Scientists on the 2 April 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 also 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 deCode, the Icelandic genetics company, 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 of 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.

    为什么有些吸烟者抽一辈子烟也不得病，而其他人却年纪轻轻就死于肺癌？科学家4月2日发表的论文首次提供了破解这个谜题的基因线索。

    三个研究小组各自独立地发现了一组基因变异，这种变异会增加患肺癌的风险，也许还会使吸烟者对尼古丁更加上瘾。他们的论文发表在《自然》(Nature)和《基因研究》(Genome Research)杂志上。

    受影响的基因似乎会产生一种蛋白质，在大脑中发挥尼古丁“受体”或停靠点的作用。

    这三个小组分别来自冰岛基因公司deCode、德克萨斯大学(University of Texas)和里昂的国际癌症研究所(International Agency for Research on Cancer)，它们对增加的风险达成了一致意见。从父亲或母亲那里遗传了这种基因变异的人，患肺癌的机率比没有变异的人高出30%。那些从父母双亲那里都遗传了基因变异的人，患肺癌的可能性会增加80%。

    deCode首席执行官卡里•斯蒂芬森(Kari Stefansson)估计，携带双亲遗传变异的人占欧洲所有肺癌患者的18%。约有一半的人口至少有单亲遗传。

    但对于这种变异是通过引发导致肺癌的生物过程直接增加风险，还是通过让人们对吸烟更上瘾间接增加风险，科学家们没有达成一致。

    科学家需要进行更多研究，才能阐明相关生物机制，然后予以阻止，并由此找出肺癌的预防措施或治疗方法。

    里昂研究小组负责人保罗•布伦南(Paul Brennan)表示：“这些结果尤其令人兴奋，因为它们首次确认了一种会增加肺癌风险的主要基因因素。但这不应有损于人们从癌症中得到的主要教训的重要性：吸烟者应该戒烟。”

    德克萨斯小组的负责人克里斯•阿摩司(Chris Amos)表示，这些发现表明，尼古丁不仅是香烟中主要的致瘾化学物质，而且是肺癌的直接诱因。