It is well established that colorectal cancer develops from a series of precursor epithelial polyps, including tubular adenomas, villous/tubulovillous adenomas (VA/TVA), sessile serrated adenomas (SSA) and traditional...It is well established that colorectal cancer develops from a series of precursor epithelial polyps, including tubular adenomas, villous/tubulovillous adenomas (VA/TVA), sessile serrated adenomas (SSA) and traditional serrated adenomas (TSA). Of these, TSAs are least common and account for only 5% of all serrated polyps. TSAs are characterised by the presence of a “pinecone-like” architecture, granular eosinophilic cytoplasm, luminal serrations, ectopic crypt foci (ECF) and elongated, pencillate nuclei. However, the distinct slit-like luminal serrations, reminiscent of small bowel mucosa, appear to be the most unique and reproducible feature to distinguish TSAs from other polyps. There is a contention that TSAs are not inherently dysplastic and that the majority do not show cytological atypia. Two types of dysplasia are associated with TSA. Serrated dysplasia is less well recognised and less commonly encountered than adenomatous dysplasia. In addition, it is now becoming increasingly evident that TSAs can be admixed with HP, SSA and VA/TVA. At a genetic level, polyps may switch phenotype as they accumulate genetic changes, evolving from a serrated pathway to a more conventional one, which could be the basis for a spectrum theory starting out with a TSA with serration and ECF evolving into a TSA with conventional dysplasia and, eventually, to a well-developed conventional adenoma. Nevertheless, there is an exigency for future studies to provide further illumination and bridge the gaps in our present understanding.展开更多
文摘It is well established that colorectal cancer develops from a series of precursor epithelial polyps, including tubular adenomas, villous/tubulovillous adenomas (VA/TVA), sessile serrated adenomas (SSA) and traditional serrated adenomas (TSA). Of these, TSAs are least common and account for only 5% of all serrated polyps. TSAs are characterised by the presence of a “pinecone-like” architecture, granular eosinophilic cytoplasm, luminal serrations, ectopic crypt foci (ECF) and elongated, pencillate nuclei. However, the distinct slit-like luminal serrations, reminiscent of small bowel mucosa, appear to be the most unique and reproducible feature to distinguish TSAs from other polyps. There is a contention that TSAs are not inherently dysplastic and that the majority do not show cytological atypia. Two types of dysplasia are associated with TSA. Serrated dysplasia is less well recognised and less commonly encountered than adenomatous dysplasia. In addition, it is now becoming increasingly evident that TSAs can be admixed with HP, SSA and VA/TVA. At a genetic level, polyps may switch phenotype as they accumulate genetic changes, evolving from a serrated pathway to a more conventional one, which could be the basis for a spectrum theory starting out with a TSA with serration and ECF evolving into a TSA with conventional dysplasia and, eventually, to a well-developed conventional adenoma. Nevertheless, there is an exigency for future studies to provide further illumination and bridge the gaps in our present understanding.
