The folks at Canyon Ranch in Tucson, Arizona told me all about the merits of flax seed. They told me to sprinkle it here, sprinkle it there, sprinkle it everywhere. While at this desert destination, I did just that. I dipped into the bowls of flax scattered at all dining locations, and I topped my bagels, cereals, salads, and more with this powerful substance. As soon as I got home from this little slice of paradise, I bought my own personal container of flax. I promptly placed it in my refrigerator, have used it a few times, and just recently realized I'd forgotten why exactly it's so good for me.

I've done some research, and now I know a little more about this thing called flax -- and I remember why it must become a part of my everyday life.

Flax, also known as Common Flax or Linseed, is an annual plant that grows to 120 cm tall, with slender stems. Native to the region extending from the eastern Mediterranean to India, its leaves are green, its flowers blue, its fruit round and containing glossy brown seeds. Grown for both its seeds and its fibers, parts of this plant are used to make fabric, dye, paper, medicines, fishing nets, and soap. The seeds, like what sit in my refrigerator, come in two forms -- brown and yellow or golden. The yellow, golden variety is the one most often consumed.

On Tuesday, researchers announced that a three-drug cocktail may help women with HER2-positive breast cancer better than any other drug used on its own. About one quarter of women with breast cancer make up this HER2 category.

Tests on mice revealed using the three drugs along with breast cancer drug tamoxifen helped wipe out tumors altogether. And the tumors did not come back. This is the first time mice were cured of a very aggressive human breast tumor. Incidentally, when a single drug was used, tumors returned within several weeks.

The three wonder drugs used in this study -- all are monoclonal antibodies that precisely target certain aspects of tumors -- are the experimental drug pertuzumab; trastuzumab, also known as Herceptin; and gefitinib, or Iressa.

Published in the Journal of the National Cancer Institute, this study supports the notion that HER2-positive tumors eventually become resistant to one drug and attacking them on several fronts seems to work better.

A new study of mice implanted with human breast cancer cells shows the spread of the disease to the lungs -- a common metastasis site -- is caused by the abnormal activation of four specific genes working together.

The study, published in the journal Nature, indicates that shutting off the genes one by one can slow the growth and spread of this cancer. But turning off all four at one time almost completely stops the process. In mice anyway.

These genes are no strangers to researchers who have known for some time about their existence and functions. They just know more about them now.

The four genes work together at every step of the metastatic process to allow a breast tumor to develop blood vessels, let tumor cells enter the vessel walls and lungs, and permit them to pass out of the lung vessels and resume growth. New analysis shows that blocking these genes significantly reduces the tangle of blood vessels, making it harder for cancer cells to escape.

Researchers, who say the four genes are among 18 they associate with breast cancer metastasis, report that one implication of this study is clear: combined use of drug therapy may be more effective at inhibiting the activity of multiple gene targets.

There's a new vaccine out there that stimulates the immune system to find and destroy breast cancer cells. In early experiments, the vaccine held off or stopped the growth of tumors in all of the mice studied. Some mice were even cured.

Think about this:

Research presented at the annual meeting of the American Association for Cancer Research reveals this vaccine is different from most under development that help kick-start the immune systems of sick patients. In this case, the vaccine tells the immune system to recognize breast cancer cells and to attack and kill them on the spot.

One researcher says breast cancer cells usually fly under the radar of the immune system. To combat this problem, the injectable vaccine uses a bacteria-type substance that is altered to contain the gene HER2/neu and also antibodies that rev up the immune system. This makes the body react and wipe out cells containing HER2/neu.

If continued studies prove promising, the vaccine would work for the 15 to 25 percent of women whose breast cancers overexpress HER2/neu.

Antiretroviral drugs, used to prevent HIV transmission from mother to child, are now believed to cause genetic damage in infants. This damage, leading to an increased risk of developing cancer, makes it highly plausible these children may be diagnosed with the disease in mid and late adulthood.

