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In sporadic colorectal cancer (CRC), the  BRAF V600E   mutation is associated with deficient mismatch repair (MMR) status and inversely associated with to KRAS mutations. In contrast to deficient MMR (dMMR) CRC, data on the presence of  KRAS  oncogenic mutations in proficient MMR (pMMR) CRC and their relationship with tumor progression are scarce. We therefore examined the MMR status in combination with  KRAS  mutations in 913 Chinese patients and correlated the findings obtained with clinical and pathological features. The MMR status was determined based on detection of MLH1, MSH2, MSH6 and PMS2 expression.  KRAS  mutation and dMMR status were detected in 36.9% and 7.5% of cases, respectively. Four subtypes were determined by MMR and  KRAS  mutation status:  KRAS  (+)/pMMR (34.0%),  KRAS  (+)/dMMR (2.9%),  KRAS  (-)/pMMR (58.5%) and  KRAS  (-)/dMMR (4.6%). A higher percentage of pMMR tumors with  KRAS  mutation were most likely to be female (49.0%), proximal located (45.5%), a mucinous histology (38.4%), and to have increased lymph node metastasis (60.3%), compared with pMMR tumors without  BRAF V600E   and  KRAS  mutations (36.0%, 29.3%, 29.4% and 50.7%, respectively; all  P  < 0.01). To the contrary, compared with those with  KRAS (-)/dMMR tumors, patients with  KRAS (+)/dMMR tumors demonstrated no statistically significant differences in gender, tumor location, pT depth of invasion, lymph node metastasis, pTNM stage, and histologic grade. This study revealed that specific epidemiologic and clinicopathologic characteristics are associated with MMR status stratified by  KRAS  mutation. Knowledge of MMR and  KRAS  mutation status may enhance molecular pathologic staging of CRC patients and metastatic progression in CRC can be estimated based on the combination of these biomarkers.

Distinct Clinicopathological Patterns of Mismatch Repair Status in Colorectal Cancer Stratified by KRAS Mutations