Sessile serrated lesion

Last updated on: 08.11.2024

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HistoryThis section has been translated automatically.

In the 5th edition of the WHO Classification of Tumors of the Digestive System (2019), the term "sessile serrated lesion" (SSL) was introduced to replace the term "sessile serrated adenoma/polyp" (SSA/P). SSLs are early precursor lesions in the serrated neoplasia pathway that give rise to colorectal carcinomas with BRAF mutations, methylation for DNA repair genes, a CpG island methylator phenotype and a high degree of microsatellite instability. Some of these lesions can rapidly become dysplastic or invasive carcinomas with a high potential for lymphatic invasion and lymph node metastasis (Murakami T et al. 2022).

DefinitionThis section has been translated automatically.

"Sessile serrated lesion" (from the Latin sessilis - sessile and serra - saw) is a pathological-anatomical term in gastroenterology for an adenomatous, flat, broad-based colonic polyp with histologically widened and sawtooth-like crypts up to the base. This lesion is considered a precancerous condition.

General informationThis section has been translated automatically.

Serrated lesions (SSL) in the colorectum represent a problem area for clinicians and pathologists; this is mainly due to the risk of progression of the various serrated polyps, which has not yet been conclusively clarified. Molecular biological research in recent years has clearly shown that, in addition to the classic "adenoma-carcinoma sequence", there is also a so-called "serrated pathway" of carcinogenesis, via which sessile serrated adenomas can develop intocolon carcinomas.

In serrated adenocarcinomas, a low-risk subtype (frequency <20%, with mostly proximal localization, the sessile serrated adenoma as a precursor lesion, BRAF mutation, high microsatellite instability, CpG methylation/hMLH1 failure and a 5-year survival rate of >70%) and a high-risk subtype (frequency >80%, with mostly distal localization, the traditional serrated adenoma as a precursor lesion, KRAS mutation, low microsatellite instability/microsatellite stability, CpG methylation/p53 accumulation and a 5-year survival rate of <30%). A molecular pathological determination of the microsatellite status and a BRAF or KRAS mutation in conjunction with hMLH1 and p53 immunohistochemistry allows a better differentiation of these two types and is becoming increasingly clinically relevant.

OccurrenceThis section has been translated automatically.

SSLs are typically found in the right-sided colon. They are usually > 5 mm in size and show a morphological similarity to hyperplastic polyps. In molecular biology, a sessile serrated lesion is associated with a mutation of the BRAF protooncogene. In the 2019 WHO classification, it was determined that dysplasia occurring in an SSL is most likely an advanced polyp, regardless of the morphologic grade of the dysplasia. Recognition of SSLs with or without dysplasia is crucial; however, the detection of SSLs is difficult and their identification inconsistent

LiteratureThis section has been translated automatically.

  1. Murakami T et al. (2022) Sessile serrated lesions: Clinicopathological characteristics, endoscopic diagnosis, and management. Dig Endosc 34:1096-1109.

Last updated on: 08.11.2024