Two new studies indicate there are cancer-causing effects of transplacental exposure to AZT, an antiretroviral drug. These effects -- like increased incidence of tumors and tumors with genetic changes -- have been demonstrated in mice and rats and seem to be cause for concern in humans too.

"The cumulative mutagenesis data suggest that infants exposed transplacentally to AZT may be at increased risk for cancer as they age," said one researcher, whose findings are published in Environment and Molecular Mutagenesis.

A new study shows men are three times more likely to develop certain types of skin cancer than women. But it doesn't have as much to do with sun exposure as we might think.

According to researchers at Ohio State University, gender differences put men at greater risk for non-melanoma skin cancers than their female counterparts.

Researchers tested the effects of UVB rays on mice and found male mice developed tumors earlier. The tumors were also larger and more aggressive than those found in female mice.

The study, published in the April 1 issue of Cancer Research, indicates it could be the higher levels of antioxidants females have in their skin that allow them to fight off tumors better.

It might not be possible at this time to eradicate cancer altogether. But we may be able to stop cancer cells in their tracks through a process called senescence.

In senescence, cells don't divide. And when cells don't divide, they don't grow. In such a scenario then, cancer cells wouldn't divide and therefore couldn't grow.

Think about this:

According to lab tests on mice, triggering senescence in certain cells hampers the growth of some tumors.

Researchers at the University of Texas M.D. Anderson Cancer Center in Houston are the ones behind the scenes on this project -- the study appears online in EMBO Reports, a publication of the European Molecular Biology Organization -- and all eyes are on the p53 gene.

The p53 gene lives within cells and works to nip cancer in the bud by springing to action in damaged cells that may be spinning themselves into a cancer frenzy.

Researchers say senescence ordered by the p53 gene is extremely important in suppressing tumor formation and is as important as apoptosis -- a type of programmed cell death. But in some cancers, senescence might not be enough to halt cancer, they found.

OK, so senescence is not a perfect approach to halting all cancers. But it seems to work for some -- so I say for now, let's take what we can get.

When Dr. Jian-Wei Gu went to Mississippi to study the cardiovascular system and the process of blood vessel growth, he had no idea he'd make national headlines about his research into the world of cancer.

Gu, assistant professor of physiology and biophysics at the University of Mississippi Medical Center, says his discovery of the mechanism by which alcohol consumption causes tumor growth was purely accidental.

And extremely significant.

Scientists have known for a hundred years about the link between alcohol consumption and cancer. A study from Paris in 1910 showed that 80 percent of patients with cancer of the esophagus or gastric track were alcoholics. More recently, scientists have found correlations between alcohol consumption and cancer of the mouth, pharynx, larynx, esophagus, liver, large bowel, and even the breasts. Yet lab experiments have always failed to show the effects in animals that investigators knew to be true in humans.

Until now.

It seems past studies used too much alcohol -- in concentrations of 20 percent -- and the animals just wasted away while showing no tumor growth. But when Gu used concentrations of one percent -- about one to two drinks per day in humans -- to study blood vessel growth, he detected stimulated tumor growth in both chick embryos and mice. Thus, his cancer discovery was born.

Gu has further concluded that melanoma cancers in mice grew significantly faster and larger in the mice who consumed the equivalent of one or two alcoholic drinks a day than the mice receiving no alcohol.

Gu's findings, now confirmed by other scientists, are evidence of what many have long suspected -- alcohol, even in moderation, increases cancer risk.

Lung cancer tumors in mice are shrinking -- with the help of a hormone important in the control of blood pressure.

This new discovery, led by scientists at Wake University School of Medicine, suggests some drugs used to manage blood pressure might also prevent or treat lung cancer.

This all came about when it was noticed that lung cancer rates were lower among those treated for high blood pressure with angiotensin-converting enzyme, or ACE, inhibitors. These drugs, including Capoten and Lotensin, increase levels of angiotensin-(1-7) in the bloodstream.

