PDF file - 1.3MB, Proliferation of MDA MB231 and A549 cells grown in different conditions.

PDF file - 235K, Clinical relevance of AXL in CRC tissues.

Table S1: Top 20 pathways identified by IPA containing genes significantly upregulated between poor and good prognostic BRAFMT stage II/III CRC in GSE39582; Table S2: Top 20 pathways identified by IPA containing genes significantly downregulated between poor and good prognostic BRAFMT stage II/III CRC in GSE39582; Table S3: Top 20 pathways identified by IPA containing genes differentially expressed between poor (disease free survival <5 years) and good prognostic BRAFMT stage II CRC (disease free survival >5 years) in E-MTAB-863 and E-MTAB-864; Table S4: Results of siRNA screen in BRAFMT CRC.

PDF file - 179K, Effect of AXL siRNA on migration, proliferation and survival of CRC cells.

Supplementary Table 2: Differentially expressed gene list contrasting tumour region of origin between Central Tumor and Invasive Front. Supplementary Table 3: Differentially expressed gene list contrasting tumour region of origin between CT-LN. Supplementary Table 4: Differentially expressed gene list contrasting tumour region of origin between LN-IF.

Figure legends for Supplementary Figures

PDF file - 3.5, MTT assay showing that cancer cells with K-Ras activation mutation (HCT116/Hkh-2 and DLD1/DKO3 isogenic pairs) and c-Met (HCC827 parental/GR5 pair) are more susceptible to Ran silencing-induced apoptosis. (A) In HCT116/Hkh-2 colon cancer isogenic pair, HCT116 cells, which contain K-Ras activation mutation, are more susceptible to apoptosis induction by the 5 shRNAs targeting Ran, compared to the K-Ras wild-type counterpart, Hkh-2. (B) In DLD1/DKO3 colon cancer isogenic pair, DLD1 cells, which contain K-Ras activation mutation, are more susceptible to apoptosis induction by the 2 shRNAs targeting Ran, compared to the K-Ras wild-type counterpart, DKO3. (C) In HCC827 parental/GR5 lung cancer pair, the GR5 cells, which contain c-Met amplification, are more susceptible to apoptosis induction by the 2 shRNAs targeting Ran, compared to the wild-type HCC827 cells. Results are plotted as histogram showing the mean SD from three independent experiments. Key; *, ** and *** represent p < 0.05, <0.01 and <0.001, respectively. Representative blots from three independent experiments are shown.

Figure S1: Discovery and validation datasets used in the study; Figure S2: Sensitivity of BRAFMT and WT CRC cells to acute ER stress induction; Figure S3: Sensitivity of BRAFMT and WT CRC cells to ACY-1215 and carfilzomib; Figure S4: Effect of combined ACY-1215 and carfilzomib on survival of BRAFMT and WT CRC cells; Figure S5: Effect of combined ACY-1215 and carfilzomib on accumulation of ubiquitinated proteins; Figure S6: Tolerability of combined ACY-1215/carfilzomib treatment in BALB/c nude mice

PDF file - 223K, Univariate and multivariate analyses for OS, DSS, DFS and AXL-LOW and AXL-HIGH in stage II/III CRC group (publicly-available CRC microarray dataset).

Supplementary Figures S1-S2 and Supplementary Tables S1-S3.

Supplementary Data from Clinical Determinants of Response to Irinotecan-Based Therapy Derived from Cell Line Models

PDF file - 213K, Migration, proliferation rates and RTK profiling of HCT116 parental and invasive cells.

Supplementary materials and methods

PDF file - 80K, Pathway analysis

PDF file - 157K, Candidate genes for RNAi screen

Impact of each predictor included in the Random Forest classifier on the probability of recurrence alone and in combination with the others.

This Supplementary Figure indicates the project plan

Supplementary Figure S7. MEK1/2 regulates levels of decoy MET in BRAFMT in vitro and in vivo models.

Detailed description of the patients data handling and inclusion criteria for downstream analyses of the discovery, expansion and validation cohorts.

This Supplementary Table indicates the sample source for the study