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Scientists Discover How Stomach Tumors Form

Blocking IL-11 protein prevents inflammation, hints of new treatments for disease

WEDNESDAY, April 23 (HealthDay News) -- Scientists say they may have discovered how tumors develop in the stomach, a finding that could lead to new treatments for gastric cancer.

In a study done on mice, scientists at the Melbourne Branch of the International Ludwig Institute for Cancer Research (LICR) found that blocking the signaling pathway of the IL-11 protein -- either through genetic manipulation or with medications -- would prevent certain inflammation, hyperplasia (an abnormal increase in the number of cells), and tumor formation in pre-clinical models of stomach cancer.

Stomach cancer, the second most common cause of cancer-related deaths worldwide, has been shown previously to be correlated with chronic inflammation.

The findings were published online April 22 in The Journal of Clinical Investigation.

The study shows that IL-11 promotes chronic inflammation and the formation of tumors in the stomach by increasing activation of the Stat3 protein, a known player in inflammation-associated carcinogenesis. Excessive Stat3 activity is often found in gastric and other types of cancer. The underlying cause of the Stat3 issue had previously been unknown.

"The clear link between inhibition of IL-11/Stat3 activity and suppression of gastric tumorigenesis that we identified supports the further development of pharmacologic agents that target these molecules for the treatment of gastric and potentially other cancers," study author Matthias Ernst, from the LICR Melbourne Branch, said in a prepared statement. "We believe that we have a very relevant model in our hand for the preclinical assessment of such compounds as well as for the identification of potential markers that may ultimately help in the early detection of disease."

More information

The American Cancer Society has more about stomach cancer.

-- Kevin McKeever

SOURCE: Ludwig Institute for Cancer Research, news release, April 22, 2008

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