Scientists have for the first time pinpointed a protein that explains how smoking can directly lead to genetic changes that cause cancer – research published in the British Journal of Cancer reveals.
Researchers have now discovered that the production of a protein called FANCD2 is slowed when lung cells are exposed to cigarette smoke. Low levels of FANCD2 leads to DNA damage, triggering cancer.
These findings may help scientists improve treatments for the disease in the future.
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.”
Cigarette smoke curbs the production of “caretaker” proteins, such as FANCD2, which normally prevents cancer by fixing damages in DNA and causing faulty cells to commit suicide.
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.
Dr Lesley Walker, director of cancer information at Cancer Research UK, said: “This interesting piece of science adds to our understanding of why smoking is so deadly. Smoking is the single biggest preventable cause of cancer and causes nine out of 10 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 10 years your risk of lung cancer will have halved too.”
