Most human CRCs are thought to arise From adenomas (adenomatous polyps) that become dysplastic.
Understanding of the so called serrated carcinogenesis pathway is an important step forward in expanding possibilities in the prevention of CRC..
An important step to reduce the incidence of CRC initiated by the serrated pathway is to improve the detection of serrated polyps and to ensure their complete removal during endoscopy.
Moreover, the data indicate that the SSA/P are the precursors of Colorectal carcinoma by MSI and may be subject to rapid progression to malignancy.
Evidence suggests that subtypes of serrated polyps, particularly TSA and SSA/P, can lead to adenocarcinoma through the serrated pathway.
These tumors seem to have a better prognosis, stage for stage, than typical Colorectal carcinomas.
Carcinomas associated with DNA mismatch repair mutations are more likely to be poorly differentiated and incite a host lymphocytic response.
Generally, as polyps increase in size, the degree of dysplasia worsens, the villous component increases, the number of genetic abnormalities increases, and the likelihood of harboring invasive carcinoma increases.
Adenomatous polyps are classified as tubular, tubulovillous, or villous.
Over time, as this lesion acquires additional mutations, it evolves into a classic adenomatous polyp.
The earliest lesion detected with dysplasia is the aberrant crypt focus.
All adenomas contain dysplastic epithelium that arises From mutations in either the adenomatous polyposis coli gene or DNA mismatch repair genes.
The adenoma carcinoma sequence postulates that Colorectal carcinomas arise From precursor lesions, called adenomas.
Th hypothesis that invasive CRCs develop From intermediate precancerous precursors is supported by pathologic, epidemiologic, and observational clinical data.
This ordered process is increasingly disrupted as adenomas increase in size, become dysplastic, and eventually attain invasive potential.
As cells move towards the luminal surface, they cease proliferating and terminally differentiate.
Typically, proliferation occurs exclusively at the crypt base.
Surface cells lining the intestine are continuously lost into the bowel lumen due to apoptosis and exfoliation and must be continuously replaced.
Adenomatous polyps form in the colon when normal mechanisms regulating epithelial renewal are disrupted.
Most human CRCs are thought to arise From adenomas (adenomatous polyps) that become dysplastic
