A key mechanism by which smoking triggers genetic changes that cause lung cancer has been unravelled.
Researchers have shown exposure to cigarette smoke slows production of a protein called FANCD2 in lung cells.
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.
It raises hopes of improved treatments for the disease.
Lead researcher Dr Laura Hays said: “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.”
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.
*Most common cancer in the world with 1.3 million people diagnosed every year
*Second most common form of cancer in the UK after breast cancer
*Over 38,300 new cases, and more than 33,000 deaths in the UK each year
*Smoking responsible for 90% of cases in the UK
The researchers created an artificial windpipe in the lab to replicate the environment of a smoker’s lung.
They 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.
“Smoking is the single biggest preventable cause of cancer and causes nine out of ten cases of lung cancer.
“But the good news is that 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.”
Sources: BBC NEWS:MAY 14,’08