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TLR4 gene found to protect against tumor development

A new study finds that a gene which plays an important role in immune function, known as toll-like receptor 4 (TLR4), may also play a critical role in suppressing chronic lung inflammation and tumor development in mice.

"We know that chronic inflammation predisposes people to many types of cancer," says NIH Director Elias Zerhouni, M.D. "By using this new information we may be able to suppress chronic inflammation and reduce our Nation's cancer burden."

In the December 7, 2005 issue of the Journal of the National Cancer Institute, researchers at the National Institute of Environmental Health Sciences (NIEHS), a part of the National Institutes of Health, report that mice prone to lung cancer that had TLR4 removed or altered had 60 percent more tumors than mice that had intact receptors, illustrating a new protective role for this gene. There were no differences in overall tumor size or structure between the mice. TLR4 is part of what immunologists refer to as the "innate immune system" which acts as the body's first line of defense against harmful substances.

Researchers explain the immune system actually is comprised of two components or systems, the innate and the acquired. The innate system can be thought of as the way the body is naturally programmed to respond, forming the front line of defense against infection. The acquired depends on the development of antibodies and other systems to recognize pathogens and other foreign objects that might upset the body's ability to fight off diseases. Understanding more about how the innate system works will help inform how the more complex, acquired system works.

"We have recently learned a lot about TLR4, its different mutations, and the role they play in immunity," said David A. Schwartz, MD, the NIEHS Director, "but discovering this novel function of TLR4 in tumor biology may provide new therapeutic targets for many chronic diseases, including cancer."

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Contact: Robin Mackar
rmackar@niehs.nih.gov
919-541-0073
NIH/National Institute of Environmental Health Sciences
7-Dec-2005


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