Figure 5 | Scientific Reports

Figure 5

From: Ex vivo treatment of patient biopsies as a novel method to assess colorectal tumour response to the MEK1/2 inhibitor, Selumetinib

Figure 5

Influence of KRAS mutational status on ERK1/2 activity and tumour sensitivity to Selumetinib. (a–f) Twenty two tumours were analysed for codon 12/13 mutations in KRAS, and for BRAFV600E mutations. (a–c) Graphs showing mean (+/− s.e.m) basal (T0) levels of (a) p-ERK1/2, (b) proliferation and (c) apoptosis in wild type and KRAS/BRAF mutant tumours collectively. See also Supporting Fig. 3. (d) Fold change in relative p-ERK1/2 activity in wild type and KRAS mutant tumours. (e and f) Mean (+/− s.e.m, N = 22) percentage (e) apoptosis and (f) proliferation in untreated (0 µm) and treated (0.1–3 µM Selumetinib) wild type and KRAS mutant tumours. (g) Subsets 1, 2 and 3 refer to subsets 1, 2 and 3 outlined in Fig. 4. Subset 1-A significant decrease in proliferation in response to 3 µM Selumetinib but not necessarily 0.1 µM. Subset 2- Significant response only at 0.1 µM Selumetinib. Subset 3: No significant response.

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