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Background  BRAF is a member of RAF family of serine/threonine kinases and mediates cellular responses to growth signals through the RAS-RAF-MAP kinase pathway. Activating mutations in  BRAF  have recently been found in about 10% of colorectal cancers, with the vast majority being a V600E hotspot mutation. The aim of the present study was to evaluate the clinical, pathological and molecular phenotype of colorectal tumors with  BRAF  mutations.    Results  Mutations in  BRAF  were identified in 8% (23/275) of colorectal cancers. They were 5–10-fold more frequent in tumors with infiltrating lymphocytes, location in the proximal colon, poor histological grade and mucinous appearance ( P  < 0.002 for each). Tumors with  BRAF  mutation were also 10-fold more likely to show microsatellite instability and frequent DNA methylation ( P  < 0.0001) compared to tumors without this mutation. The characteristic morphological features of tumors with  BRAF  mutation (infiltrating lymphocytes, poor grade, mucinous) remained after stratification according to microsatellite instability and methylator phenotypes. Mutations in  BRAF  were mutually exclusive with mutations in  KRAS  but showed no clear association with the presence of  TP53  mutation.    Conclusion   BRAF  mutation identifies a colorectal cancer subgroup with distinctive phenotypic properties independent of microsatellite instability status and thus could be a valuable marker for studies into the clinical properties of these tumors.

molecular cancer

BRAF mutations are associated with distinctive clinical, pathological and molecular features of colorectal cancer independently of microsatellite instability status