Study Reveals How Common Painkillers Fight Cancer

FRIDAY, Dec. 15 (HealthDay News) -- For years, experts have noted that people who take nonsteroidal anti-inflammatory drugs (NSAIDs) for pain relief also lower their risk for a variety of cancers.

Now, scientists believe they know why that happens.

New research shows that NSAIDs -- which include aspirin, ibuprofen, Aleve and Celebrex -- boost the level of a cellular molecule that causes malignant cells to die off.

The finding "opens up our understanding of how anti-inflammatory drugs are effective against cancer cells. This could also lead to new drug development and of monitoring drugs' effect on cancer cells," said study senior author Towia Libermann, director of the Genomics Center at Beth Israel Deaconess Medical Center in Boston.

His team published its findings in the Dec. 15 issue ofCancer Research.

The millions of Americans who regularly take a daily NSAID to ease arthritis or other pain have long gotten an added bonus in terms of reduced cancer risk. For example, a study released this spring found that women who took daily aspirin had lower odds of developing a particularly aggressive form of breast cancer. Trials have also been conducted that suggest that Celebrex might reduce risks for precancerous colorectal polyps.

There are other indicators linking chronic inflammation and cancer. "For example, people with inflammatory bowel disease have a significantly higher risk for colon cancer than the regular population," Libermann said, and there's also a highly aggressive breast malignancy -- called inflammatory breast cancer -- that is marked by tissue inflammation.

So, it makes sense that drugs that subdue inflammation might also beat back cancer. But how?

To answer that question, Libermann's team used high-tech gene microarray analyses to examine more than 20,000 genes they knew were activated in the presence of NSAIDs.

They discovered that one gene, in particular, was highly activated to produce a particular cytokine (a protein-signaling molecule) called MDA-7/IL-24.

As the level of this cytokine rose, the ability of cancer cells to avoid programmed cell death declined.

"We showed this in different types of cancer cells and with different types of anti-inflammatory drugs," said Libermann, who is also associate professor of medicine at Harvard Medical School. "In fact, drugs that were not active in killing cancer cells did not induce this cytokine, while drugs that were able to kill cancer cells did induce this cytokine."