified

Scientists studying cancer development have known about micronuclei for some time. These erratic, small extra nuclei, which contain fragments or whole chromosomes that were not incorporated into daughter cells after cell division, are associated with specific forms of cancer and are predictive of poorer prognosis.

In a new study, published on July 3 inCell, a team of scientists at the Salk Institute for Biological Studies finds that disrupted micronuclei, which can trigger massive DNA damage on chromosomes, might play an even more active role in carcinogenesis than previously thought. They also found that disrupted micronuclei can be an objective biomarker for the genetic instability common to many solid tumors, including non-small cell lung cancer (NSCLC).

"Our study shows that more than 60 percent of micronuclei undergo catastrophic dysfunction in solid tumors such as NSCLC," says Martin Hetzer, a professor in Salk's Molecular and Cell Biology Laboratory and holder of the Jesse and Caryl Phillips Foundation Chair. "We identified disrupted micronuclei in two major subtypes of human non-small cell lung cancer, which suggests that they could be a valuable tool for cancer diagnosis."

As a result of a glitch in cell division, whole chromosomes can sometimes end up outside the nucleus. During normal division, a cell duplicates its chromosomes and sends them to two newly formed daughter cells. One set of chromosomes goes to each daughter cell, but, for a variety of reasons, the chromosomes sometimes are not divided evenly, with one cell receiving an extra set and the other cell coming up short. These lagging chromosomes, which acquire their own nuclear membrane and are called micronuclei, often don't make it to the nucleus, ending up elsewhere within the cell and becoming wrapped in their own nuclear envelope. Micronuclei appear at a higher frequency in cancer cells.

In their study, Hetzer and his team found that during a certain phase of cancer cell division previously undetected defects in the nuclear lamina, filaments that provide support and stability to the cell's nucleus, cause the nuclear envelope surrounding micronuclei to catastrophically collapse, leading to the loss of basic nuclear functions such as replication, transcription, and DNA damage recognition and repair. More than 60 percent of micronuclei undergo this irreversible loss of function following nuclear envelope collapse, precipitating cancer-causing aneuploidy, the accumulation of an abnormal number of intact chromosomes within cancer cells.

"In the micronuclei," says Emily Hatch, a research associate in the Hetzer laboratory, "we saw holes developing in the lamina. We think the membrane has no support at the site of these holes, so it weakens and ruptures. We don't fully understand why this happens in micronuclei."

Previous studies have found that the DNA damage and arrest of gene transcription caused by nuclear envelope collapse can promote aneuploidy. This damaged DNA can then enter the next generation of daughter cells and undergo chromothripsis, a rearrangement of genomic information in one chromosome, which leads to massive DNA damage and the formation of tumors.

In the current study, Hatch identified biomarkers to identify disrupted micronuclei, which may greatly increase pathologists' ability to recognize these structures in tumor sections. Currently, few objective markers exist to detect genomic instability in solid tumors, she says, although several cancers rely on the identification of aneuploidy.

"Our ability to identify disrupted micronuclei in solid tumors suggests a new way to evaluate aneuploidy in these tissues," adds Hetzer, who says that it is not clear if all or how many cancers are affected by disrupted micronuclei. In addition to NSCLC, scientists believe that micronuclei disruption may play a role in bone cancer, melanoma and other forms of lung cancer.

Because they are strongly correlated with mitotic errors, micronuclei are regarded as an accurate indicator of genomic stability and aneuploidy, two hallmarks which characterize non-small cell lung cancer. Hetzer's team found disrupted micronuclei in pulmonary adenocarcinomas, the most common form of primary lung cancer and roughly 50 percent of all NSCLCs, and squamous cell carcinomas, which make up about 30 percent of NSCLCs.

Other researchers on the study were Andrew H. Fischer of the University of Massachusetts Medical School and Thomas J. Deerinck of the University of California, San Diego. The work was supported by the National Institutes of Health, the American Cancer Society and the National Cancer Institute.

