Supplementary Figure 1 through 7 and Supplementary Tables 1 through 6 and 8 through 14, and Supplementary Materials and Methods from Somatic Ephrin Receptor Mutations Are Associated with Metastasis in Primary Colorectal Cancer

Supplementary Fig. 1. Luciferase reporter assay reveals downregulation of BMP pathway activity upon overexpression of mutant BMPR2 Supplementary Fig. 2. Genes found in the largest number of significant outcomes when comparing mutation rate between metastatic and non-metastatic patients Supplementary Fig. 3. In situ mutation detection in FF colon tumour sections Supplementary Fig. 4. Expression levels of EPHB1 in DLD-1 cell lines overexpressing EPHB1 and its four mutant versions Supplementary Fig. 5. EPHB2 interacts with ephrinB1 ligand used as a positive control for the compartmentalisation experiment Supplementary Fig. 6. Detections of four non-synonymous mutations at the transcript level by Sanger sequencing and real time growth analysis of cell lines used in the compartmentalisation experiment Supplementary Fig. 7. The EPHB1 kinase inhibitor dasatinib abrogates the compartmentalisation phenotype of EPHB1 cells co-cultured with ephrinB1 ligand expressing cells Supplementary Table 1. Probe sequences for in situ mutation detection Supplementary Table 2. Probe performance for in situ mutation detection Supplementary Table 3. LNA primers for reverse transcription in situ Supplementary Table 4. Fluorescently labelled detection probes for RCPs Supplementary Table 5. Genes and corresponding length of the coding regions included in this study Supplementary Table 6. Patient-matched tumour and normal samples Supplementary Table 8. Comparison of pathway mutation rates in metastatic vs non-metastatic samples Supplementary Table 9. Functional annotation of mutated genes unique to metastatic patients Supplementary Table 10. Somatic mutations in Ephrin receptor genes Supplementary Table 11. Mean read depth of Eph receptor tyrosine kinases Supplementary Table 12. Prediction scores for amino acid conservation and effect of point mutations Supplementary Table 13. Mutation counts for Eph receptor mutations in situ Supplementary Table 14. Primer sequences for Sanger sequencing mutant constructs. Supplementary Materials and Methods