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肺腺癌基因组综合发现一些潜在的靶点
2014-08-03 21:46:35来自“癌症基因组图谱研究网络(The Cancer Genome Atlas Research Network)”的这篇报告发布了230个切除的、未处理过的肺腺癌样本的分子特征。对转录组、基因组、甲基化组和蛋白质组所做的综合分析识别出了高速度的体细胞突变、包括NF1, MET, ERBB2 and RIT1 在13%患者中有突变发生。RIT1 和MGA在内的显著突变的基因以及由体细胞基因组变化驱动的剪接改变,并且说明存在使MAPK 和PI(3)K通道活性发生改变的尚未被识别出的病变。这些数据为对全世界因癌症而造成死亡的主要原因进行分类和进一步研究奠定了基础。
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.
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