Cancer's Origins Revealed: Genetic Imprints and Signatures Left by DNA-Damaging Processes That Lead to Cancer Identified

Researchers have provided the first comprehensive compendium of mutational processes that drive tumour development. Together, these mutational processes explain most mutations found in 30 of the most common cancer types. This new understanding of cancer development could help to treat and prevent a wide-range of cancers.

Each mutational process leaves a particular pattern of mutations, an imprint or signature, in the genomes of cancers it has caused. By studying 7,042 genomes of people with the most common forms of cancer, the team uncovered more than 20 signatures of processes that mutate DNA. For many of the signatures, they also identified the underlying biological process responsible.

All cancers are caused by mutations in DNA occurring in cells of the body during a person's lifetime. Although we know that chemicals in tobacco smoke cause mutations in lung cells that lead to lung cancers and ultraviolet light causes mutations in skin cells that lead to skin cancers, we have remarkably little understanding of the biological processes that cause the mutations which are responsible for the development of most cancers.

"We have identified the majority of the mutational signatures that explain the genetic development and history of cancers in patients," says Ludmil Alexandrov first author from the Wellcome Trust Sanger Institute. "We are now beginning to understand the complicated biological processes that occur over time and leave these residual mutational signatures on cancer genomes."

All of the cancers contained two or more signatures, reflecting the variety of processes that work together during the development of cancer. However, different cancers have different numbers of mutational processes. For example, two mutational processes underlie the development of ovarian cancer, while six mutational processes underlie the development of liver cancer.

Some of the mutational signatures are found in multiple cancer types, while others are confined to a single cancer type. Out of the 30 cancer types, 25 had signatures arising from age-related mutational processes. Another signature, caused by defects in repairing DNA due to mutations in the breast cancer susceptibility genes BRCA1 and 2, was found in breast, ovarian and pancreatic cancers.

"Through detailed analysis, we can start to use the overwhelming amounts of information buried deep in the DNA of cancers to our advantage in terms of understanding how and why cancers arise,"says Dr Serena Nik-Zainal, author from the Wellcome Trust Sanger Institute. "Our map of the events that cause the majority of cancers in humans is an important step to discovering the processes that drive cancer formation."

The team found that a family of enzymes, which is known to 'edit' (ie mutate) DNA, was linked to more than half of the cancer types. These enzymes, known as APOBECs, can be activated in response to viral infections. It may be that the resulting signatures are collateral damage on the human genome caused by the enzymes' actions to protect cells from viruses.

Cancer Cure Plant

FAGONIA CRETICA - PLANT FROM INDIAN SUB=CONTINENT IS A CURE FOR CANCER.

Scientists have discovered that extracts from a plant found in arid regions of India and Pakistan can kill cancerous cells and produces no harmful side-effects associated with chemotherapy.

Tea from the plant known as Virgin’s mantle is already drunk by women in rural Pakistan who have breast cancer, the Daily Mail reported.

Researchers from Aston University, Birmingham, and Russells Hall Hospital, Dudley, found that it contains potent anti-cancer agents that act singly or in combination against the proliferation of cancer cells.

Laboratory tests showed they arrested the growth of cells within five hours of application and caused them to die within 24 hours.

The plant, which has the botanical name Fagonia cretica, is found in arid, desert regions of Pakistan, India, Africa and parts of Europe.

Professor Helen Griffiths and Professor Amtul R Carmichael, who headed the study, found herbal tea made from the extract of the plant destroys cancer cells but unlike conventional chemotherapy, treatment does not damage normal breast cells, thus reducing side effects.

Reports from breast cancer sufferers in Pakistan suggested the plant extract does not trigger any serious side effects such as loss of hair, drop in blood count or diarrhoea.

The plant extract had a novel mechanism which could remedy defects in cell DNA that would normally resist tumour growth.

An impaired DNA response not only allows the cancer to flourish, it also inhibits the way chemotherapy works which reduces its effectiveness.

“A small hospital 100 miles north of Lahore in Pakistan started using the herbal tea 40 years ago to treat breast cancer patients. It appears to keep them in remission, although we can’t use the word cure at this stage,” Carmichael said.

