Sessile Serrated Adenoma / Polyp (SSA/P) Carcinogenic Mechanism and Gene Mutations Caused by Fusobacterium Nucleatum - Problems to be Clarified in the Future |Biomedgrid

The carcinogenic pathways of colorectal cancer include the classical pathway in which adenoma grows to colorectal cancer and the serrated pathway in which colorectal cancer grows from serrated adenoma. In the former adenoma, the diversity of gut flora (α diversity) is reduced, but not in SSA/P, and there is a difference in the change of gut flora depending on the carcinogenic route [1]. The serrated pathway is a concept recently proposed by Torlakovic et al. [2]. Sessile serrated adenoma / polyp (SSA/P) predominates in the right-side colon [3] and SSA/P is caused by mutations in the BRAF gene. In SSA/P, DNA methylation is observed genome-wide, and p16 and IGFBP7 are methylated to shift cells from the resting phase to the proliferative phase [4]. In addition, the methylation of the mismatch repair gene MLH1 suppresses MLH1 protein expression, causing microsatellite instability (MSI), resulting in atypia from SSA/P.