Scientists today publish the first genetic clues to unravelling the mystery of why some smokers puff their way through life without developing disease while others die young of lung cancer. Three research teams have independently discovered a set of genetic variations that increase the risk of lung cancer and may make smokers more addicted to nicotine. Their papers appear in the journals Nature and Nature Genetics. The gene affected seems to make a protein that acts as a "receptor", or docking point, for nicotine in the brain. The three teams - from the Icelandic genetics company deCode, the University of Texas and the International Agency for Research on Cancer in Lyons - agreed on the added risk. People who inherit the variants from one parent have a 30 per cent higher chance of developing lung cancer than those who do not have the variants. Those with two copies of the variations are 80 per cent more likely to get lung cancer. The set of variants accounts for 18 per cent of all lung cancers among Europeans, estimated Kari Stefansson, chief executive of deCode. About half the population carries at least one copy of the variants. But the scientists disagreed about whether the variants increased the risk directly by triggering biological processes that lead to lung cancer or indirectly by making people more addicted to smoking. More research will be needed to elucidate the biological mechanism responsible and then to block it in a way that could lead to preventative measures or treatments for lung cancer. "These results are particularly exciting as they provide the first identification of a major genetic factor that contributes to lung cancer risk," said Paul Brennan, who led the IARC team in Lyons. "They should not, however, detract from the main lung cancer message that people who smoke should quit." Chris Amos, head of the Texan team, said the findings suggested nicotine was not only the prime addictive chemical in cigarettes but also played a direct causative role in lung cancer. The studies used a method called "genome-wide association", which is only now becoming technically feasible. It aims to find the genetic causes of common diseases by scanning human DNA for genes that vary between patients and those who are not affected by the disease. The teams studied 35,000 people with and without lung cancer, including smokers and non-smokers. Copyright The Financial Times Limited 2008