“However, they live for a long time without losing their hair or putting on a large amount of weight, or experiencing other toxic side effects associated with chemotherapy, so we are confident this extract has something to contribute,” Carmichael was quoted by the paper as saying.

At present the herbal tea is being used to treat Asians but there might be different effects in Caucasian patients, she added.

Plants that Fight Cancer
In 1996, 555,000 Americans alone died as a result of cancer or complications associated with the disease. It is expected that by the year 2000 cancer will pass heart disease as the number one killer in this country. Since every treatment for cancer and other illnesses at one time was considered "alternative" until its effects were proven, in hope of a cure, many American (15-25% of cancer patients) have turned to "alternative therapies" such as herbal medicine.

Out of over 30,000 tests and 2500 plants tested by the National Cancer Institute, the plant of Chinese origin,Zizyphus mauritiana proved to be helpful against combating melanoma cells. The major component responsible for this effect is betulinic acid, which inhibits growth of cancer cells. Three weeks after the treatment with the herb ended, there were no signs of tumor growth, no signs of toxic effects and was effective in small amounts. With the toxic effects of chemotherapy drugs such as vincristine and taxol, this appears to be a promising alternative, yet more studies have to be conducted until the drug can be marketed. For example, vincristine is known to cause sensory impairment and shortness of breath shortly after the medication is taken. Betulinic acid can also be extracted from betulin found in birch trees, so that if the acid is approved as a cancer treatment, then it can be produced from the birch tree much easier than from the Zizyphus mauritiana plant.

Lignans are a group of phytochemicals that may be responsible for fluctuations in sex steroids in women such as testosterone, estradiol and estrone. Lignans can be found in many fiber-containing foods, and since Americans are known for low fiber diets, then they often have low consumption of fiber. As a result, disorders such as ovarian dysfunction, suppression of ovulation, and lower amounts of corpus luteum occur more readily in women. Ovarian disorders are probable links to breast and other cancers. The flax seed contains concentrated forms of 2 lignans-enterodiol and enterolactone-so a study was conducted to see if intake of flax seed correlated to a lower breast cancer risk.
The study conducted from 18 participants at the University of Rochester and Minnesota included 10 grams of flax seed power in conjunction with her regular low fiber diet. The results showed increase in the luteal phase, less suppression of ovulation, and a decreased frequency of ovarian dysfunction. This study therefore suggested that an intake of greater amounts of lignans could result in a decreased risk cancers, such as breast cancer, that are hormone dependent.

Another plant used in cancer treatment is called Astragalus. Research has shown that it is a powerful stimulator of the immune system. It increases and stimulates the number and growth of stem cells in the marrow tissue and lymph. In the area of cancer research, the University of Texas showed that Astragalus completely restored cancer patients immune cells to work at a higher degree than those not affected by cancer in some cases. With a belief that cancer arises when foreign cells are not removed from the system, this plant could be used as a stimulus to the immune system as a way to prevent cancer before it begins. It could also aid in quickening a cancer patient's recovery from damaged immune system as a result of chemotherapy, radiation and bone marrow treatment.

Although herbal medicine is still controversial in the medical community, it is gaining ground in cancer treatment as a therapy used with conventional medicine such as chemotherapy and radiation.

Local scientist wants you to pick the cure for cancer

Dr. Jim Olson is leading a team of researchers searching for medical treatments in plants and animals. You can decide which organisms they investigate first. (Courtesy Fred Hutch Cancer Research Center)

SEATTLE -- Could a scorpion hold the cure for cancer? How about a sunflower? A Seattle oncologist is inviting the public to choose which plants or animals researchers should use to treat the world’s toughest diseases.

Dr. Jim Olson, a pediatric brain cancer specialist at the Fred Hutch Cancer Research Center, has founded “Project Violet,” a program that allows citizen scientists to invest in the development of new cancer drugs made from organisms ranging from spiders to potatoes.

