Dousing the Flames of Cancer
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By Alexandra Goho

Dousing the Flames of Cancer

Treating chronic inflammation may be crucial to preventing the disease

By Alexandra Goho


The idea that cancer begins with a series of genetic mutations that cause cells to proliferate out of control has dominated cancer research for nearly half a century. But starting a decade ago, another idea began to take hold: Could inflammation, the immune response that normally protects the body from injury and foreign invaders, be a key player in turning cells cancerous?

As much as 20 percent of all cancers arise from tissue that is chronically inflamed. For instance, infection with Helicobacter pylori, a bacterium that causes gastritis—inflammation of the stomach lining—greatly increases the risk of stomach cancer. And infection with the human papillomavirus (HPV) causes the cervical tissue to become inflamed, spurring the development of cervical cancer. A host of studies have also linked persistent inflammation to prostate, ovarian and colorectal cancers.

Because inflammatory cells are known to release toxic, gene-mutating compounds called free radicals, many cancer researchers have assumed that inflammation was just one more way that normal cells could mutate into cancer cells. But recent studies are showing that inflammation plays an even larger role and can lead to cancer in surprising ways.

“What many of us are finding is that cancer cells set up an environment in which they usurp some of the responses of the immune system,” says cancer biologist Raymond DuBois, the provost and executive vice president for academic affairs at M. D. Anderson Cancer Center in Houston and an expert on the role of inflammation in colon cancer. For instance, studies show that tumor cells hijack inflammatory cells called macrophages, which normally scavenge foreign microorganisms from the body’s tissues, and use the macrophages to proliferate and evade cell death.

When chronic inflammation is caused by an infection, eliminating the offending virus or bacteria can dramatically reduce the risk of cancer. However, treatment can be more difficult for inflammatory diseases that have no infectious agent, as is the case with inflammatory bowel disease, which can lead to colon cancer, or gastroesophageal reflux disease, which can lead to esophageal cancer. In these situations, researchers and physicians rely on drugs that eliminate the inflammation. The trick is finding ways to do that without making the immune system—a sophisticated collection of specialized cells and chemical signals—go awry. “It’s a very difficult system to play around with because it’s so important in protecting the body from infections and other pathogens,” says DuBois.

As researchers continue to uncover the mechanisms linking inflammation and cancer, new ideas are emerging for ways to block the process. Not only could these lead to more effective ways of treating patients with cancer, they also suggest ways of preventing the disease altogether in patients at risk. “If you remove the inflammation, there’s a really good chance it will reduce the risk for cancer,” says DuBois.


THE COX-2 CONUNDRUM
In the mid-1990s, DuBois, who was then at the Vanderbilt-Ingram Cancer Center in Nashville, Tenn., made an important discovery. He and his team showed that cyclooxygenase-2 (COX-2), an enzyme found mainly in inflammatory cells, was overproduced in human colorectal cancers. And blocking COX-2’s activity halted the growth of human colon cancer cells in the lab. Since then, a number of research groups have found elevated COX-2 levels in other types of cancer, including breast cancer, lung cancer and prostate cancer.



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