Relationships among KRAS mutation status, expression of RAS pathway signaling molecules, and clinicopathological features and prognosis of patients with colorectal cancer

Figure 1 Real-time polymerase chain reaction detection of mutated KRAS in formalin-fixed paraffin-embedded colorectal cancer tissues. Left to right representative amplification plots for samples with wild-type, uncertain mutation status, and mutated KRAS genes.

Figure 2 Expression of RAS pathway proteins in colorectal cancer. A-D: KRAS negative (A and B) and positive (C and D) expression at magnification × 40 (A and C) and × 100 (B and D). E-P: As described for (A-D), except that staining for BRAF protein (E-H), MEK protein (I-L), and ERK protein (M-P) is shown.

Figure 3 Effect of KRAS gene status on expression of KRAS protein on the cell membrane. H-score: Histochemistry score.

Figure 4 Effect of KRAS gene status on expression of KRAS protein in the cytoplasm. H-score: Histochemistry score.

Figure 5 Effect of KRAS gene status on BRAF protein expression. H-score: Histochemistry score.

Figure 6 Effect of KRAS gene status on MEK protein expression. H-score: Histochemistry score.

Figure 7 Effect of KRAS gene status on ERK protein expression. H-score: Histochemistry score.

Figure 8 Effect of RAS pathway protein expression on progression-free survival and overall survival in patients with stage II/III colorectal cancer. A-H: Effects of KRAS (A and B), BRAF (C and D), MEK (E and F), and ERK (G and H) protein expression on progression-free survival (A, C, E, and G) and overall survival (B, D, F, and H). PFS: Progression-free survival; OS: Overall survival.