Investors can “adopt a drug candidate” for $100 through the project website. Donors choose from five organisms – spider, petunia, potato, scorpion or horseshoe crab – and then choose a drug molecule inspired by that protein. The investor names the drug candidate and can give their email address so they can stay in contact with the scientists working on that drug and learn if their investment leads to a lifesaving discovery.

“Every donation really helps launch a program that might not otherwise be possible,” Olson said. “A hundred dollars gets the drug out of the computer screen and into testing for diseases like pediatric cancers.”

Donors can also adopt drug candidates for schools or classrooms.

“You become part of a community that is working together to find new cures,” Olson said. “I believe people’s lives will be enriched and our program will be able to continue at full speed.”

The drug candidates in Project Violet are part of a new class of anti-cancer compounds derived from plants and animals: “optimized peptides,” also known as “optides.” It is believed these peptides can be used to attack cancer cells while leaving healthy cells untouched, sparing patients from the toxic effects of chemotherapy including hair loss and nausea.

Project Violet was built on the success of Olson’s initial invention of Tumor Paint, a molecule derived from scorpion venom that safely travels through the body and causes cancer cells to light up to help surgeons distinguish cancer from normal tissue.

“We were impressed that scorpions have evolved amazing drugs, which led us to begin looking deeply into the drugs produced by other plants and animals,” Olson said. “For example, sunflower petals are not eaten by bugs because they make a compound that protects them from hungry insects. Likewise, we found exquisite examples of drugs made by potatoes, spiders, cone snails, sea slugs and, yes, violets.”

Olson and colleagues are developing optides that target some of the most treatment-resistant malignancies: brain cancer, melanoma, breast cancer and tumors of the neck and throat. These drugs may also lead to treatments for epilepsy, depression, anxiety and other disorders of the central nervous system, Olson said.

“Optides offer unprecedented accuracy – an entirely new class of drugs that are far less toxic, far more effective and flexible enough to be used in a wide range of applications,” he said.

Other researchers have tried to create drugs derived from plants and animals, but most efforts have failed because it is so challenging to make optides inexpensively, rapidly and in large enough quantities to conduct rigorous scientific experiments.

But, Olson and his collaborators have developed a new optide production system to quickly synthesize thousands of optide variants that can then be evaluated for therapeutic potential.

“Whereas it takes some companies a decade to make hundreds of peptide drug candidates, we can make 12,000 a month and are ramping up beyond that,” he said. “Nature provides the raw materials and we provide the expertise to turn them into lifesaving therapies.”

Project Violet was named after Violet O’Dell, one of Olson’s patients from Sequim, who was diagnosed with a diffuse intrinsic pontine glioma brain tumor in 2011 when she was 10 years old. The disease kills 90 percent of patients within nine months, and the remaining 10 percent rarely live past one year. In his 23 years practicing oncology, Olson has never had a child survive this type of cancer. When Violet learned she was likely going to die from her brain tumor, she focused her hope on others. She asked Olson if she could donate her brain tumor to research after she died.

“That spirit of generosity led to the most exciting scientific project I’ve worked on in my life. It was only fitting that it be named after Violet,” Olson said. “I knew that we were going to do this in her spirit, memory and honor.”Violet’s mom Jess is confident Olson’s work will lead to significant discoveries.

“He is going to find a cure this way because of his humble values,” she said. “It take a village. It doesn’t matter where the credit goes, just that it happens.”

There Is No Mistaking The Evidence,

Cannabis Cures Cancer

Cannabis is one of the most powerful healing plants in the world and it makes cancer essentially disappear. Cannabis compounds are responsible for halting the growth factors that are responsible for metastatic growth.

Although there has been scientific evidence that marijuana can shrink and even kill tumors since the 1970s, much of the recent public interest in this research has been inspired by Run From The Cure , a documentary about a Canadian man who claims that the concentrated oil from the cannabis plant has cured his skin cancer. He then tries the cure on a number of other cancer victims in his community with similar results .

Researchers have now found that the compound, called cannabidiol, has the ability to ‘switch off’ the gene responsible for metastasis in an aggressive form of breast cancer. Importantly, this substance does not produce the psychoactive properties of the cannabis plant.

