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Supplementary Figure Legends Figure S1. Somatic mutations of each tumor. Missense, nonsense and splicing identified by whole-exome sequencing analysis Figure S2. EML4-ALK fusion gene detected from TH2 and TH5. (A) The break point region is located within intron 19 of ALK and intron 6 of EML4. (B-D) The IGV visualization of EML4-ALK fusion in TH1 from RNA-seq data, in TH1 from panel-sequencing data and in TH4 from RNAseq data. Figure S3. The genomic and transcriptomic differences between multiple lymph nodes of patients TH2, TH3, TH4 and TH6. The density plots of cancer cell fraction (CCF) between the primary site and lymph node metastases are shown in upper panels. The scatter plots for similarity of gene expression profiles between the primary site and lymph node metastases are shown in lower panels. Differentially expressed cancer related-genes (>2-fold change) are highlighted in red and green colors. Figure S4. The genomic and transcriptomic pattern of TH6 case. (A) The mutation heatmap. (B) The scatter plot shows the similarity of gene expression profiles between nodes (using 15,842 genes with at least > 5 reads) by measuring Pearson’s correlation coefficient (r). (C) The density plot of cancer cell fraction (CCF) between the primary and the lymph node. (D) The gene expression pattern of genes belonging to SQCCs, PI(3)K/RTK/RAS signaling. Gene expression values in lymph nodes were mapped on the distribution of gene expression in TCGA SQCCs (n=495), represented by the boxplot. AKT2 and RASA1 show significant clinical outcome difference in the gene expression of TCGA SQCCs patients; *P < 0.05. Figure S5. The measurement representing early vs. late metastasis. (A) The percentage of trunk/non-trunk mutations for six cases. (B) The expression levels of AKT2 gene as a potential early event in tumorigenesis.