Therapeutic approaches targeting the serrated pathway of colorectal cancer characterized by mutation in the BRAF gene and overexpression of GTPase RAC1b

Abstract

Around 30% of all colorectal cancer cases are derived from the serrated polyp pathway and mostly carry a mutation in the BRAF gene. Here, we review the current knowledge about the association of this tumor subtype with the CpG island methylator and microsatellite instability phenotypes, immune cell infiltration, and overexpression of GTPase Rac1b. The corresponding therapeutic approaches for targeting these molecular characteristics are presented and critically discussed.