A team from the California Pacific Medical Center, in San Francisco, first spotted its potential five years ago, after it stopped the proliferation of human breast cancer cells in the lab.

Another Spanish team, led by Dr Manuel Guzmon, wanted to see whether they could prevent a form of cancer (glioblastoma multiforme) from growing by cutting off its blood supply. Glioblastoma multiforme is one of the most difficult cancers to treat – it seldom responds to any medical intervention, especially conventional methods which poisoning and primatively destroy cells such as radiotherapy, chemotherapy and surgery.

The mice were given a cancer similar to the human brain cancer (glioblastoma multiforme). The mice were then given cannabinoids and the genes examined. The genes associated with blood vessel growth in tumors through the production of a chemical called vascular endothelial growth factor (VEGF) had their activity reduced.

Cannabinoids halt VEGF production by producing Ceramide. Ceramide controls cell death.

Dr Guzmon said: “As far as we know, this is the first report showing that ceramide depresses VEGF pathway by interfering with VEGF production.”

They then wanted to see if this would also happen with humans.

They selected two patients who had glioblastoma multiforme and had not responded to chemotherapy, radiotherapy or surgery. The scientists took samples from them before and after treating them with a cannabinoids solution – this was administered directly into the tumor.

Amazingly, both patients experienced reduced VEGF levels in the tumor as a result of treatment with cannabinoids.

Confirmed: Flaxseed Contains ‘Estrogens’ That Regress Cancer

Flaxseed has remarkable therapeutic properties, with over 50 potential applications in the prevention and treatment of disease, as documented in the peer-reviewed biomedical literature itself*

Flaxseed’s role in breast cancer is one of the more compelling areas of research, considering this is the #1 form of cancer afflicting women today, and that most women still equate “prevention” with subjecting themselves to annual breast screenings involving highly carcinogenic 30 kVp gamma rays — overlooking entirely the role of diet, as well as avoidable chemical exposures. (More on this topic)

Given that flaxseed already has an exceptional nutritional profile, there are a broad range of reasons to incorporate it into the diet, even if only as a nourishing food. The main reason why the public is so enthralled by flaxseed (and rightly so!) is for its relatively high levels of omega-3 fatty acids, and the density of soothing, mucilaginous fiber it contains. Now, an accumulating body of scientific research reveals flaxseed’s hitherto secret ‘second life’ as a medicinal powerhouse, confirming how timelessly true was Hippocrates proclamation that food is also medicine.

In 2005, the journal Clinical Cancer Research published a placebo-controlled study involving patients who received a 25 gram flaxseed-containing muffin over the course of 32 days. After observing a reduction in tumor markers and an increase in programmed cell death (apoptosis) in the flaxseed-treated patients, the authors concluded: “Dietary flaxseed has the potential to reduce tumor growth in patients with breast cancer.”

Additional animal research supports flaxseed’s role in suppressing human breast cancer. In immunosuppressed mice (thymus removed), flaxseed and an extract of pure secoisolariciresinol diglucoside from flaxseed was capable of suppressing the estrogen-fed (estradiol-17 beta) growth of transplanted human breast cancer tumors. Flaxseed does not just suppress estradiol production, as do blockbuster hormone-suppressive chemotherapy drugs like Arimidex (created by the chemical company which founded Breast Cancer Awareness Month!), but nudges estradiol metabolism into a positive direction bygenerating a higher ratio of the beneficial metabolite 2-hydroxyestrone versus the more harmful 16-hydroxylestrone.

The anti-cancer effects of flaxseed are not limited to breast cancer. Prostate cancer, another archetypally hormone-senstive cancer, is also benefited from this remarkable seed. In a 2008 study published in the journal Cancer Epidemiology, Biomarkers & Prevention, prostate cancer patients scheduled at least 21 days before prostate removal were randomnly assigned to one of 4 groups: 1) control (usual diet) 2) flaxseed-supplemented diet (30 g/d) 3) low-fat diet 4) flaxseed-supplemented, low-fat diet. The authors noted “Proliferation rates were significantly lower (P < 0.002) among men assigned to the flaxseed arms.” The study concluded: “Findings suggest that flaxseed is safe and associated with biological alterations that may be protective for prostate cancer.”

