The spectrum of serrated colorectal lesions—new entities and unanswered questions

Abstract

The spectrum of serrated colorectal lesions-new entities and unanswered questions Hyperplastic polyps (HPs) of the colon and rectum were historically thought not to be associated with an increased risk of development of colorectal cancer (CRC). The recognition of variants of serrated colorectal lesions that possessed relatively subtle but significant morphological differences from those of HPs and that could be associated with epithelial dysplasia and CRC led to the characterisation of sessile serrated lesions (SSLs) and traditional serrated adenomas (TSAs). These links were supported by the identification of genetic alterations that are commonly found in HPs, SSLs, TSAs, and CRC, e.g. BRAF and KRAS mutations. The 'serrated pathway' to CRC may progress faster than the traditional 'adenoma-carcinoma sequence', underlining the importance of identifying these lesions. The diagnostic histological criteria for SSLs have since been more clearly defined, in parallel with a drive to increase the recognition of these lesions at endoscopy. The existence of lesions showing overlapping morphological and molecular features with those of HPs, SSLs and TSAs has most recently been highlighted-including mucin-rich TSA, serrated tubulovillous adenoma, and those showing mixed histological features, e.g. comprising differing combinations of HP, SSL, and TSA. Morphological and molecular studies of this range of lesions are providing insights into the relationships of serrated colorectal lesions with each other and with CRC. This article provides an overview of the current understanding of serrated colorectal lesions, including a discussion of those with overlapping and mixed features.

NTRK oncogenic fusions are exclusively associated with the serrated neoplasia pathway in the colorectum and begin to occur in sessile serrated lesions

“…The 132 SSLs without morphological dysplasia were collected in our previous study, and the detailed histological criteria for the selection of SSLs were described in our previous reports [18,19]. Other precursor lesions, including SSLDs, TSAs, HPs, conventional adenomas with low-grade dysplasia, and conventional adenomas with high-grade dysplasia, were selected mainly based on the histological criteria of the latest WHO classification [19,[24][25][26]. This study was conducted in compliance with the ethical guidelines of the 2013 Declaration of Helsinki.…”

Real-time colorectal polyp detection using a novel computer-aided detection system (CADe): a feasibility study

“…Although we are optimistic about these detection rates, future well-designed randomized trials powered to detect a clinically and statistically significant improvement in the quality indicator ADR are needed. As 15-20% of CRCs develop from the serrated pathway and SSLs seem to be over-represented among iCRCs, it will be of high interest to evaluate SDR as additional outcome [7]. Finally, future studies should also focus on the detection of lesions that are easily overlooked without an CADe system, such as small (< 10 mm) and nonpolypoid lesions [23].…”

“…Missed lesions have a risk of developing into CRC, and it is thought that at least 50% of all interval cancers (iCRCs; defined as CRC diagnosed between screening and post-screening surveillance colonoscopies) develop from missed lesions during colonoscopy [6]. Interestingly, CRCs deriving from the serrated neoplasia pathway seem to be overrepresented among interval carcinomas, making it even more important to early detect and resect SSLs [7].…”

Clinicopathological and molecular analyses of hyperplastic lesions including microvesicular variant and goblet cell rich variant hyperplastic polyps and hyperplastic nodules—Hyperplastic nodule is an independent histological entity

“…To histologically characterize each lesion, we selected nine histological features found among the 142 hyperplastic lesions. As listed in Table S1 and illustrated in Figure S1 these were: (1) goblet cell abundance; (2) limited serrated change, only at the surface of the crypt; (3) serration of the crypt within the upper half of the crypt; (4) branching of the crypt; (5) dilatation of the crypt; (6) lateral spread of the crypt base (e.g., boot‐shaped or anchor‐shaped crypts); (7) asymmetrical branching; (8) narrowing of the lower crypt; and (9) elongated straightforward crypt without serration 2,8–12 . The first eight factors were defined as a lesion with at least greater than one factors.…”

“…As listed in Table S1 and illustrated in Figure S1 these were: (1) goblet cell abundance; (2) limited serrated change, only at the surface of the crypt; (3) serration of the crypt within the upper half of the crypt; (4) branching of the crypt; (5) dilatation of the crypt; (6) lateral spread of the crypt base (e.g., boot‐shaped or anchor‐shaped crypts); (7) asymmetrical branching; (8) narrowing of the lower crypt; and (9) elongated straightforward crypt without serration. 2 , 8 , 9 , 10 , 11 , 12 The first eight factors were defined as a lesion with at least greater than one factors. A finding of “elongated straightforward crypt without serration” was termed as a lesion with more than 50% present within the same tumor.…”