However, SSA/Ps can be difficult to detect, are inconsistently identified by endoscopists and pathologists, and are often incompletely resected. Therefore, the detection of serrated lesions, including SSA/Ps with and without dysplasia, is critical. Furthermore, we reported that the submucosal invasive carcinomas that arose in SSA/Ps exhibited higher potentials for lymphatic invasion and lymph node metastasis than their conventional counterparts that arose from tubular adenomas. Some researchers have suggested that some serrated lesions might progress rapidly to dysplasia or invasive carcinomas. This pathway is thought to be distinct from the conventional adenoma-carcinoma pathway in which adenomas progress to invasive colorectal carcinomas as a result of a series of genetic alterations, including adenomatous polyposis coli ( APC) and KRAS mutations. Recent studies have shown associations between SSA/Ps with and without dysplasia or carcinoma and the methylation or loss of protein expression for DNA repair genes, including MLH1, a CpG island methylator phenotype, BRAF mutations, and a lack of genetic alterations in CTNNB1, which is the gene that codes for β-catenin protein. SSA/Ps are early precursor lesions in the serrated neoplasia pathway, which results in colorectal carcinomas with high levels of microsatellite instability. Crypts with a serrated architecture include those that are irregularly dilated, branch irregularly, and are horizontally arranged (basal). Typical histology of a sessile serrated adenoma/polyp. Greater awareness may promote further research into improving the detection, identification, and complete resection rates of SSA/Ps with and without dysplasia/carcinoma and reduce the interval cancer rates. The lesions’ endoscopic characteristics, which include their (semi)pedunculated morphologies, double elevations, central depressions, and reddishness, and the use of magnifying endoscopy, might help to detect dysplasia/carcinoma within SSA/Ps. Magnifying narrow-band imaging findings, which include dark spots inside the crypts and varicose microvascular vessels, in addition to the type II-open pit patterns detected using magnifying chromoendoscopy, effectively differentiate SSA/Ps from hyperplastic polyps. Unlike hyperplastic polyps, SSA/Ps are usually larger than 5 mm, frequently covered by a thin layer called the ‘‘mucus cap’’, and are more commonly located in the proximal colon. Endoscopically, these subtle polyps are like hyperplastic polyps, because they are slightly elevated and pale. Here, the endoscopic features of SSA/Ps with and without dysplasia/carcinoma, including the characteristics determined using magnifying endoscopy, are reviewed in the context of previous reports. If colonoscopists can identify the specific endoscopic characteristics of SSA/Ps, their detection and the effectiveness of colonoscopy may improve. Therefore, SSA/Ps are considered to be major contributors to “interval cancers”. Detecting serrated lesions, including SSA/Ps with and without dysplasia/carcinoma, is critical, but SSA/Ps can be difficult to detect, are inconsistently identified by endoscopists and pathologists, and are often incompletely resected. Some of these lesions can rapidly become dysplastic or invasive carcinomas that exhibit high lymphatic invasion and lymph node metastasis potentials. Sessile serrated adenoma/polyps (SSA/Ps) are early precursor lesions in the serrated neoplasia pathway, which results in colorectal carcinomas with BRAF mutations, methylation for DNA repair genes, a CpG island methylator phenotype, and high levels of microsatellite instability.
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