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Review
Traditional serrated adenoma: an overview of pathology and emphasis on molecular pathogenesis
  1. Aoife J McCarthy,
  2. Stefano Serra,
  3. Runjan Chetty
  1. Division of Anatomical Pathology, Laboratory Medicine Program, University Health Network and University of Toronto, Toronto, Ontario, Canada
  1. Correspondence to Dr Runjan Chetty; runjan.chetty{at}gmail.com

Abstract

Objective To provide an overview of the pathology and molecular pathogenesis of traditional serrated adenomas (TSA).

Design Describe the morphology and molecules that play a role in their pathogenesis.

Results These exuberant polypoid lesions are typified by tall cells with deeply eosinophilic cytoplasm, elongated nuclei bearing delicate chromatin, ectopic crypt foci, deep clefting of the lining mucosa and an overall resemblance to small bowel mucosa.

Broadly, TSAs arise via three mechanisms. They may be BRAF mutated and CpG island methylator phenotype (CIMP)-high: right sided, mediated through a microvesicular hyperplastic polyp or a sessile serrated adenoma, may also have RNF43 mutations and result in microsatellite stable (MSS) colorectal cancers (CRC). The second pathway that is mutually exclusive of the first is mediated through KRAS mutation with CIMP-low TSAs. These are left-sided TSAs, are not associated with another serrated polyp and result in MSS CRC. These TSAs also have RSPO3, RNF43 and p53 mutations together with aberrant nuclear localisation of β-catenin. Third, there is a smaller group of TSAs that are BRAF and KRAS wild type and arise by as yet unknown molecular events. All TSAs show retention of mismatch repair proteins.

Conclusion These are characteristic unusual polyps with a complex molecular landscape.

  • traditional serrated adenoma
  • serrated polyp
  • BRAF
  • KRAS
  • colorectal cancer

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/bmjgast-2019-000317

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    Footnotes

    • Contributors The three authors (AJMC, SS, RC) are authors based on the following four criteria applying to all three authors: substantial contributions to the conception or design of the work; or the acquisition, analysis, or interpretation of data for the work: AJMC, SS, RC; drafting the work or revising it critically for important intellectual content: AJMC, SS, RC; final approval of the version to be published: AJMC, SS, RC; agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved: AJMC, SS, RC. All individuals listed as coauthors of the manuscript (AJMC, SS, RC) qualify for every one of the four criteria listed above.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data availability statement No additional data are available.