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Gene variations directly link inflammation to an increased risk for lung cancer

amage to lung tissue leads to cancer, Engels said. Knowing more about the downstream effects of these polymorphisms, and discovering others like them, will increase our understanding of how some people are predisposed to developing cancer.

To examine the relationship between inflammation and lung cancer risk, the researchers compared differences in genes related to inflammation between more than 1,500 lung cancer patients and 1,700 controls at M. D. Anderson Cancer Center in Houston, Texas. More than 80 percent of the cancer patients in the study were current or former smokers. Among the 59 variations in 37 inflammation-related genes studied, the researchers discovered that some variants in the genes for interleukin (IL) 1A and 1B, are found more frequently in patients with lung cancer -- and especially among heavy smokers. The effect was most profound in polymorphisms in IL1B, which is central to the inflammation process, the researchers said.

According to Engels, the IL1B protein is an integral part of the chemical cascade by which cell signals moderate the response to inflammation. Variations in the gene may lead to greater expression of the protein, which is more likely to turn on the cascade and sustain the damaging effects of inflammation. Over time, the constant damage of inflammation could lead to genetic damage and cancer, Engels said.

The researchers believe their findings will provide the basis for further lung cancer research as well as a model for examining the nature of inflammation in other types of cancer.

While smoking is still the greatest risk factor, we still do not understand how other factors play a role, Engels said. A better understanding of the risks involving inflammation will lead to a better understanding of cancer prevention.


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Contact: Greg Lester
lester@aacr.org
267-646-0554
American Association for Cancer Research
3-Jul-2007


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