Figure 3 from Precision Oncology and Systemic Targeted Therapy in Pseudomyxoma Peritonei

Treatment with BRAF inhibitor is enough to block RAS/ERK signaling pathway and reduce cell viability in PMP models. BRAFWT (T70) or BRAFV600E (CTAX34) colorectal cancer PDXO and BRAFV600E PMP PDXO (PMP5.1) or PDO (PMP5.2) derived from two different peritoneal metastasis from PMP patient 5 treated with vehicle, mitomycin C 150 ng/mL, cetuximab 100 μg/mL, encorafenib 1 μmol/L, doublet (encorafenib + cetuximab). A and B, Cell viability (A) and caspase 3/7 activation (B) were measured after 5 days or 48 hours on treatment, respectively. Mean ± SD of triplicates is shown. Significant differences were assessed using one-way ANOVA and Dunnett’s multiple comparisons tests compared to control (*, P value < 0.05; **, P value < 0.01; ***, P value < 0.001; ****, P value < 0.0001). C and D, Western blot analysis of phospho-ERK, phospho-EGFR, ERK, and EGFR was performed after 30 minutes or 24 hours on treatment. Quantification of phospho-EGFR/EGFR (C) and phospho-ERK/ERK (D) ration in all the samples. r.u, relative units. PMP, Pseudomyxoma peritonei; CRC, Colorectal cancer; PDO, Patient-derived organoid; PDXO, Patient-derived xenografts organoid.