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. 2019 Apr 11;10:1670. doi: 10.1038/s41467-019-09255-1

Fig. 1.

Fig. 1

Heterogeneity of driver mutations across 39 ESCC individuals. a Sequencing and analytical pipeline in this study. Multisite samples including metastatic lymph nodes, lymphocytes, and primary tumors. Primary tumors were divided into five regions for each patient. b The top panel shows the number of coding mutations detected in each individual; the bottom panel shows the percentages of trunk or branch coding mutations. c Heat map shows somatic driver mutations with different clonal status. The right panel shows the proportion of the variants found as trunk/branch in ESCC; the bottom panel shows key clinicopathological characteristics. d Schematics of ErbB4 protein alterations resulted from mutations identified from the 39-Mseq ESCCs and additional TCGA, early Chinese and Japanese cohorts. e The effect of ERBB4 wild type and mutants on ErbB4 phosphorylation and cell proliferation as monitored by NRG-1 stimulation (left), MTT (middle), and colony formation assay (right), respectively. Experiments were performed with KYSE150 cells in triplicate and all data are mean ± SD. *P< 0.05, **P< 0.01, ***P< 0.001. Source data are provided as a Source Data file