Boffins have found that a variation in two genes related to inflammation, might increase risk for developing lung cancer.
The study was conducted by a team of researchers led by Eric Engels at the National Cancer Institute and the University of Texas M. D. Anderson Cancer Center.
As part of the study, researchers compared differences in genes related to inflammation between more than 1,500 lung cancer patients and 1,700 controls to examine the relationship between inflammation and lung cancer risk.
More than 80 percent of the cancer patients in the study were current or former smokers.
Researchers found that among the 59 variations in 37 inflammation-related genes studied some variants in the genes for interleukin (IL) 1A and 1B were found frequently in patients with lung cancer and especially among heavy smokers.
The genes' strong effect on heavy smokers suggested that the inflammatory response is important in modulating the damage caused by tobacco smoke.
The effect was most profound in polymorphisms in IL1B, which was central to the inflammation process.
The researchers noted that the IL1B protein was an integral part of the chemical cascade by which cell signals moderate the response to inflammation.
Variations in the gene might 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.
"Inflammation is part of the immune system's arsenal to combat the effects of infection and cell damage. However, prolonged or intense inflammation could lead to conditions within the lung environment that foster cancer," Engels said.
The findings of the study were published in the July issue of Cancer Research, a publication of the American Association for Cancer Research.