How does flaxseed work to prevent and/or regress hormone-associated cancers? The surprising answer is it is due to flaxseed’s distinctively hormonal and/or hormone-modulating activity. Flaxseed contains compounds known as phytoestrogens which have the ability to interact with cellular estrogen receptors. Although an increasingly common mantra in the conventional medical community (particularly in the field of oncology) is to identify all estrogens, including phytoestrogens, as “carcinogenic,” the weight of the evidence stands against this accusation, both in the case of soy and flaxseed. Our indexing project, for instance, has identified 36 studies on soy’s anti-breast cancer properties. It helps to understand the biochemistry in order to make sense of how a plant estrogen may actually reduce estrogen activity in the body…

The byproducts of flaxseed fermentive biotransformation in the colon: namely, enterodiol (END) and enterolactone (ENL), are known to modulate estrogen levels in tissues affected by these compounds. They are weakly estrogenic, which explains why they may alleviate hot flash symptoms in women dealing with hormone insufficiency, but are also antiestrogenic, capable of binding to estrogen receptors and blocking out more powerful estrogens (both endogenous and xenobiotic) at the same time. This is also known as Selective Estrogen Receptor Modulation (SERM): the ability to down-regulate estrogen activity in one tissue (breast), and up-regulate it in another (bone or brain). Soy contains the phytoestrogen compound genistein, also a byproduct of the bacterial biotransformation, which shares in this dual-acting SERM activity. Although drug companies have attempted to reproduce SERM-like affects with novel, synthetic compounds, often the unintended, adverse affects far outnumber the intended therapeutic ones. This is one reason why the discovery of pharmacologically active principles in foods, i.e. food as medicine, holds so much promise as the drug-driven system of conventional medicine begins to collapse under the growing weight of its own incompetence.

In the meantime, while you are enjoying flaxseed as a nourishing food, it is reassuring to know you may gain protection from the following health conditions in the process:

Just One Can of Soda a Day Raises Aggressive Cancer Risk By 40 Percent

Men who drink one 300ml can of soda per day are much more likely to require treatment for a serious form of cancer than those who never consumed the drink.

A 15-year study found those who drank 300ml of a fizzy drink a day — slightly less than a standard can — were 40 percent more likely to develop prostate cancer than men who avoid the drinks.

Worryingly, the risk applied not to early-stage disease that was spotted via blood tests but to cancers that had progressed enough to cause symptoms.

This is significant as faster-growing forms of prostate cancer are more likely to be fatal.

It is thought that sugar triggers the release of the hormone insulin, which feeds tumours.

In America in 1850, about 13 ounces of soda were consumed per person per year. In the late 1980s, more than 500 twelve-ounce cans of sodas were consumed per person per year. The 1994 annual report of the beverage industry shows that per-capita consumption of sodas is 49.1 gallons per year. Of this amount, 28.2 percent of consumption is diet soda. Current estimates per-capita is approximately 60 gallons per year. The United States are the largest consumers of soft drink consumption and at least double the consumption of almost every country in the world.

Carbonated soda pop provides more added sugar in a typical 2-year-old toddler’s diet than cookies, candies and ice cream combined.

Fifty-six percent of 8-year-olds down soft drinks daily, and a third of teenage boys drink at least three cans of soda pop per day.

Prostate cancer is the second most common cancer in men, affecting more than one billion worldwide annually.

The study, published in the respected American Journal of Clinical Nutrition, is far from the first to link the sugary soft drinks which lead to poor health. Previous research has flagged up heart attacks, diabetes,weight gain, brittle bones, pancreatic cancer, muscle weakness and paralysis as potential risks.

In the spring of 2005, research showed a strong correlation between esophageal cancer and the drinking of carbonated beverages.

