SMolecular Cancer BiologyFigure 1. Intraindividual heterogeneity between liver metastases as determined by

Notably, in five patients, KRAS or TP53 mutations seemed to evolve over time either between the primary and the metastases or between the first and second liver resection (see details in Supporting Information Table S2). Mutation frequencies in subgroups of patients with different chemotherapy exposure are listed in Supporting Information Table S3.C Int. J. Cancer: 139, 647?56 (2016) V 2016 The Authors Ssion of lipoxygenase pathway of arachidonic 1940-0640-8-15 acid metabolism CAPE getting the International Journal of Cancer published by John Wiley Sons Ltd on behalf of Union for International Cancer ControlL s et al.Influence of chemotherapy exposureFigure 2. Kaplan eier survival curves illustrating time to relapse (left panels) and disease-specific survival (right panels) after liver surgery for metastatic colorectal cancer with respect to mutation status for KRAS, BRAF, KRAS title= 02699931.2015.1049516 and BRAF combined, PIK3CA and TP53 (n 5 151 in each panel). A patient was classified as harboring a gene mutation as long as it was present in at least one lesion. pvalues are from log-rank tests.Mutation status and prognosis after liver resectionTo evaluate the prognostic impact of the mutations described above in patients treated with liver resections, we excluded patients who had undergone a previous liver resection (n 5 13) before inclusion in the present study, leaving a total of 151 patients. In univariate analyses (Fig. 2), we found KRAS and BRAF mutations both to be associated with reduced median TTR (7 vs. 22 and 3 vs. 16 months; p title= srep43317 Comparing all the four treatment groups together, a significant effect on TRR (p