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.

    為什么有些吸煙者抽一輩子煙也不得病，而其他人卻年紀輕輕就死于肺癌？科學家4月2日發(fā)表的論文首次提供了破解這個謎題的基因線索。

    三個研究小組各自獨立地發(fā)現(xiàn)了一組基因變異，這種變異會增加患肺癌的風險，也許還會使吸煙者對尼古丁更加上癮。他們的論文發(fā)表在《自然》(Nature)和《基因研究》(Genome Research)雜志上。

    受影響的基因似乎會產(chǎn)生一種蛋白質(zhì)，在大腦中發(fā)揮尼古丁“受體”或停靠點的作用。

    這三個小組分別來自冰島基因公司deCode、德克薩斯大學(University of Texas)和里昂的國際癌癥研究所(International Agency for Research on Cancer)，它們對增加的風險達成了一致意見。從父親或母親那里遺傳了這種基因變異的人，患肺癌的機率比沒有變異的人高出30%。那些從父母雙親那里都遺傳了基因變異的人，患肺癌的可能性會增加80%。

    deCode首席執(zhí)行官卡里•斯蒂芬森(Kari Stefansson)估計，攜帶雙親遺傳變異的人占歐洲所有肺癌患者的18%。約有一半的人口至少有單親遺傳。

    但對于這種變異是通過引發(fā)導致肺癌的生物過程直接增加風險，還是通過讓人們對吸煙更上癮間接增加風險，科學家們沒有達成一致。

    科學家需要進行更多研究，才能闡明相關生物機制，然后予以阻止，并由此找出肺癌的預防措施或治療方法。

    里昂研究小組負責人保羅•布倫南(Paul Brennan)表示：“這些結果尤其令人興奮，因為它們首次確認了一種會增加肺癌風險的主要基因因素。但這不應有損于人們從癌癥中得到的主要教訓的重要性：吸煙者應該戒煙。”

    德克薩斯小組的負責人克里斯•阿摩司(Chris Amos)表示，這些發(fā)現(xiàn)表明，尼古丁不僅是香煙中主要的致癮化學物質(zhì)，而且是肺癌的直接誘因。