Lung cancer remains the world’s deadliest cancer, with cigarette smoke as its main cause. Tobacco contains chemicals like polycyclic aromatic hydrocarbons (PAHs) that damage DNA and trigger mutations leading to tumors. Despite this, surprisingly, 80 to 90 percent of smokers never develop lung cancer, a puzzling fact scientists have long sought to understand.
Recent research offers new insights. Scientists have discovered that some smokers may have built-in protective mechanisms that limit DNA damage in lung cells, helping prevent cancer development. This study, led by researchers from Albert Einstein College of Medicine, used advanced single-cell whole-genome sequencing (WGS) to analyze DNA mutations in bronchial epithelial cells—the lung cells most likely to become cancerous.
The study compared lung cells from smokers and non-smokers across various ages. It confirmed that smoking significantly increases DNA mutations, but found that mutation accumulation plateaus after about 23 pack-years of smoking. This plateau suggests some smokers’ cells can effectively repair DNA damage or detoxify harmful chemicals, preventing further mutation buildup.
Dr. Simon Spivack, co-author of the study, explained, “The heaviest smokers didn’t always have the highest mutation burden. Their bodies may be better equipped to counteract DNA damage from cigarette smoke.”
These findings open doors for new approaches to lung cancer prevention and early detection by identifying individuals’ DNA repair and detoxification abilities. Such personalized insights could revolutionize risk assessment and help target interventions before cancer develops.
While quitting smoking remains the best way to reduce lung cancer risk, understanding why some smokers remain cancer-free despite long exposure offers hope for future breakthroughs in precision medicine.
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