In studies, the angiotensin-(1-7) hormone caused a 30 percent decrease in tumor volume in mice. Tumors in mice not treated with the hormone more than doubled.

This study, published in the journal Cancer Research, is the first demonstration of the effect in animals.

Katherine Schaefer was investigating methods for treating the inflammation seen in Crohn's disease and ulcerative colitis when something terrible happened -- she noticed her carefully cultured cells were dead. And then something wonderful happened -- she realized she had stumbled upon a potential new method of attacking cancerous tumors that have become resistant to existing drugs.

Schaefer and her colleagues at the University of Rochester Medical Center in New York were testing a compound called a PPAR-gamma modulator -- a compound never considered a cancer drug, or a drug of any kind really -- when Schaefer made a calculation error and used a lot more of the compound than she should have. And her cells died.

Upon further study, Schaefer found the compound killed just about every possible epithelial tumor cell. These cells line organs such as the colon and also the skin. The compound, that works like taxane drugs but without eventual tumor resistance, also killed colon tumors in mice without making them sick.

The research team, whose findings are published in the journal International Cancer Research, plans more safety tests in mice. And eventually, if their outcomes are promising, they plan to design something they can patent as a new drug -- because they would love to see this disastrous lab experiment one day lead to treatment for cancers of the colon, esophagus, liver, and skin.

A drug commonly used to minimize the toxic effects of chemotherapy has been shown in mice to cause bone loss and promote tumor growth, according to the results of a recent study.

This drug, granulocyte colony-stimulating factor (G-CSF) -- also known as Neupogen, Neulasta, and Granocyte -- helps restore white blood cell counts that take a beating during chemotherapy, protecting cancer patients from an increased risk of infection.

According to researchers, G-CSF -- essentially a growth factor -- encourages bone breakdown. And any therapy that decreases bone density can enhance tumor growth in bones. So doctors are urged to closely monitor their patients during chemotherapy with regular bone density scans. They can also prescribe medications to prevent bone loss if necessary. And patients can protect their bones by consuming enough calcium and vitamin D and engaging in regular exercise.

Currently, research on cancer patients treated with G-CSF have not yielded the same strong results researchers found among mice.

The details of this study appear online in the journal Blood, and will be published in an upcoming print issue.

Canadian researchers have made an unexpected discovery in a molecule that appears to drastically boost the ability of standard drugs to kill breast cancer cells. Currently, the discovery has been confined to the lab -- but researchers hope the power of this molecule, the ANK peptide, can one day be used to counter drug resistance for many women with breast cancer.

Scientists from Queen's University say the ANK peptide, not a drug by itself, gives drugs like taxol and nocodazole more than triple the ability to kill breast cancer cells. One scientist says the process of enhancing drug effectiveness is much like adding flavor to coffee to make it taste better.

This is exciting news, but the results -- published Monday in the journal Cancer Research -- only apply to lab experiments at this point. Researchers must now proceed with testing the peptide-drug combination in lab mice. If successful, they will move on to human testing. The whole process could take years. But early results are so promising that application for a U.S. patent on the peptide has already been made.

According the medical experts, breast cancer patients can become resistant to some drugs depending on duration of treatment, dose of medication, and genetic makeup.

"This peptide would be able to give them another chance," said a researcher from this study. "For those who respond reasonably well, they will do even better; for those who don't respond to this drug treatment ... we greatly hope this will make the current drug more useful by extending its impact to a wider range of people, particularly those with a resistance problem."

In a radical new approach to attacking cancer, researchers will soon attempt to kill tumors by infecting them with viruses that cause ailments like the common cold.

This virus therapy treatment -- considered the third pillar alongside chemotherapy and radiation -- could one day become standard battle against cancer.

One Belfast doctor says anything that could improve the lives of cancer patients is worth a try. And try is exactly what Leonard Seymour, Professor of Gene Therapy at Oxford University, plans to do when he begins leading trials later this year.

