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Brennan and Amos, working on different teams, linked the genetic variation itself -- when triggered by smoking -- directly to lung cancer. Brennan said the nicotine receptors that the variants act on also can stimulate tumor growth. Brennan's study also found that lung cancer risk for nonsmokers with the variants was higher than for those without the variants. However, his small sample size of nonsmokers requires further study. Amos' study didn't find increased lung cancer risk for people with the set of variants who have never smoked. But Kari Stefansson, lead author of the largest of the three studies and chief executive of deCode Genetics of Iceland, said the increased lung cancer risk was indirect, and that the variant caused more addiction and more smoking. It was the extra cigarettes from increased daily smoking and the inability to quit that contributed to the higher cancer risk, Stefansson said. "It's very likely that in the end there's going to be a test and this is going to be folded into a panel of tests for the risk of cancers," said Stefansson, whose company already does prostate cancer genetic tests. The tests will lead to better treatments, but probably not prevention of smoking, he said. Stefansson and others emphasize that people without the variants should not take that genetic finding as a green light to smoke. There are other smoking-related diseases and they would still be at high risk of lung cancer. For Stefansson, the research hits home. His father, a smoker, died of lung cancer. And Stefansson, who doesn't smoke, frequently lectures his 23-year-old daughter "who smokes like a chimney." She acts like she is immortal and smoking can't kill her, Stefansson said. But his own research shows that her genes are probably stacked against her. Related Links: |
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