Phenotypic attributes and survival in mismatch repair deficient/microsatellite instability-high colorectal carcinomas

Figure 1 The consort diagram of the patients included in the study. MMR: Mismatch repair; MSI: Microsatellite instability; NACT: Neoadjuvant chemotherapy.

Figure 2 Histopathological features of mismatch repair deficient/microsatellite instability-high colorectal cancers. A: Moderately differentiated adenocarcinoma with expansile pattern of invasion; B: Low tumor budding (arrows); C: Peritumoral lymphocytic response or Cron’s like lymphoid reaction (arrows); D: Marked intraepithelial tumor infiltrating lymphocytes; E: Loss of MutL homolog 1 protein immune expression; F: Intact MutS homolog 2 protein immune expression; G: Intact MutS homolog 6 protein immune expression; E and H: Loss of postmeiotic segregation increased 2 protein immune expression (note the positive internal control i.e. nuclear staining of MutL homolog 1 or postmeiotic segregation increased 2 in stromal cells or lymphocytes).

Figure 3 Box plot analysis of mismatch repair deficient/microsatellite instability-high colorectal cancers with the mismatch repair proficient/microsatellite stable colorectal cancer group. A: Comparing the lymph node yield; B: Lymph node ratio; C: Size of largest uninvolved lymph node. MMR: Mismatch repair; LNY: Lymph node yield; LNR: Lymph node ratio.

Figure 4 Overall survival curve of mismatch repair proficient and microsatellite instability-high colorectal cancer patients. A and B: Respect to tumor budding, P = 0.049; C and D: Intraepithelial lymphocytes, P = 0.014; E and F: Peritumoral lymphocytes, P value not evaluable.