Stress, Inflammation and Cancer

Cancer causes include methylation and inflammation

(RxWiki News) Cancer is a lot like a runaway train. In order for it to happen, not only did a lot of things go wrong, but the built-in safety mechanisms failed as well.

A team of researchers studied chronic inflammation of tissues and found that inflammation can cause those anti-cancer safety mechanisms to quit working.

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Inflammation over a long period of time does not give the tissue a chance to rest. These cells don't repair damage, including damage to the DNA, because they are in alert mode.

When no DNA repair proteins are made, this is known as gene silencing. Genetic silencing occurs by a chemical process to the DNA itself, known as methylation.

The group from The University of Texas MD Anderson Cancer Center looked at how a process known as DNA methylation was influenced by a chemical produced during stress called PGE2.

Mice in the study were given drugs to reverse the methylation process, stop the inflammation, or they received both drugs together.

Combination therapy produced the best results, reducing the number of tumors by 93 percent and shrinking tumor sizes by half as cancer fighting genes came back to life.

"We've known that chronic inflammation increases the risk of developing cancer and progression of disease," said senior author Raymond DuBois, M.D., Ph.D., and executive VP at MD Anderson.

Studying this mechanism of methylation in inflammation could lead to better information about the most influential factors in preventing and reversing cancer.

The drugs used in the study were most effective when used together. Combining the anti-inflammatory drugs such as Celebrex (celecoxib) with demethylating agents such as Vidaza (azacitidine) produced much better results than either alone did.

"One potential application of our research would be a clinical trial for patients who are at extremely high risk for developing colorectal cancer, such as those with a genetic predisposition, to see if treatment with these agents would decrease their risk," Dr. DuBois said.

Research was published in the January, 2012 edition of Nature Medicine.

The authors declared no competing financial interests.

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Review Date: 
February 2, 2012