Additional file 2: of Combined blockade of MEK and PI3KCA as an effective antitumor strategy in HER2 gene amplified human colorectal cancer models

Table S1. Evaluation of protein expression level in parental (SW48 and LIM1215) and in HER2-amplified human colon cancer cell lines. Legend: Negative symbol (-) no protein expression detected; Positive symbols: (+) expression and (++) over-expression levels of each protein detected. Table S2. Antitumor efficacy of oxaliplatin plus trastuzumab followed by maintenance treatment in human HER2-amplified colon cancer xenograft. (DOCX 613 kb

Additional file 1: of Combined blockade of MEK and PI3KCA as an effective antitumor strategy in HER2 gene amplified human colorectal cancer models

Figure S1. Expression and phosphorylation of HER2 in parental SW48 and LIM1215 human colon cancer cell lines and in their HER2-amplified derivatives (SW48-HER2 and LIM1215-HER2) cells (Additional file 3: Supplementary Methods). Figure S2. Phenotypic characterization of parental SW48 and LIM1215 human colon cancer cell lines and of their HER2-amplified derivatives (SW48-HER2 and LIM1215-HER2) cells. Figure S3. Expression and phosphorylation of HER family receptors and their downstream signaling pathways in parental SW48 and LIM1215 human colon cancer cell lines and in their HER2-amplified derivatives (SW48-HER2 and LIM1215-HER2) cells. Figure S4. Effects of chemotherapeutic agents and of anti-EGFR monoclonal antibodies on cell proliferation in parental SW48 and LIM1215 human colon cancer cell lines and in their HER2-amplified derivatives (SW48-HER2 and LIM1215-HER2) cells. (DOCX 5258 kb

Additional file 3: of Combined blockade of MEK and PI3KCA as an effective antitumor strategy in HER2 gene amplified human colorectal cancer models

Supplementary Methods. (DOCX 18 kb

Supplementary Figure 2 from EPHA2 Is a Predictive Biomarker of Resistance and a Potential Therapeutic Target for Improving Antiepidermal Growth Factor Receptor Therapy in Colorectal Cancer

Supplementary Figure 2. A-B: Synergistic anti-proliferative effects of the combination of ALW-II-41-27 and cetuximab.C: Effect of Epha2 gene knockdown on cetuximab sensitivity in HCT116 and LOVO cell lines. D: Effects of combination treatment with ALW-II-41-27 and cetuximab on induction of apoptosis. E: Cell cycle distribution for HCT15 and SW48-CR following treatment with ALW-II-41-27 and/or cetuximab for 24, 48 and 72 hrs at indicated doses. F: Effects of EPHA2 blockade alone and in combination with cetuximab on intracellular signalling pathways of cell proliferation and survival.</p

Supplementary Figure 1 from EPHA2 Is a Predictive Biomarker of Resistance and a Potential Therapeutic Target for Improving Antiepidermal Growth Factor Receptor Therapy in Colorectal Cancer

Supplementary Figure 1. A: Phosphoarray analysis of SW48 and SW48-CR cell lines. B: Silencing of EPHA2 decreases the sensitivity to ALW-II-41-27 in HCT15 and SW48-CR cell lines.</p

Supplementary Table 1 from EPHA2 Is a Predictive Biomarker of Resistance and a Potential Therapeutic Target for Improving Antiepidermal Growth Factor Receptor Therapy in Colorectal Cancer

Supplementary Table 1: Treatment with ALW-II-41-27 or cetuximab as single agents</p

Supplementary Table 2 from EPHA2 Is a Predictive Biomarker of Resistance and a Potential Therapeutic Target for Improving Antiepidermal Growth Factor Receptor Therapy in Colorectal Cancer

Supplementary Table 2: EPHA2 expression in tumor samples of 82 RAS WT colorectal cancer patients from the GOIM-CAPRI trial</p

Supplementary Table 3 from EPHA2 Is a Predictive Biomarker of Resistance and a Potential Therapeutic Target for Improving Antiepidermal Growth Factor Receptor Therapy in Colorectal Cancer

Supplementary Table 3: EPHA2 expression in tumor samples with HSCORE</p

Supplementary Materials and Methods from EPHA2 Is a Predictive Biomarker of Resistance and a Potential Therapeutic Target for Improving Antiepidermal Growth Factor Receptor Therapy in Colorectal Cancer

Supplementary materials and methods</p