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发稿时间：2015-08-06来源：圣谷同创

近日，刊登在国际杂志science上 的一篇研究论文中，来自英国癌症研究中心的研究人员通过研究发现，肺癌在转化成为恶性之前可以在人类机体中潜伏长达20年之久；文章中研究人员对7位肺癌 病人进行研究，包括吸烟者、已戒烟者及从不吸烟的个体，结果发现，在机体中发生第一次促发癌症的遗传突变后，该突变会在机体中隐藏很多年直到新发突变产 生，最终这些突变会联合起来引发疾病的恶化。
  charles swanton教授表示，尽管针对肺癌有很多靶向性的疗法，但是肺癌患者的生存率依然很低，通过揭示肺癌的发病原因或许就可以为我们后期开发治疗肺癌的新型疗法提供一定的帮助。
  文章中研究人员阐明了吸烟在引发肺癌过程中的重要作用，研究者表示，许多早期的遗传突变都是由于吸烟引发的，但是随着疾病发生这些突变就会变得不再占据主导地位，而随之而来的将是由蛋白质apobec控制产生的肿瘤突变。
  在肺癌患者机体中发现的多种遗传突变就可以帮助解释靶向疗法为何屡屡受挫，每年大约有4 万人会患上肺癌，研究者nic jones指出，目前的研究急需我们开发出肺癌的早期诊断技术来帮助预防和阻断肺癌的恶化，如果在疾病发生的萌芽阶段就将其扼杀住，那么患者治愈的希望非 常之大。（转化医学网360zhyx.com）
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science   doi: 10.1126/science.1253462
elza c. de bruin1,*, nicholas mcgranahan2,3,*, richard mitter2,*, max salm2,*, david c. wedge4,*, lucy yates4,5,†, mariam jamal-hanjani1,†, seema shafi1, nirupa murugaesu1, andrew j. rowan2, eva grönroos2, madiha a. muhammad1, stuart horswell2, marco gerlinger2, ignacio varela6, david jones4, john marshall4, thierry voet4,7, peter van loo4,7, doris m. rassl8, robert c. rintoul8, sam m. janes9, siow-ming lee1,10, martin forster1,10, tanya ahmad10, david lawrence10, mary falzon10, arrigo capitanio10, timothy t. harkins11, clarence c. lee11, warren tom11, enock teefe11, shann-ching chen11, sharmin begum2, adam rabinowitz2, benjamin phillimore2, bradley spencer-dene2, gordon stamp2, zoltan szallasi12,13, nik matthews2, aengus stewart2, peter campbell4, charles swanton1,2,‡
spatial and temporal dissection of the genomic changes occurring during the evolution of human non–small cell lung cancer (nsclc) may help elucidate the basis for its dismal prognosis. we sequenced 25 spatially distinct regions from seven operable nsclcs and found evidence of branched evolution, with driver mutations arising before and after subclonal diversification. there was pronounced intratumor heterogeneity in copy number alterations, translocations, and mutations associated with apobec cytidine deaminase activity. despite maintained carcinogen exposure, tumors from smokers showed a relative decrease in smoking-related mutations over time, accompanied by an increase in apobec-associated mutations. in tumors from former smokers, genome-doubling occurred within a smoking-signature context before subclonal diversification, which suggested that a long period of tumor latency had preceded clinical detection. the regionally separated driver mutations, coupled with the relentless and heterogeneous nature of the genome instability processes, are likely to confound treatment success in nsclc.