Seymour, who has been working with viruses that kill cancer cells while sparing healthy tissue, will use a stealth virus masked from the body's immune system with a polymer coat that could travel through the bloodstream and reach tumors.

Two viruses are likely candidates for study in the first clinical trials -- adenovirus, cause of a cold-like virus, and vaccinia, cause of cowpox and a component in the smallpox vaccine.

Preliminary research on mice shows that virus therapy works well on tumors resistant to standard cancer drugs. But several years of trials will be necessary before the therapy can be considered for use on all cancers.

Once upon a time there were two groups of mice, all genetically engineered to develop prostate cancer. Each group was fed the same amount of calories. One group of mice lived in cages warmed to 80.6 degrees. The other group lived in cages kept at 71.6 degrees. The mice in the cooler quarters burned more calories to keep warm. And after three weeks, they weighed less than the toasty warm mice. They were also less likely to develop prostate cancer.

Then there were two other groups of mice, also genetically engineered to develop prostate cancer. Both groups were kept in cages with temperatures 80.6 degrees and 71.6 degrees -- like above. But these mice got to eat whatever their little hearts desired. The mice in cooler cages ate 30 percent more than the mice in warmer cages. They got just as fat as the warm mice. And they all got prostate cancer at the same rate, despite the extra calories.

The moral of the story is this -- being lean rather than obese has a greater protective effect against cancer. Excess calorie retention, rather than consumption, raises cancer risk. This moral stands in contrast to what most researchers believe -- that a restricted diet cuts the risk of and slows the growth of cancer and this is directly related to calorie intake.

Tim Nagy, Ph.D. and professor of nutrition sciences at the University of Alabama, Birmingham and lead researcher on the mice story says when you eat more calories than you burn, you store the extra calories as fat. It's the fat cells -- not the extra calories themselves -- that affect cancer risk.

It's not a good idea for humans to chill themselves to avoid cancer, Nagy says. But perhaps people could get the same effect by exercising more since that, too, burns calories.

Nagy's study appears in the January 1 issue of the journal Cancer Research.

In an analysis of animal research used to understand and treat human diseases, the London School of Hygiene and Tropical Medicine researchers found that using animals, such as mice, had limited value. Only half of the research done using animals translated into the same outcome for humans.

In a BBC News report over the controversy that rages regarding the wisdom of using animals in research, Professor Ian Roberts is quoted as saying, "The debate over this issue is really quite hysterical. At the moment, there is too much emotion and not much science. Anti-vivisectionists say animal testing is of no use at all, and those who do them say we would have no safe and effective treatments if we didn't." Lead researcher Roberts believes animal studies should be used, but not in all cases of research.

The value of animal research was catapulted to front page news headlines earlier this year when six men experienced tragic life-threatening side-effects as they participated in a human clinical trial of the drug TGN1412, which had previously been shown safe and effective during animal studies.

Last March, six healthy young men volunteered at Northwick Park Hospital in London as participants in a clinical trial for a drug called TGN1412, designed to treat leukemia, autoimmune and inflammatory diseases. According to the men, they were told by doctors there would be no serious short-term or long-term side effects. They were each paid £2,000. Within hours, the worst that could happen did, and the men were plunged into a nightmare beyond anything they could have imagined.

The headaches began, followed by convulsions, bloating, organ failure and comas. The men came to be known as the Elephant Men because of the swollen faces and chests they suffered. One of the men suffered gangrene -- all his toes and three of his fingers were amputated. He also suffered heart failure, kidney failure, pneumonia, septicaemia and liver failure. Recently, another participant was told he might be developing cancer as a result of the drug trial. All have been told to expect early death.

Do you feel that animal research used to test drugs and medical procedures meant to treat human ailments and diseases, are credible enough to continue, or do you believe that research using animals should be abandoned?