That smoking causes lung cancer is well established. But what causes smoking? This is the question at the heart of a study publi

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问题    That smoking causes lung cancer is well established. But what causes smoking? This is the question at the heart of a study published in Nature by a group of researchers who work at deCODE, an Icelandic genomics company. They do not, quite, answer it. But they do think they have the answer to the related question of why some smokers smoke in moderation whereas others are rarely found without a fag in their hands—and thus this is the reason why some people are, genetically speaking, more susceptible to lung cancer than others.
   That answer lies in part of human chromosome 15, and depends on what is known as allele T of SNP rsl051730. A SNP, or single-nucleotide polymorphism, to give its full name (the short version is pronounced "snip"), is a place where genomes routinely differ from one another by a single genetic letter.
   In this case, the variation happens inside a gene for one of the receptor molecules that nicotine attaches itself to when it produces its buzz. Based on a study of 13,945 Icelandic smokers, deCODE’s researchers showed that having a T in the appropriate part of the gene correlates very strongly indeed with being a heavy smoker. The team estimates that the chance of their being wrong is less than one in a thousand trillion.
   Not surprisingly, having the T variant also correlates with the chance of a smoker getting lung cancer. Each copy (there may be none, one or two, since one can come from a person’s father and one from his mother) increases that chance by 30%. The T variant does not, however, increase the likelihood that someone will take up smoking in the first place. That is either a matter of free will or, if it is genetic, is controlled by genes somewhere else. It all looks neat and simple—and extremely plausible. Genes promote smoking; smoking promotes cancer. However, it might be wrong, for another paper in Nature, and a third in its sister journal Nature Genetics, report similar studies that have drawn rather different conclusions.
   Paul Brennan and Christopher Amos both agree that something significant is going on in the part of chromosome 15 studied by deCODE. But they have concluded that genetic variation there acts directly on a person’s susceptibility to lung cancer rather than acts indirectly by modifying his smoking behavior. That does not mean the gene or genes in question actually cause lung cancer. Rather, it means that they amplify the effects of smoking instead of the amount of smoking.
   Dr. Brennan and Dr. Amos both used a different method from deCODE’s. They compared lung-cancer patients directly with otherwise similar cancer-free smokers, in what is known as a case controlled study, and concluded that genetic variants in the nicotine-receptor-rich part of chromosome 15 are changing not smokers’ behavior, but their susceptibility to cancer. Moreover, Dr. Brennan also claims to have discovered an increased susceptibility to lung cancer in non-smokers with the relevant SNPs, though his sample size is small and his result is not supported by Dr. Amos’s work.
   [A] finds an increased susceptibility to lung cancer in non-smokers with the relevant SNPs.
   [B] concludes that genetic variation directly affects a person’s susceptibility to lung cancer.
   [C] appraises that their study is nearly impossible to be wrong.
   [D] is thought to be connected to the rate of a smoker getting lung cancer.
   [E] is the cause of different smoking behaviors according to deCODE’s study.
   [F] increases the possibility of someone’s smoking in the first place.
   [G] is a place in which genomes are different from one other by a genetic letter.
The T variant

选项

答案D

解析 The T variant出现在第四段。该段的第一句说,不出所料,胸腺嘧啶的变异同样和吸烟者发生肺癌的几率呈正相关关系。D中的be connected to对应原文的correlates,而rate与文中chance同义,getting lung cancer是文中的原词复现,故确定D为本题的正确答案。
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