Mini-symposium: pathology of the large bowelThe serrated polyp pathway to colorectal carcinoma
Section snippets
Basic concepts
Serration, an apt histological term for a saw-toothed glandular architecture, has been linked primarily to the common diminutive mucosal growths of the colorectum, called hyperplastic or metaplastic polyps. Although contrarian views can be found in the literature,1, 2 the conventional wisdom, since their early description and distinction from adenomatous polyps,3 has been that such serrated polyps are self-limited and unrelated to colorectal carcinoma (CRC). That view has been altered over the
Non-dysplastic serrated polyps (hyperplastic polyps)
The terms ‘hyperplastic polyp’ or ‘metaplastic polyp’ are widely used in pathology, but current knowledge justifies a classification of these non-dysplastic serrated polyps that recognizes their heterogeneity, and which identifies those categories that have a measurable level of risk of progression or association with malignant transformation. Efforts in this direction have made progress, but some confusion exists and a consensus on terminology and criteria is awaited. The classification of
Dysplastic serrated polyps (serrated adenomas)
Dysplastic serrated polyp (also known as ‘serrated adenoma’; Figure 5, Figure 6) encompasses several histological entities:
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serrated adenoma not otherwise specified
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mixed or admixed polyp
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traditional serrated adenoma
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sessile serrated adenoma with dysplasia.
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a serrated histogenesis identified by a serrated architecture in some component of the polyp
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a component that shows overt cytological dysplasia.
Serrated polyp pathway-associated colorectal adenocarcinomas–serrated carcinomas
The term ‘serrated carcinoma’ (SCa) was proposed originally by Jass and Smith62 on the basis of the striking architectural and histochemical resemblance of a CRC subset to hyperplastic polyps. It is currently applied to the endpoint carcinomas of the serrated pathway, whether identified by morphological features, residual serrated polyp or by a specific molecular genetic marker or profile. Estimates of the contribution of SCa to CRC overall can be calculated through various approaches, the most
Clinical guidelines for management and surveillance
In recent recommendations for colorectal screening and post-polypectomy surveillance, the USA National Taskforce on Colon Cancer,73 while acknowledging the serrated polyp pathway in CRC, did not offer specific recommendations for serrated polyp management and surveillance,73 citing the absence of authoritative clinical studies on which to base such recommendations. Huang et al.,52 in a clinicopathological review of the serrated polyp pathway and its implications for gastroenterology practice,
Acknowledgment
The authors thank John O’Hara, BS for his expert assistance with the preparation of the figures.
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Cited by (24)
The role of phosphatidylinositol 3 kinase (PI3K) and cycloxygenase-2 (COX2) in carcinogenesis of colorectal polyps
2018, Journal of ColoproctologyCitation Excerpt :Concerning the pathway of microsatellite instability, there is a dysfunction of deoxyribonucleic acid (DNA) repair enzymes, due to germline mutations in mismatch repair genes (MMR), with formation of tens to hundreds of repetitions of short sequences of nucleotide bases by the genome, called microsatellites.8 Regarding the serrated pathway, there is no mutation of MMR genes but an epigenetic phenomenon, called hypermethylation of promoter gene MMR enzyme that makes the silencing of their gene expression.9,10 Apparently, genetic alterations that occur in colorectal cancer follow the histologic progression of adenomas.11
Histological and molecular classification of gastrointestinal polyps
2017, Best Practice and Research: Clinical GastroenterologyCitation Excerpt :Characteristically they show a sawtooth morphology by epithelial protrusions into the crypt lumen. They are often small (less than 10 mm in diameter), stalked or broad based and most frequently found in the left hemicolon and the microvesicular variant harbors a braf mutation [68–75]. In the right hemicolon they are more frequently the starting point for the so called serrated pathway of malignant transformation.
Colorectal serrated adenocarcinoma. Histopathological, immunohistochemical and molecular description of one case
2013, Revista Espanola de PatologiaColorectal tumors: The histology report
2011, Digestive and Liver DiseaseClinicopathologic study of 85 colorectal serrated adenocarcinomas: Further insights into the full recognition of a new subset of colorectal carcinoma
2010, Human PathologyCitation Excerpt :Previous studies have given varying estimates about the frequency of cancers originating from serrated polyps, making it difficult to know the actual incidence of SAC. Morphologic studies [5,10] have yielded lower numbers (7.5%-12%) than estimates of a 10% to 20% frequency drawn from the molecular characteristics of serrated polyps and sporadic CRC with concurrent DNA hypermethylation and BRAF mutations [11]. The purpose of this study was 4-fold, as follow:
Pragmatic classification of superficial neoplastic colorectal lesions
2009, Gastrointestinal EndoscopyCitation Excerpt :They introduce an alternative pathway between neoplastic and non-neoplastic lesions because some of them do progress to neoplasia (Fig. 1). All serrated lesions share the same architecture in the upper part of epithelial crypts with a sawtooth lumen and a distinctive phenotype of somatic mutations of the BRAF gene.19,21-27 The metaplastic and serrated subtype of ACF is the monocryptal precursor of HPs and serrated lesions.