For the study, they tracked the health of more than 8,000 men aged 45 to 73 for an average of 15 years. The men, who were in good health at the start of the study, were also quizzed about what they liked to eat and drink.

At the end of the study, they compared the dietary habits of the men who had been diagnosed with prostate cancer with those who remained healthy and found a clear link between sugary drinks and the disease.

Lund University researcher Isabel Drake said: ‘Among the men who drank a lot of soft drinks we saw an increased risk of prostate cancer of around 40 percent.’ The analysis also linked large amounts of cakes and biscuits, and sugary breakfast cereals with a less serious form of the disease.

Diet drinks, and tea and coffee with sugar, were not included in the study.

April McCarthy is a community journalist playing an active role reporting and analyzing world events to advance our health and eco-friendly initiatives.

· Acute lymphoblastic leukemia (ALL)
· Acute myeloid leukemia
· Adrenocortical carcinoma
· AIDS-related cancers
· AIDS-related lymphoma
· Anal cancer
· Appendix cancer
· Astrocytoma, childhood cerebellar or cerebral
· Basal-cell carcinoma
· Bile duct cancer, extrahepatic (see Cholangiocarcinoma)
· Bladder cancer
· Bone tumor, Osteosarcoma/Malignant fibrous histiocytoma
· Brainstem glioma
· Brain cancer
· Brain tumor, cerebellar astrocytoma
· Brain tumor, cerebral astrocytoma/malignant glioma
· Brain tumor, ependymoma
· Brain tumor, medulloblastoma
· Brain tumor, supratentorial primitive neuroectodermal tumors
· Brain tumor, visual pathway and hypothalamic glioma
· Breast cancer
· Bronchial adenomas/carcinoids
· Burkitt's lymphoma
· Carcinoid tumor, childhood
· Carcinoid tumor, gastrointestinal
· Carcinoma of unknown primary
· Central nervous system lymphoma, primary
· Cerebellar astrocytoma, childhood
· Cerebral astrocytoma/Malignant glioma, childhood
· Cervical cancer
· Childhood cancers
· Chronic lymphocytic leukemia
· Chronic myelogenous leukemia
· Chronic myeloproliferative disorders
· Colon Cancer
· Cutaneous T-cell lymphoma
· Desmoplastic small round cell tumor
· Endometrial cancer
· Ependymoma
· Esophageal cancer
· Ewing's sarcoma in the Ewing family of tumors
· Extracranial germ cell tumor, Childhood
· Extragonadal Germ cell tumor
· Extrahepatic bile duct cancer
· Eye Cancer, Intraocular melanoma
· Eye Cancer, Retinoblastoma
· Gallbladder cancer
· Gastric (Stomach) cancer
· Gastrointestinal Carcinoid Tumor
· Gastrointestinal stromal tumor (GIST)
· Germ cell tumor: extracranial, extragonadal, or ovarian
· Gestational trophoblastic tumor
· Glioma of the brain stem
· Glioma, Childhood Cerebral Astrocytoma
· Glioma, Childhood Visual Pathway and Hypothalamic
· Gastric carcinoid
· Hairy cell leukemia
· Head and neck cancer
· Heart cancer
· Hepatocellular (liver) cancer
· Hodgkin lymphoma
· Hypopharyngeal cancer
· Hypothalamic and visual pathway glioma, childhood
· Intraocular Melanoma
· Islet Cell Carcinoma (Endocrine Pancreas)
· Kaposi sarcoma
· Kidney cancer (renal cell cancer)
· Laryngeal Cancer
· Leukemias
· Leukemia, acute lymphoblastic (also called acute lymphocytic leukemia)
· Leukemia, acute myeloid (also called acute myelogenous leukemia)
