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肺腺癌基因組綜合發(fā)現(xiàn)一些潛在的靶點(diǎn)
2014-08-03 21:46:35來自“癌癥基因組圖譜研究網(wǎng)絡(luò)(The Cancer Genome Atlas Research Network)”的這篇報(bào)告發(fā)布了230個(gè)切除的、未處理過的肺腺癌樣本的分子特征。對轉(zhuǎn)錄組、基因組、甲基化組和蛋白質(zhì)組所做的綜合分析識(shí)別出了高速度的體細(xì)胞突變、包括NF1, MET, ERBB2 and RIT1 在13%患者中有突變發(fā)生。RIT1 和MGA在內(nèi)的顯著突變的基因以及由體細(xì)胞基因組變化驅(qū)動(dòng)的剪接改變，并且說明存在使MAPK 和PI(3)K通道活性發(fā)生改變的尚未被識(shí)別出的病變。這些數(shù)據(jù)為對全世界因癌癥而造成死亡的主要原因進(jìn)行分類和進(jìn)一步研究奠定了基礎(chǔ)。
a, GISTIC analysis of focal amplifications in oncogene-negative (n = 87) and oncogene-positive (n = 143) TCGA samples identifies focal gains of MET and ERBB2 that are specific to the oncogene-negative set (purple). b, TP53, KEAP1, NF1 and RIT1 mutations are significantly enriched in samples otherwise lacking oncogene mutations (adjusted P < 0.05 by Fisher’s exact test). c, Co-mutation plot of variants of known significance within the RTK/RAS/RAF pathway in lung adenocarcinoma. Not shown are the 63 tumours lacking an identifiable driver lesion. Only canonical driver events, as defined in Supplementary Fig. 9, and proposed driver events, are shown; hence not every alteration found is displayed. d, New candidate driver oncogenes (blue: 13% of cases) and known somatically activated drivers events (red: 63%) that activate the RTK/RAS/RAF pathway can be found in the majority of the 230 lung adenocarcinomas.留言新發(fā)布 -
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