Fig. 10
Schematic of the serrated neoplasia pathway. Most sessile serrated polyps harbor a BRAF mutation and may develop possibly from a microvesicular hyperplastic polyp or de novo (dotted line). Sessile serrated polyps progress to malignancy by either acquiring mismatch repair deficiency caused by MLH1 promoter methylation or through other molecular events such as TP53 mutation to mismatch repair-proficient colorectal carcinoma. Traditional serrated adenoma may develop possibly from sessile serrated polyp or some goblet cell hyperplastic polyps (dotted lines) and progress to malignancy via the BRAF or the KRAS pathway to high grade dysplasia and mismatch repair proficient-colorectal carcinoma. WNT signaling pathway activation occurs in all pathways through different mechanisms, at the transition to dysplasia or earlier in traditional serrated adenoma
