Liver cancer -- the fifth most common cancer type worldwide -- may have do do more with a patient's DNA rather than any specific environmental variable, according to new research.

Liver cancer was found to be affected by the genome of a particular patient after the process of methylation (the extent can vary widely), which then could be tied to a particular liver cancer patient's outcome.

This really does not suggest anything surprising, since most cancers tend to be sunk deeply into a person's DNA, then expressed in various ways based on the witch's brew of lifestyle variables unique to every patient.

I honestly think we're just now starting to scratch the surface on the understanding of how cancer develops, even after decades of specific, billion-dollar research.

In a study recently published in Molecular Cell, two molecular biologists at Tufts have used yeast artificial chromosomes to show that there is a highly flexible DNA sequence that increases fragility and stalls replication, causing the chromosome to break. The site that is prone to breaking lies in the middle of a tumor suppressor gene and breakage is highly associated with cancer.

According to Catherine Freudenreich, lead author on the study, "If you delete that gene or delete part of that gene so it doesn't work anymore, that can lead to tumors. The fact that there is fragility in the same region that this gene is located is a bad coincidence."

Four more breast cancer genes have been uncovered by a team of international scientists, a discovery that may rival in importance the cloning of the BRCA2 gene in 1995. Scientists say women with mutated versions of these genes have a pretty low risk of contracting breast cancer, though, and it's unlikely that screening tests for such mutations will be developed.

Genetic causes of breast cancer account for 5 to 10 percent of all cases. Lifestyle factors, such as smoking and environmental influences, account for the rest.

Until now, only 25 percent of the genes suspected to cause inherited breast cancer had been identified. The four new genes -- FRFR2, TNRC9, MAP3K1, and LSP1 -- are believed to be fairly common yet account for only four percent of all cases. The genes BRCA1 and BRCA2, in contrast, are not very common but indicate a high risk for disease.

A high intake of vitamin C has been shown to reduce the risks for virtually all forms of cancer, including leukemia, lymphoma, and lung, colorectal, and pancreatic cancers as well as sex hormone related cancers like breast, prostate, cervix, and ovarian cancers. Vitamin C is your body's first and most effective line of antioxidant protection. Vitamin C protects cell structures like DNA from damage and it helps the body deal with environmental pollution and toxic chemicals. Vitamin C enhances immune function, and it inhibits the formation of cancer causing compounds in the body (such as the nitrosamines, chemicals produced when the body digests processed meats containing nitrates).

Dr. Douglas Brodie states in the book, Alternative Medicine Definitive Guide to Cancer, "Each one of us produces several hundred thousand cancer cells every day of our lives. Whether we develop clinical cancer or not depends upon the ability of our immune systems to destroy these cancer cells. That's because cancer thrives in the presence of a deficient immune system."

Here is a list of foods high in vitamin C. Adding these foods to your daily diet will help boost your immune system which will aid you in fighting off many diseases as well as cancer.
Fruits and vegetables are both high in Vitamin C. The highest are papaya, raw red and green peppers, oranges, cantaloupe, broccoli, cauliflower, strawberries, Brussels sprouts, baked potato, cabbage, green peas, kiwi fruit, and kale.

There are a few good vitamin C supplements on the market but one that I particularly am using at present to super charge my immune system is Emergen-C Super Energy Booster which has 1,000mg of vitamin C along with vitamin B and 32 mineral complexes.

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.

Cancer is a complicated disease often described by those who know it well in confusing medical, technical, and scientific terms. There's a way to understand it in simple terms, though. And a recent CBS news story features a great run-down on the disease, its causes, how it grows, and more.

Think about this:

• Cancer refers to any one of a large number of diseases characterized by the uncontrollable growth of abnormal cells. These cells have the ability to infiltrate and destroy normal tissue and can spread -- metastasize -- throughout the body.

• Cancer is caused by damage in the DNA. DNA is like a set of instructions for cells and tells cells how to grow and divide. Normal cells can develop mutations in their DNA but can repair most of them. If they cannot make a repair, the cells often die. But certain mutated cells don't repair and don't die. They instead grow and become cancerous.

