A cluster of genes that influence the risk of developing lung cancer has been found, offering insights that could lead to new treatments and ways of helping people to quit smoking.

People who inherit a particular genetic variant are 30 per cent more likely to develop lung cancer than those who do not; in those who inherit two copies of the variant, the risk rises by up to 80 per cent.

However, the link between the disease and a genetic region that holds three nicotine receptor genes has divided the three independent teams that have identified it, which disagree over its relationship with smoking.

The largest of the studies, from deCODE Genetics, an Icelandic company, found that the increased risk occurs entirely because the variant makes smokers more likely to become addicted and to smoke more heavily.

A French group, however, found that the raised risk applies to people who have never smoked as well as to smokers, suggesting that the gene may have a biological effect independent of its impact on tobacco use.

The third study, led by Richard Houlston, of the Institute of Cancer Research in Sutton, Surrey, also found an independent effect, though this was studied only in current and former smokers.

Further research will be needed to settle the issue.

Whatever the explanation, variations in a region of chromosome 15 appear to be sufficiently important to account for nearly one in five cases of lung cancer, and for one in ten cases of peripheral artery disease (PAD) — a circulatory disorder also linked to smoking.

That is because while the variant adds only slightly to individuals’ risk, it is very common. About 44 per cent of people of European descent carry one copy and another 11 per cent have two copies. As well as its effect on the risk of lung cancer, each copy raises the risk of PAD by 20 per cent.

Even if the variant does affect non-smokers, however, all three studies agreed that its impact will be far outweighed by that of smoking.

Paul Brennan, of the French National Institute of Cancer, said that before genetics are considered, smokers have a lifetime risk of lung cancer of about 15 per cent, compared with 6 per cent for former smokers who quit by middle age, and less than 1 per cent for non-smokers. The risk rises to 23 per cent for smokers with the most vulnerable genetic profile, but hardly falls at all for smokers with the least susceptible genotype, who still have a 14 per cent lifetime risk.

This is still about ten times greater than it is for people who have never smoked, but who have two copies of the variant, according to Dr Brennan’s results. “If people don’t smoke, the background risk is so low that having one or even two copies really doesn’t make a difference,” he said.

One of the most interesting aspects of the findings, which are published in the journals Nature and Nature Genetics, is that they show how a disease that clearly has a strong environmental component can also be affected by genetics.

In a commentary for Nature, Stephen Chanock, of the US National Institutes of Health, and David Hunter, of Harvard Medical School, said that the results could have important medical implications. “We may be able to evaluate smoking-cessation treatments informed by knowledge of a person’s genetic predisposition to start smoking or to nicotine addiction, and thus add new weapons to the anti-smoking arsenal,” they said.

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