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. 2020 May 28;16(5):e1008743. doi: 10.1371/journal.pgen.1008743

Fig 3. Metastasis-specific mutations are recurrent and stratify patient outcome.

Fig 3

IGV screen shots showing allele frequency in the blue and red boxes, representative SNV reads, mutated codon letter, tissue type, and mouse strain. A, Exome-seq identified a C (blue) to T (red) SNV within Kras resulting in the G12D amino acid substitution in metastases from two C57BL/6J x PyMT animals. B. RNA-seq identified a T (red) to C (blue) SNV within Kras resulting in the Q61R amino acid substitution in a metastatic lesion from one FVB/NJ x PyMT animal. C, Exome-seq identified C (blue) to T (red) and C (blue) to A (green) SNVs in metastases from three animals (FVB/NJ, CAST/Ei (2 mets from 1 mouse with same SNV), and C57BL/6J x PyMT) resulting in the P561S/T or H amino acid substitutions, respectively. D, RNA-seq identified a C (blue) to G (orange) SNV resulting in the P561A amino acid substitution in one FVB/NJ x PyMT animal. E. Kaplan-Meier plots generated using METABRIC for the top six genes identified with metastasis-driver SNVs by exome-seq in mice that most significantly stratify patient survival when altered in primary tumor tissue (blue = no CNV, red = CNV present). PT, primary tumor; Met, metastasis.