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About a third of bowel cancers do not come from the familiar polyp at all. They come from flat, saw-toothed lesions that are hard to see at colonoscopy and follow a different molecular route, driven by chemical silencing of genes rather than by chromosome loss.
Approximately 30% of colorectal carcinomas develop through a serrated neoplasia pathway, named for the pattern of crypts in the precursor polyps. Molecular abnormalities consistently involve CpG island methylation of low or high degree and activating mutations of BRAF or KRAS; microsatellite instability of high level is often present. That allows a molecular classification into BRAF-mutant CIMP-high tumours, either microsatellite-unstable or stable, and KRAS-mutant CIMP-low microsatellite-stable tumours. Precursor polyps include the sessile serrated adenoma, proximal, with crypt architectural disturbance and BRAF mutation, probably preceded by the microvesicular hyperplastic polyp, with borderline lesions between them. Cytological dysplasia in a sessile serrated adenoma indicates advanced genetic abnormality and a high risk of progression. The traditional serrated adenoma favours the left colon, has tubulovillous architecture, eosinophilic cytoplasm and frequent KRAS mutation. Serrated morphology carcinoma is a World Health Organization subtype with frequent KRAS or BRAF mutation and a poor prognosis.
It is the reason colonoscopy quality standards now count sessile serrated lesion detection separately, and the reason a right-sided, BRAF-mutant, MSI-high cancer is read as serrated in origin rather than as an odd adenoma.
Shares Sidedness (left vs right colon), Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2), Mismatch repair & microsatellite instability, Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR).
Shares Colonoscopy, Epigenetic reprogramming, Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR), BRAF.
Shares Epigenetic reprogramming, Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2), Mismatch repair & microsatellite instability, Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR).
Shares Sidedness (left vs right colon), Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR), KRAS, Colorectal cancer.
Shares Sidedness (left vs right colon), Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2), Mismatch repair & microsatellite instability, Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR).
Shares Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2), Mismatch repair & microsatellite instability, Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR), BRAF.
Shares Epigenetic reprogramming, Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2), Mismatch repair & microsatellite instability, Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR).
Shares Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2), Mismatch repair & microsatellite instability, Microsatellite instability (MSI-H) / mismatch repair deficiency (dMMR), Colorectal cancer.