• Normal, healthy cells grow in an orderly, well-controlled way. They live for a set period of time and then die on schedule. Dead cells are replaced by new normal cells. Cancer cells, in contrast, grow in an uncontrolled manner. They don't die. They accumulate. One malignant cell becomes two, two become four, four become eight, and so on, until a mass of cells -- a tumor -- is created. Tumors remain small until they're able to attract their own blood supply, which allows them to obtain the oxygen and nutrients they need to grow larger.

• Not all cancers form tumors. Leukemia, for example, is a cancer of the blood, bone marrow, lymphatic system, and spleen.
  
  
• Cancer can take decades to develop. By the time a cancerous mass is detected, it's likely that 100 million to one billion cancer cells are present, and the original cancer may have been dividing for five years or more.

• Lung cancer is the top cancer killer among men and women and will kill 160,390 people in 2007.

New research has stated that eating a bowl of watercress, a salad leaf, can significantly reduce DNA damage to blood cells.

The report was published in the American Journal of Clinical Nutrition and it involved 30 men and 30 women, half of whom were smokers. They ate a small bag of prepared salad for eight weeks, in addition to their regular diet.

The results of the blood tests on the participants showed a 22.9 percent reduction in DNA damage to white blood cells. Damage to DNA is considered by experts to be an important trigger in the development of cancer.

The benefits of watercress were especially notable among smokers.

The research concluded "The results support the theory that consumption of watercress can be linked to a reduced risk of cancer via decreased damage to DNA and possible modulation of antioxidant status by increasing carotenoid concentrations."

So, I think next time instead of skipping over the watercress for the arugula I will grab both!

A lab in Oklahoma is studying genes for combinations that predict breast cancer risk. A look into the 100 genes gathered from each woman -- via mouthwash -- allows researchers to categorize women with standard, moderate, or high risks of developing the disease.

The study begins with a lengthy questionnaire about medical history and leads to the collection of a DNA sample. Women simply rinse their mouths with a standard mouthwash and wait for results.

Geneticist Dr. Kara Casas says she hopes that regardless of results, women will choose a healthy lifestyle with a diet low in fat and alcohol consumption and with lots of exercise too. But those in the moderate and high-risk groupings will be advised to make other lifestyle changes to help decrease their chances of getting breast cancer. They may be asked to regulate estrogen levels, for example, and to report regularly for mammograms at an earlier age.

Casas says all women have some risk of developing breast cancer. But knowing what these risks are can help them better protect themselves -- which makes tests like this so important.

A total of 12,000 samples will collected for an FDA trial. For more information about this study in mouthwash, call 903-510-1173.

The earlier a cancer is detected, the greater the chances for cancer survival. One of the problems in surviving colon cancer is that people are reluctant to undergo colonoscopies, and therefore, colon cancer is not always detected in its earliest stages before symptoms develop.

Mount Sinai School of Medicine and EXACT Sciences Corporation are publishing study findings that show a DNA stool test can accurately predict colorectal cancer 88 percent of the time, regardless of where in the colon the cancer is located.

"This study confirms that stool-based DNA technologies can achieve high sensitivities for detecting colorectal cancer," stated Steven Itzkowitz, M.D., principal investigator and Professor and Associate Director of Gastroenterology at Mount Sinai School of Medicine. "For those individuals who are unwilling or unable to undergo colonoscopy, stool DNA testing offers a valuable and patient-friendly screening option. These results also underscore that as new markers and technologies are developed and validated, they can readily be incorporated into existing stool DNA tests to improve cancer detection and, ultimately, patient outcomes."

According to statistics, colorectal cancer is the second leading cause of cancer deaths in the U.S. and more than half of the over 80 million people over the age of 50 have never been screened. I agree with the researchers who suggest that it is time to develop new non-invasive technologies for colorectal screening.

Researchers have identified a damaged gene -- BRIP1 -- that doubles the risk of familial breast cancer in a small percentage of women. BRIP1 is a DNA repair gene that can lead to uncontrollable cell growth if not functioning properly. Researchers have concluded that the damaged gene increases risk for breast cancer from eight to 16 percent by age 70.

These findings won't change patient care but they may offer comfort to women who develop breast cancer and cannot pinpoint the occurrence to the commonly mutated BRCA1 and BRCA2 genes -- mutations that are responsible for the disease 80 percent of the time. And while the study of BRIP1 does add to the pool of research on breast cancer, it does not warrant screening at this time. It's just a small piece of the puzzle that one day may prove significant. For now, the risk of breast cancer resulting from a damaged BRIP1 gene is modest.

