Hyperplastic polyps and colorectal cancer: is there a link?1 Jeremy R Jass  Clinical Gastroenterology and Hepatology  Volume 2, Issue 1, Pages 1-8 (January 2004) DOI: 10.1016/S1542-3565(03)00284-2

Figure 1 Mixed polyp comprising hyperplastic polyp on the left and serrated adenoma on the right (A). The hyperplastic component shows an irregular crypt architecture including dilatation, and some would regard this component of the mixed lesion as a sessile serrated adenoma despite the absence of overt dysplasia. The more obviously dysplastic component to the right of panel A shows loss of expression of the DNA mismatch repair gene hMLH1 (B). (A) Hematoxylin-eosin; (B) anti-hMLH1 immunostaining (G168-15; Pharmingen, San Diego, CA). Clinical Gastroenterology and Hepatology 2004 2, 1-8DOI: (10.1016/S1542-3565(03)00284-2)

Figure 2 Schema illustrating possible key rate-limiting steps in 3 pathways to ACF, hyperplastic polyp and hyperplastic-like polyps, or sessile serrated polyps. The molecular steps that determine growth of ACF into hyperplastic polyps are not known. CRC is envisioned to arise from hyperplastic-like polyps (or sessile serrated polyps) in which the earliest events might be BRAF mutation synergizing with a methylated and silenced pro-apoptotic gene. Subsequent methylation of hMLH1 or MGMT then predisposes to mutation, dysplastic change, and finally to malignancy that is frequently characterized by MSI-H or MSI-low status. K-ras mutation may substitute for BRAF in methylator pathways culminating in MSI-low and some MSS CRC. Clinical Gastroenterology and Hepatology 2004 2, 1-8DOI: (10.1016/S1542-3565(03)00284-2)