Hepatitis B virus infects hundreds of millions of people worldwide, causing jaundice, fatigue, liver damage, and joint pain. More ominously, investigators have indicted it in another role: as co-conspirator in a far-ranging case they've been building for years linking chronic inflammation and cancer. Researchers have long known that patients with persistent hepatitis B infections experience inflammation and scarring of liver tissue and an increased risk of liver cancer. Other sources of chronic inflammation, including the ulcer-causing bacterium Helicobacter pylori and an immune disorder known as ulcerative colitis, predispose patients to cancers of the stomach and colon.
Based on their experience with these diseases, researchers estimate that inflammation contributes to the development of at least 15% of all cancers. Much less clear, however, is exactly how it does its dirty work. The inflammation-cancer connection is especially puzzling in light of other work suggesting that in some circumstances the immune system, which sustains inflammation, has the opposite effect: inhibiting tumor development. A flurry of results published over the past few months may now be resolving the mystery.
The new work has implicated an inflammation-induced protein called NF-[kappa]B as a key player. It is an intermediary in promoting the cellular changes leading to the uncontrolled growth of cancer cells and also to later changes that help metastatic cells escape from the original tumor and spread to new sites in the body.
Other studies have pointed to a source of trouble in the inflammatory cells that creep into a growing tumor, suggesting that they produce numerous substances that can contribute to tumor growth and survival, including some that might trigger increased NF-[kappa]B activity. Research into the inflammation-cancer link "is a very exciting area that is developing very rapidly," says Raymond DuBois of Vanderbilt University Medical Center in Nashville, Tennessee.
The excitement stems in part from the expectation that this emerging understanding could lead to improved cancer prevention and treatment. Epidemiological studies have already shown that people who regularly take NSAIDs--nonsteroidal anti-inflammatory drugs--have a lower risk of developing cancer than people who don't take the drugs. But the efficacy of NSAIDs is not ideal, and the first generation of these drugs, such as aspirin, can cause life-threatening stomach ulcers. Now, even the newer NSAIDs--the so-called COX-2 inhibitors, which were designed to avoid that side effect--may have problems: On 30 September, the pharmaceutical company Merck removed its blockbuster COX-2 inhibitor Vioxx from the market because it increased patients' risks of having heart attacks and strokes.
Researchers hope that if they learn how chronic inflammation leads to cancer, they will be able to design new drugs that counter its effects. The information may also aid the development of vaccines and other strategies to enhance immune attacks on tumors. But researchers will have to toe a fine line: The new work suggests that some approaches might enhance the growth of tumors rather than kill them. "It's a complicated field, but it's extremely important," says Albert Baldwin of the University of North Carolina School of Medicine in Chapel Hill...
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