A protein responsible for repairing damaged DNA may be a vital link to explaining how smoking causes lung cancer, US researchers reported on Tuesday. Lung cells exposed to cigarette smoke produce less of the protein, called FANCD2, the team at Oregon Health & Science University Cancer Institute reported. Without FANCD2, damaged DNA can cause cells to proliferate out of control instead of destroying them selves as normal cells do. The study, published in the British Journal of Cancer, could lead to better treatments for lung cancer, the leading cause of cancer death globally, the researchers said. Lung cancer kills more than 1 million people every year and only 15 per cent of patients live for 5 years or longer. "These findings show the important role FANCD2 plays in protecting lung cells against cigarette smoke, and may explain why ciga rette smoke is so toxic to these cells," said Laura Hays, who worked on the study. "Although there are probably other proteins involved in this process, we know this is a key one because cells with very high levels of FANCD2 were resistant to the toxic effects of the smoke," added Dr Grover Bagby, who oversaw the work. Hays and colleagues created an artificial windpipe in the lab to study the effects of cigarette smoke on cells. FANCD2 had already been linked with cancer. It is part of a family of proteins involved in an inherited condition called Fanconi anaemia. People with Fanconi anaemia have low levels of the proteins and are more likely to develop cancers at a young age. "This interesting piece of science adds to our understanding of why smoking is so deadly," director of cancer information at Cancer Research UK, said.