美国科学家近日成功发现了人类26个促使肺癌发生的重要基因，当它们遭到破坏时就会诱发肺癌的发生。
这项成果将有助于为一些病情特殊的患者度身定制适合他们的疗法。这项研究由美国联邦政府资助，旨在检测在肺癌这种常见病中基因的变化情况。相关结果发表在最新一期《自然》（Nature）杂志上。
肺癌是在美国和全世界致死人数最多的癌症。这项研究的观察重点是生长在肺部而后被手术切除的肿瘤，但是研究人员也希望了解，他们的发现在那些肿瘤转移到身体别处的患者身上是否同样成立。他们利用188个肿瘤样本来观察其中623个基因的结构，目的是寻找最容易产生变异的那些基因。他们假设，如果一个基因在多个肿瘤样本中都出现变异，那么可以肯定它在肺癌的发病过程中有重要的意义，而这些变异在肺癌患者体内的健康组织中是不会出现的。
这项成果显示，一些目前已经被使用或者正在处于研发阶段的药品将对肿瘤发生特定变异的人群才会有效。而知道了哪些基因在癌症的发展中产生作用也将使科学家在制定新的疗法时更加有的放矢。
此外，这项成果也为将来为肿瘤患者制定适合他们自身病情的疗法奠定了方法论的基础。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature，455, 1069-1075，Li Ding，Richard K. Wilson
Somatic mutations affect key pathways in lung adenocarcinoma
Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFRhomologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers—including NF1, APC, RB1 and ATM—and for sequence changes inPTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.