· Leukemia, chronic lymphocytic (also called chronic lymphocytic leukemia)
· Leukemia, chronic myelogenous (also called chronic myeloid leukemia)
· Leukemia, hairy cell
· Lip and Oral Cavity Cancer
· Liposarcoma
· Liver Cancer (Primary)
· Lung Cancer, Non-Small Cell
· Lung Cancer, Small Cell
· Lymphomas
· Lymphoma, AIDS-related
· Lymphoma, Burkitt
· Lymphoma, cutaneous T-Cell
· Lymphoma, Hodgkin
· Lymphomas, Non-Hodgkin (an old classification of all lymphomas except Hodgkin's)
· Lymphoma, Primary Central Nervous System
· Macroglobulinemia, Waldenström
· Malignant Fibrous Histiocytoma of Bone/Osteosarcoma
· Medulloblastoma, Childhood
· Melanoma
· Melanoma, Intraocular (Eye)
· Merkel Cell Carcinoma
· Mesothelioma, Adult Malignant
· Mesothelioma, Childhood
· Metastatic Squamous Neck Cancer with Occult Primary
· Mouth Cancer
· Multiple Endocrine Neoplasia Syndrome, Childhood
· Multiple Myeloma/Plasma Cell Neoplasm
· Mycosis Fungoides
· Myelodysplastic Syndromes
· Myelodysplastic/Myeloproliferative Diseases
· Myelogenous Leukemia, Chronic
· Myeloid Leukemia, Adult Acute
· Myeloid Leukemia, Childhood Acute
· Myeloma, Multiple (Cancer of the Bone-Marrow)
· Myeloproliferative Disorders, Chronic
· Nasal cavity and paranasal sinus cancer
· Nasopharyngeal carcinoma
· Neuroblastoma
· Non-Hodgkin lymphoma
· Non-small cell lung cancer
· Oral Cancer
· Oropharyngeal cancer
· Osteosarcoma/malignant fibrous histiocytoma of bone
· Ovarian cancer
· Ovarian epithelial cancer (Surface epithelial-stromal tumor)
· Ovarian germ cell tumor
· Ovarian low malignant potential tumor
· Pancreatic cancer
· Pancreatic cancer, islet cell
· Paranasal sinus and nasal cavity cancer
· Parathyroid cancer
· Penile cancer
· Pharyngeal cancer
· Pheochromocytoma
· Pineal astrocytoma
· Pineal germinoma
· Pineoblastoma and supratentorial primitive neuroectodermal tumors, childhood
· Pituitary adenoma
· Plasma cell neoplasia/Multiple myeloma
· Pleuropulmonary blastoma
· Primary central nervous system lymphoma
· Prostate cancer
· Rectal cancer
· Renal cell carcinoma (kidney cancer)
· Renal pelvis and ureter, transitional cell cancer
· Retinoblastoma
· Rhabdomyosarcoma, childhood
· Salivary gland cancer
· Sarcoma, Ewing family of tumors
· Sarcoma, Kaposi
· Sarcoma, soft tissue
· Sarcoma, uterine
· Sézary syndrome
· Skin cancer (nonmelanoma)
· Skin cancer (melanoma)
· Skin carcinoma, Merkel cell
· Small cell lung cancer
· Small intestine cancer
· Soft tissue sarcoma
· Squamous cell carcinoma – see Skin cancer (nonmelanoma)
· Squamous neck cancer with occult primary, metastatic
· Stomach cancer
· Supratentorial primitive neuroectodermal tumor, childhood
· T-Cell lymphoma, cutaneous – see Mycosis Fungoides and Sézary syndrome
· Testicular cancer
· Throat cancer
· Thymoma, childhood
· Thymoma and Thymic carcinoma
· Thyroid cancer
· Thyroid cancer, childhood
· Transitional cell cancer of the renal pelvis and ureter
· Trophoblastic tumor, gestational
· Unknown primary site, carcinoma of, adult
· Unknown primary site, cancer of, childhood
· Ureter and renal pelvis, transitional cell cancer
· Urethral cancer
· Uterine cancer, endometrial
· Uterine sarcoma
· Vaginal cancer
· Visual pathway and hypothalamic glioma, childhood
· Vulvar cancer
· Waldenström macroglobulinemia
· Wilms tumor (kidney cancer), childhood