Researchers have unraveled a key mechanism by which smoking triggers genetic changes that cause lung cancer.
Exposure to cigarette smoke slows production of a protein called FANCD2 in lung cells and this protein plays a key role in repairing damage to DNA, and causing faulty cells to commit suicide before they go on to become cancerous, BBC reported Wednesday, quoting a study by American researchers which appears in the British Journal of Cancer.
Researchers at Oregon Health and Science University created an artificial windpipe in the lab to replicate the environment of a smoker's lung, then studied the effects of cigarette smoke on different proteins in cells and found that FANCD2 levels were low enough to allow DNA damage.
FANCD2 is part of a family of proteins involved in an inherited condition called Fanconi anaemia. People with the condition are more likely to develop cancers at a young age and have low levels of these proteins.
"These findings show the important role FANCD2 plays in protecting lung cells against cigarette smoke and may explain why cigarette smoke is so toxic to these cells," lead researcher Laura Hays was quoted as saying.
The researchers suspect other proteins also play a role in fixing DNA and weeding out defective cells. However, their work showed that cells with very high levels of FANCD2 were resistant to the toxic effects of smoke, suggesting this protein is key.
Smoking is known as the single biggest preventable cause of cancer and causes nine out of ten cases of lung cancer, but quitting works. After five years without smoking your risk of a heart attack will have fallen to half that of a smoker and after ten years your risk of lung cancer will have halved too, according to published researches.
(Xinhua News Agency May 15, 2008)