I hesitate to bring this up, as the hot dog is a bonafide American icon, associated so closely as it is to the all-American pastimes of baseball and backyard barbeques -- and to sacrilegiously make the suggestion or malign the hot dog on any level I realize puts me at risk of having my patriotism brought into question.

Still, knowing this, I have chosen to throw pickle relish caution to the wind in the name of science and better health.

According to University of Nebraska researchers (you note I point directly to the researchers as the originators of this news) some hot dogs might cause DNA mutation and increase colon cancer risks. Not all hotdogs, but they cannot tell you at this time which hotdogs are a cancer menace.

Hot dogs do not stand alone as culprits to cancer. Salted dried fish and soy sauce have been identified as potential offenders. But I am not nearly as skittish in mentioning the latter two.

The National Hot Dog and Sausage Council estimates that more than seven billion hot dogs will be eaten by Americans between Memorial Day and Labor Day. Statistics estimate the breakdown of hot dog consumption per American is 60 hot dogs a year.

Next? Brushing up on my French.

Charlie Emrich, in Glowing chickens bring hope in fight against cancer, calls fluorescent chickens, "cool in a creepy, mad-scientist sort of way." When you consider that scientists have combined jellyfish DNA with chickens to create illuminated birds, you can kind of see it from Emrich's descriptive perspective.

The purpose of chickens that glow, is that scientists can track antibody-based therapies that might prove valuable in treating human cancers.

UC Davis Cancer Center Dr. Joseph Tuscano explains that, "One of the problems with modern drugs is that they're not very specific. Even aspirin is not very specific. Antibodies, on the other hand are highly, highly specific meaning that, like an archer's arrow, they can effectively target a disease. Antibody-based therapies are one of the biggest advances in cancer treatment in the last 40 years."

Emrich quotes researchers of the project and takes you through the purpose and process of genetically-modified glow-in-the-dark chickens in the potential development of antibody-based therapies to one day treat cancer here.

Republican Senator Gordon Smith of Oregon calls home DNA kits for cancer and other diseases as nothing more than modern day snake oil and he believes consumers are being misled and exploited.

Smith, chairman of the Senate Special Committee on Aging, released a report from the Government Accountability Office on home DNA test products. He stated he is shocked to learn how little the federal government is doing to protect consumers in awareness and education regarding the uselessness of these products.

According to a Congressional report, home DNA tests or nutrigenetic tests, are not clinically valid and companies selling them are making unproven and ambiguous health-related predictions.

The Food and Drug Administration (FDA) and the Centers for Medicare and Medicaid Services said they were investigating the companies to determine is oversight was needed.

If you count yourself among the working poor, or one of the vanishing middle-class in a constant struggle to make ends meet, do not read this -- it is not going to cheer you up.

The most significant and unavoidable risk factor that increases the chance of being diagnosed with cancer is the aging process. The older we get, the more susceptible we are to developing cancer. Because of this fact, research into the aging process, how we age, and why we age -- even if the research is not specifically looking at the link between aging and increased cancer risk -- still might one day provide some insight into the potential for reducing cancer risks associated with aging.

Oregon Health & Science University Cancer Institute researchers have developed a new method of identifying abnormalities that cause cells to develop into cancerous ones that is much quicker and far less expensive than the traditional method of identification.

According to the researchers, DNA sequencing to find cancer-causing mutations in genes is time consuming and expensive, and the vast majority of mutations it identifies don't cause cancer. With the new method, in less than two months they were able to find three activating mutations of the tyrosine kinase JAK3 in acute myeloid leukemia cells.

"It may have taken years to find these mutations with DNA sequencing alone," said Jeffrey Tyner, Ph.D, a senior author of the study. "As we streamline our process, we will be able to analyze cancer cells for mutations in a matter of just weeks."

"It moves forward the personalized medicine model where cancer treatment is tailored for each patient based on the molecular mutations at the heart of his or her cancer," states Dr. Brian Druker, JELD-WEN chair of leukemia research in the OHSU Cancer Institute and an investigator with the Howard Hughes Medical Institute.

One day Dr. Druker believes this new method of identifying abnormalities that cause cells to turn into cancerous ones can be applied to many cancers and that there will be a targeted drug developed for each cancer. For more information, visit OHSU Cancer Institute news.