Arthritis Villain May Also Play Role in Cancer

Study finds interleukin-1 promotes vessels tumors need

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HealthDay Reporter

MONDAY, Feb. 17, 2003 (HealthDayNews) -- Interleukin-1, the immune system molecule that causes joint damage in rheumatoid arthritis, also appears to spur the growth of cancers by promoting the formation of the blood vessels they need to flourish, Israeli scientists report.

The finding could open a new way to fight cancer, says Dr. Ron N. Apte, a professor of immunology at the faculty of health sciences of Ben-Gurion University in Beer-Sheva.

"A substance that neutralizes IL-1 is already in use in rheumatoid arthritis patients in the United States," Apte says. "It has very favorable effects on the inflammatory responses in the joints and on the well-being of patients. So, if found appropriate for cancer patients, it can be used immediately."

However, that won't happen quickly, Apte says. "Neutralizing IL-1 is not that easy, as it is part of the 'good' inflammatory responses of our defense," he says. "So, to my opinion, we need more basic research to characterize the role of IL-1 in various phases of the malignant process, in murine [mouse] models of tumors."

If Apte is right, IL-1 becomes part of a new and somewhat controversial effort to fight cancer by blocking angiogenesis, the growth of blood vessels needed for cancers to survive and spread. The idea of angiogenesis prevention was developed two decades ago by Dr. Judah Folkman of Harvard University. Efforts to apply it to treat cancers in human patients have produced mixed results.

The IL-1 finding seems to open a new front in the fight against cancer angiogenesis, Apte says. IL-1 "activates a whole cascade of cytokines and small molecules that mediate inflammation and also angiogenesis of tumors," he says. "That means that neutralizing a single molecule has potential to inhibit the production of many other molecules that control angiogenesis in a redundant manner."

Apte and his colleagues describe their research in the Feb. 18 issue of the Proceedings of the National Academy of Sciences.

They have created a strain of mice lacking the gene for IL-1. When skin, breast or prostate cancer cells were injected into normal mice, they all developed cancer and died within 20 days. The IL-1 "knockout" mice stayed cancer-free for much longer, and some never developed cancer at all. However, cancer did develop when they were injected with IL-1. And angiogenesis stopped in the normal mice when they were injected with a chemical that blocks the action of IL-1.

Apte says he isn't thinking about any human trials since his business is basic research. What he is doing, he says, is more experiments with mice designed to lack specific genes of the IL-1 family. Those experiments "have further verified and extended the findings of the PNAS paper," he says.

More information

You can learn more about angiogenesis by consulting the National Cancer Institute. Meanwhile, the Arthritis Foundation has a primer on rheumatoid arthritis.

SOURCES: Ron N. Apte, M.D., professor, immunology, Ben-Gurion University, Beer-Sheeve, Israel; Feb. 18, 2003, Proceedings of the National Academy of Sciences

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