Campbell James, Ryan Colm J, Brough Rachel, Bajrami Ilirjana, Pemberton Helen N, Chong Irene Y, Costa-Cabral Sara, Frankum Jessica, Gulati Aditi, Holme Harriet, Miller Rowan, Postel-Vinay Sophie, Rafiq Rumana, Wei Wenbin, Williamson Chris T, Quigley David A, Tym Joe, Al-Lazikani Bissan, Fenton Timothy, Natrajan Rachael, Strauss Sandra J, Ashworth Alan, Lord Christopher J
The Breast Cancer Now Research Centre and CRUK Gene Function Laboratory, The Institute of Cancer Research, London SW3 6JB, UK.
Systems Biology Ireland, University College Dublin, Dublin 4, Ireland.
Cell Rep. 2016 Mar 15;14(10):2490-501. doi: 10.1016/j.celrep.2016.02.023. Epub 2016 Mar 3.
One approach to identifying cancer-specific vulnerabilities and therapeutic targets is to profile genetic dependencies in cancer cell lines. Here, we describe data from a series of siRNA screens that identify the kinase genetic dependencies in 117 cancer cell lines from ten cancer types. By integrating the siRNA screen data with molecular profiling data, including exome sequencing data, we show how vulnerabilities/genetic dependencies that are associated with mutations in specific cancer driver genes can be identified. By integrating additional data sets into this analysis, including protein-protein interaction data, we also demonstrate that the genetic dependencies associated with many cancer driver genes form dense connections on functional interaction networks. We demonstrate the utility of this resource by using it to predict the drug sensitivity of genetically or histologically defined subsets of tumor cell lines, including an increased sensitivity of osteosarcoma cell lines to FGFR inhibitors and SMAD4 mutant tumor cells to mitotic inhibitors.
一种识别癌症特异性脆弱点和治疗靶点的方法是分析癌细胞系中的基因依赖性。在此,我们描述了一系列siRNA筛选的数据,这些筛选确定了来自十种癌症类型的117个癌细胞系中的激酶基因依赖性。通过将siRNA筛选数据与分子谱分析数据(包括外显子组测序数据)相结合,我们展示了如何识别与特定癌症驱动基因突变相关的脆弱点/基因依赖性。通过将其他数据集整合到该分析中,包括蛋白质-蛋白质相互作用数据,我们还证明与许多癌症驱动基因相关的基因依赖性在功能相互作用网络上形成密集连接。我们通过利用该资源预测遗传或组织学定义的肿瘤细胞系亚群的药物敏感性,证明了其效用,包括骨肉瘤细胞系对FGFR抑制剂以及SMAD4突变肿瘤细胞对有丝分裂抑制剂的敏感性增加。