Researchers from the National Cancer Institute and the University of Texas M. D. Anderson Cancer Center said the effect of the genes is especially strong among heavy smokers, suggesting the inflammatory response is important in modulating damage caused by tobacco smoke.

The scientists said their study is the first to pinpoint the mechanism by which damage to the lung might trigger an overzealous inflammatory response by the immune system, leading to lung cancer.

The variants, or polymorphisms, were found in genes for interleukin 1A and interleukin 1B -- two signaling molecules that immune system cells secrete in response to infection or tissue damage.

"Our findings help explain how heavy smoking, for example, combines with a genetic predisposition to create a besieged environment within the lungs," said lead author Dr. Eric Engels of the National Cancer Institute. "Essentially, sustained inflammation alters the microenvironment of the lung tissue, damaging cells and altering DNA."

The study appears in the July 1 issue of the journal Cancer Research.