'Inflammation genes' shed light on lung cancer development
Researchers at the National Cancer Institute and the University of Texas have found that subtle variations in two inflammation genes seem to be involved in the development of lung cancer.
The gene variants seem to have a particularly strong effect in heavy smokers.
Short-term inflammation is one of the body's ways of combating the effects of infection and cell damage. However, some researchers think that prolonged inflammation, lasting years or more, may produce the kind of conditions which enable cancer to develop.
The study, published in the journal Cancer Research, compared differences in genes related to inflammation in over 1,500 lung cancer patients, more than 80 per cent of whom were current or former smokers.
It found that particular variations in the genes which produce proteins called interleukin (IL) 1A and 1B - which are secreted in response to infection or tissue damage - were particularly common in patients with lung cancer, especially those who were heavy smokers.
Dr Eric Engels, a researcher at the Viral Epidemiology Branch of the National Cancer Institute's (NCI) division of cancer epidemiology and genetics, explained that variations in the genes may lead to more of the protein being formed, sustaining the damaging effects of inflammation and eventually leading to genetic damage and cancer.
Dr Engels commented: "Our findings help explain how heavy smoking, for example, combines with a genetic predisposition to create a besieged environment within the lungs.
"Essentially, sustained inflammation alters the microenvironment of the lung tissue, damaging cells and altering DNA."
Dr Engels concluded: "A better understanding of the risks involving inflammation will lead to a better understanding of cancer prevention."