(ORDO NEWS) — Cigarette smoking is the number one risk factor for lung cancer, with tobacco products causing up to 90 percent of lung cancer deaths in the US.
Undoubtedly, the most reliable way to protect yourself from lung cancer is not to smoke cigarettes, but at the same time, it is also true that not all lifelong smokers are doomed to develop cancer.
In fact, the vast majority do not develop it. Scientists have long wondered why, and a new study supports the idea that genetics play a role.
Among people who smoke but never get lung cancer, researchers have found an innate advantage. The cells lining their lungs appear to be less likely to mutate over time.
The results suggest that DNA repair genes are more active in some people, which may protect against cancer even with regular cigarette smoking.
The study used genetic profiles taken from the bronchi of 14 never-smokers and 19 light, moderate, and heavy smokers.
Surface cells harvested from participants’ lungs were individually sequenced to measure mutations in their genomes.
“These lung cells live for years, even decades, and therefore can accumulate mutations with age and smoking,” explains epidemiologist and pulmonologist Simon Spivak of the Albert Einstein College of Medicine.
“Of all the lung cell types, these cells are the most prone to cancer.”
According to the authors, the results “clearly indicate” that mutations in the human lungs increase with natural age, and DNA damage is even more significant in smokers.
Tobacco smoke has long been associated with DNA damage in the lungs, but a new study has found that not all smokers are in the same boat.
Although the number of cigarettes smoked is associated with an increase in the number of cellular mutations, after 23 years of smoking a pack a day, this risk is reduced.
“The heaviest smokers didn’t have the highest burden of mutations,” says Spivak.
“Our data suggest that these people may have survived so long despite heavy smoking because they were able to suppress further accumulation of mutations. This leveling of mutations may be due to the fact that these people have very efficient DNA damage repair systems or cigarette smoke detoxification.
The findings may help explain why 80-90% of lifetime smokers never develop lung cancer. It may also help explain why some people who have never smoked in the first place develop tumors.
While toxic tobacco smoke appears to cause additional cell mutations in the lungs, whether these mutations develop into tumors depends on how well the body can repair DNA or reduce DNA damage.
Genes associated with DNA repair can be inherited or acquired, and silencing of repair genes has been associated with the development of tumors in previous studies.
Genes are not the only factors influencing cancer risk. Environmental factors, such as diet, can also influence the nutrient content of the body, which influence tumor development.
The question of what makes the human body better repair DNA is still open and likely to be complex, but new results suggest that this process is closely associated with the development of lung cancer.
“Now we want to develop new assays that measure a person’s ability to repair DNA or detoxify, which could offer a new way to assess lung cancer risk,” says geneticist Jan Wiig.
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