Smoking is one of the biggest preventable causes of lung cancer, but an interesting question remains: if tobacco smoke damages DNA and increases cancer risk, why does every smoker not develop lung cancer? A new study from the University of Cambridge offers fresh clues, suggesting that our inherited genetic background may influence how cells respond to DNA damage caused by environmental exposures such as cigarette smoke and UV radiation. The study, published in Nature on July 27, found that genetic differences can influence the mutations that develop in tumours and the biological pathways through which cancer progresses. Researchers analysed nearly 600 tumours in mice with different genetic backgrounds and found that although the tumours often followed similar developmental patterns, the mutations varied depending on the animals' inherited genetics.

Does Genetics Influence Cancer Risk?

Cancer develops when DNA accumulates mutations that allow cells to grow uncontrollably and avoid the signals that normally cause damaged cells to stop dividing or die. Environmental exposures can increase the amount of DNA damage. Cigarette smoke, for example, contains numerous carcinogens that can damage cells in the lungs. Sunlight can similarly cause DNA damage in skin cells. However, researchers have long suspected that inherited genetic differences may influence how the body responds to such damage.

The Cambridge study provides new evidence for this possibility. Although the research was conducted in mice, it suggests that genetic background may influence both the mutation processes and the pathways that eventually contribute to tumour development.

Why Do Some Smokers Develop Lung Cancer While Others Don't?

According to Dr Mayank Saxena, Additional Director, Pulmonology, Fortis Hospital, Noida, smoking increases the risk of lung cancer but does not determine an individual's fate on its own. “Lung cancer develops after a series of changes accumulate within cells, and how quickly that happens varies from person to person. The amount and duration of tobacco exposure matter, but so do genetics, environmental exposures and the body's ability to repair DNA damage,” he explains.

This means that two people with seemingly similar smoking histories may not necessarily experience exactly the same biological response. Some individuals may have biological mechanisms that are more effective at repairing or limiting DNA damage, while others may be more vulnerable to the effects of carcinogens. Over years of exposure, these differences could potentially influence whether cancer-driving mutations accumulate.

What Did The Cambridge Study Find?

Researchers from the University of Cambridge, along with scientists from the University of Edinburgh and institutions across Europe and the US, conducted controlled experiments using mice with different genetic backgrounds.

They analysed nearly 600 tumours and found that tumours across different mouse strains often followed similar overall cancer-driving pathways. However, the specific mutations and genetic changes that developed within those tumours were influenced by the animals' inherited genetic background. “Cancer does not arise entirely by chance. Although tumours often reach the same biological endpoint, the path to that endpoint is determined by an individual's genetic background,” Professor Duncan Odom said. The researchers said the findings could eventually help explain why people exposed to similar environmental risks can have different cancer outcomes.

Does This Mean Some People Can Smoke Safely?

Absolutely not. Dr Saxena stresses that the research should not be interpreted as suggesting that some smokers are naturally protected from cancer. “What it does not mean is that certain people can smoke safely. We currently have no way of identifying a smoker who is ‘protected' from cancer,” he says.

Smoking repeatedly exposes the lungs to carcinogens, increasing the likelihood that DNA damage and harmful mutations will accumulate over time. The risk generally increases with the amount and duration of tobacco exposure. Even if genetic differences influence individual susceptibility, they do not eliminate the harmful effects of tobacco smoke.

Smoking Can Damage More Than The Lungs

The health consequences of smoking extend far beyond lung cancer. Tobacco use is a major cause of chronic obstructive pulmonary disease (COPD) and also increases the risk of heart disease and stroke. Smoking is linked to several other cancers as well. This is why an individual's genetic susceptibility should never be used as a reason to continue smoking. At present, there is no reliable test that can tell a smoker that their genes make them safe from tobacco-related cancer.

Could Genetics Help Personalise Cancer Screening?

The Cambridge research could eventually have implications for personalised cancer prevention and treatment, although the findings are still preliminary. Understanding why some individuals accumulate particular mutations more readily could potentially help researchers identify people at higher risk and develop more personalised approaches to screening.

The study also raises questions about cancer treatment. Researchers noted that inherited genetic background may influence how tumours respond to DNA-damaging treatments, potentially strengthening the case for more personalised cancer therapies in the future. However, it is important to remember that the current findings come from experiments in mice. More research is needed to establish whether the same patterns occur in humans.

What Should Smokers Do?

The new research does not change the most important message about smoking: quitting remains one of the most effective ways to reduce the risk of lung cancer and other serious diseases. People who smoke should not assume that the absence of symptoms means their lungs are unaffected. Tobacco-related damage can accumulate silently over many years.

Dr Saxena says, “Understanding why susceptibility differs may eventually allow us to assess risk and target screening more precisely. Until then, the practical message remains unchanged: the safest cigarette is the one you don't smoke.” Not every smoker develops lung cancer, but that does not mean smoking is harmless or that some people are immune to its effects. Cancer risk is influenced by multiple factors, including the intensity and duration of exposure, genetics, environmental factors and the body's ability to respond to DNA damage. The Cambridge study offers a better understanding of why cancer susceptibility can vary between individuals, but it is not evidence that anyone can safely smoke. Smoking increases cancer risk. Your genes may influence how your body responds, but they cannot make tobacco smoke safe.



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