Cambridge study explains why some smokers get cancer, others don't

Why do some smokers escape cancer?

For decades, doctors have puzzled over a medical mystery: why do some lifelong smokers never develop lung cancer, while occasional smokers—and even non-smokers—sometimes get the disease? A new study from the University of Cambridge has found an answer. It lies not in how much someone smokes, but in how their cells repair damage.

Researchers at the Cambridge Institute for Therapeutic Immunology and Infectious Diseases have shown that a person's genetic background plays a decisive role in whether DNA damage from smoking or UV rays leads to cancer. The findings, published in the journal Nature Genetics, offer the first direct evidence that cancer risk is shaped as much by inherited repair mechanisms as by exposure to carcinogens.

How DNA damage turns into cancer

Every cigarette introduces thousands of chemical compounds into the lungs. These compounds damage DNA, creating mutations. But the body has repair systems that fix most of this damage before it becomes permanent. The Cambridge team found that in people with efficient repair systems, even heavy smoking may not produce enough mutations to trigger cancer.

In others, however, the repair process is slower or less accurate. Damaged DNA accumulates over years. Eventually, a cell acquires enough mutations to start dividing uncontrollably. That is the beginning of cancer. The study calls this process 'experimental cancer evolution'—the step-by-step accumulation of genetic errors that drives tumour growth.

What the study actually found

The researchers tracked how DNA damage evolved in cells from different genetic backgrounds. They exposed cells to carcinogens found in tobacco smoke and UV radiation. Some cells repaired the damage quickly and completely. Others showed persistent mutations that grew more complex over time.

Lead author Dr. Serena Thakkar said the results explain a long-observed pattern. 'We now understand why two people with identical smoking histories can have completely different cancer outcomes. It is not luck. It is biology.' The study also sheds light on why some non-smokers develop lung cancer—they may inherit less efficient DNA repair systems, making them vulnerable to even low-level carcinogen exposure.

Implications for screening and prevention

The findings could change how doctors assess cancer risk. Currently, screening recommendations are based largely on age and smoking history. The Cambridge study suggests that genetic testing for DNA repair efficiency could identify high-risk individuals who need earlier or more frequent screening.

It also raises the possibility of preventive treatments. If researchers can find ways to boost DNA repair in people with weaker systems, they might reduce cancer risk even in those who continue smoking. However, the study's authors caution that quitting smoking remains the single most effective way to lower risk.

The research was supported by Cancer Research UK and the Wellcome Trust. YaleNews and ET HealthWorld have also reported on the findings, which ThePrint originally covered on 28 July 2026.

What happens next

The Cambridge team is now working to identify the specific genes that control DNA repair efficiency. If they succeed, a simple blood test could one day tell a person their intrinsic cancer risk—and help doctors decide who needs the closest monitoring.