title: Traditional serrated adenoma: an update.
abstract: Although recognized 25 years ago, the traditional serrated adenoma (TSA) remains an ongoing source of diagnostic and biologic debate. Recent research has greatly improved our understanding of the morphological and molecular aspects of these polyps. In particular, the recognition of ectopic crypt foci (ECFs) in combination with typical cytology and slitlike serrations improves diagnostic reproducibility. Awareness that many TSAs, particularly BRAF-mutated TSAs, arise in precursor microvesicular hyperplastic polyps and sessile serrated adenomas can aid in making this diagnosis and should not be confused with a sessile serrated adenoma with dysplasia. At a molecular level, TSAs can be divided into 2 groups based on their BRAF or KRAS mutation status. The development of overt cytologic dysplasia is accompanied by TP53 mutation, Wnt pathway activation, and, in some cases, silencing of CDKN2A. Importantly, however, mismatch repair enzyme function is retained. Thus, the TSA is an important precursor of aggressive molecular subtypes of colorectal carcinoma.
authors.affiliation: The Conjoint Gastroenterology Laboratory, QIMR Berghofer Medical Research Institute, School of Medicine, University of Queensland, Envoi Specialist Pathologists, Brisbane 4072, Queensland, Australia.
authors.forename: Mark L
authors.initials: ML
authors.lastname: Bettington
authors.affiliation: Department of Pathology, Laboratory Medicine Program, University Health Network, University of Toronto, Toronto, Ontario M5G 2C4, Canada. Electronic address: runjan.chetty@gmail.com.
authors.forename: Runjan
authors.initials: R
authors.lastname: Chetty
mesh_terms: D018256:Adenomatous Polyps / Q000145:classification / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism; D001706:Biopsy; D003111:Colonic Polyps / Q000145:classification / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D003113:Colonoscopy; D015179:Colorectal Neoplasms / Q000145:classification / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D004252:DNA Mutational Analysis; D003937:Diagnosis, Differential; D015972:Gene Expression Regulation, Neoplastic; D020022:Genetic Predisposition to Disease; D006801:Humans; D007150:Immunohistochemistry; D009154:Mutation; D010641:Phenotype; D011237:Predictive Value of Tests; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000235:genetics; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics; D016283:Proto-Oncogene Proteins p21(ras); D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D018631:ras Proteins / Q000235:genetics
chemical_list: D014408:Biomarkers, Tumor; C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins
keywords: BRAF; CIMP; KRAS; Serrated polyp; Traditional serrated adenoma