美國科學家近日成功發(fā)現(xiàn)了人類26個促使肺癌發(fā)生的重要基因,，當它們遭到破壞時就會誘發(fā)肺癌的發(fā)生,。
這項成果將有助于為一些病情特殊的患者度身定制適合他們的療法,。這項研究由美國聯(lián)邦政府資助,，旨在檢測在肺癌這種常見病中基因的變化情況,。相關(guān)結(jié)果發(fā)表在最新一期《自然》（Nature）雜志上,。
肺癌是在美國和全世界致死人數(shù)最多的癌癥,。這項研究的觀察重點是生長在肺部而后被手術(shù)切除的腫瘤,，但是研究人員也希望了解，他們的發(fā)現(xiàn)在那些腫瘤轉(zhuǎn)移到身體別處的患者身上是否同樣成立,。他們利用188個腫瘤樣本來觀察其中623個基因的結(jié)構(gòu),，目的是尋找最容易產(chǎn)生變異的那些基因。他們假設(shè),，如果一個基因在多個腫瘤樣本中都出現(xiàn)變異,，那么可以肯定它在肺癌的發(fā)病過程中有重要的意義，而這些變異在肺癌患者體內(nèi)的健康組織中是不會出現(xiàn)的,。
這項成果顯示,，一些目前已經(jīng)被使用或者正在處于研發(fā)階段的藥品將對腫瘤發(fā)生特定變異的人群才會有效。而知道了哪些基因在癌癥的發(fā)展中產(chǎn)生作用也將使科學家在制定新的療法時更加有的放矢,。
此外,，這項成果也為將來為腫瘤患者制定適合他們自身病情的療法奠定了方法論的基礎(chǔ)。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
