Blog
About

1
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Screening Relevance of Sessile Serrated Polyps

      Clinical Endoscopy

      Korean Society of Gastrointestinal Endoscopy

      Colorectal neoplasms, Screening, Colonoscopy

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Conventional adenomas have historically been considered to be the only screening-relevant colorectal cancer (CRC) precursor lesion. The prevailing paradigm was that most CRCs arise along the chromosomal instability pathway, where adenomas accumulate incremental genetic alterations over time, leading eventually to malignancy. However, it is now recognized that this “conventional” pathway accounts for only about two-thirds of CRCs. The serrated pathway is responsible for most of the remainder, and is a disproportionate contributor to postcolonoscopy CRC. Hallmarks of the serrated pathway are mutations in the BRAF gene, high levels of methylation of promoter CpG islands, and the sessile serrated polyp (SSP). Accumulating evidence shows that SSPs can be considered adenoma-equivalent from the standpoint of CRC screening. SSPs have a higher prevalence than previously thought, and appear to have a relatively long dwell time similar to that of conventional adenomas. In addition, SSPs, whether sporadic or as part of the serrated polyposis syndrome, are associated with increased risk of synchronous and metachronous neoplasia. These features collectively support that SSPs are highly relevant to CRC prevention.

          Related collections

          Most cited references 25

          • Record: found
          • Abstract: found
          • Article: not found

          Long-term colorectal-cancer incidence and mortality after lower endoscopy.

          Colonoscopy and sigmoidoscopy provide protection against colorectal cancer, but the magnitude and duration of protection, particularly against cancer of the proximal colon, remain uncertain. We examined the association of the use of lower endoscopy (updated biennially from 1988 through 2008) with colorectal-cancer incidence (through June 2010) and colorectal-cancer mortality (through June 2012) among participants in the Nurses' Health Study and the Health Professionals Follow-up Study. Among 88,902 participants followed over a period of 22 years, we documented 1815 incident colorectal cancers and 474 deaths from colorectal cancer. With endoscopy as compared with no endoscopy, multivariate hazard ratios for colorectal cancer were 0.57 (95% confidence interval [CI], 0.45 to 0.72) after polypectomy, 0.60 (95% CI, 0.53 to 0.68) after negative sigmoidoscopy, and 0.44 (95% CI, 0.38 to 0.52) after negative colonoscopy. Negative colonoscopy was associated with a reduced incidence of proximal colon cancer (multivariate hazard ratio, 0.73; 95% CI, 0.57 to 0.92). Multivariate hazard ratios for death from colorectal cancer were 0.59 (95% CI, 0.45 to 0.76) after screening sigmoidoscopy and 0.32 (95% CI, 0.24 to 0.45) after screening colonoscopy. Reduced mortality from proximal colon cancer was observed after screening colonoscopy (multivariate hazard ratio, 0.47; 95% CI, 0.29 to 0.76) but not after sigmoidoscopy. As compared with colorectal cancers diagnosed in patients more than 5 years after colonoscopy or without any prior endoscopy, those diagnosed in patients within 5 years after colonoscopy were more likely to be characterized by the CpG island methylator phenotype (CIMP) (multivariate odds ratio, 2.19; 95% CI, 1.14 to 4.21) and microsatellite instability (multivariate odds ratio, 2.10; 95% CI, 1.10 to 4.02). Colonoscopy and sigmoidoscopy were associated with a reduced incidence of cancer of the distal colorectum; colonoscopy was also associated with a modest reduction in the incidence of proximal colon cancer. Screening colonoscopy and sigmoidoscopy were associated with reduced colorectal-cancer mortality; only colonoscopy was associated with reduced mortality from proximal colon cancer. Colorectal cancer diagnosed within 5 years after colonoscopy was more likely than cancer diagnosed after that period or without prior endoscopy to have CIMP and microsatellite instability. (Funded by the National Institutes of Health and others.).
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Update on the serrated pathway to colorectal carcinoma.

             D C Snover (2010)
            Adenocarcinoma of the large intestine can no longer be considered one disease but rather a family of diseases with different precursor lesions, different molecular pathways, and different end-stage carcinomas with varying prognoses. Approximately 60% of colorectal carcinomas arise from conventional adenomas via the suppressor pathway leading to microsatellite stable carcinomas. These carcinomas represent the pathway that has been the target of screening and prevention programs to date. However, approximately 35% of carcinomas arise along the serrated pathway developing from the precursor lesion known as the sessile serrated adenoma (also referred to as the sessile serrated polyp). Sessile serrated adenomas/polyps lead to carcinomas with extensive CpG island promoter methylation (CpG island methylated phenotype positive carcinomas), which can be either microsatellite instable high or microsatellite stable. The remaining 5% of carcinomas arise from conventional adenomas in patients with germ line mutations of mismatch repair genes (Lynch syndrome), leading to CpG island methylated phenotype negative microsatellite instable carcinomas. Carcinomas arising from sessile serrated adenomas/polyps are not prevented by removing conventional adenomas and hence may be missed in routine screening programs. In addition, a subset of these lesions may potentially progress rapidly to carcinoma; hence, it is likely that these lesions will require a different screening strategy from that used for conventional adenomas. This article reviews the various pathways to colorectal carcinoma with emphasis on the serrated pathway and evaluates the implications of this pathway for colorectal carcinomas screening programs. Copyright © 2011. Published by Elsevier Inc.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Incomplete polyp resection during colonoscopy-results of the complete adenoma resection (CARE) study.

              Although the adenoma detection rate is used as a measure of colonoscopy quality, there are limited data on the quality of endoscopic resection of detected adenomas. We determined the rate of incompletely resected neoplastic polyps in clinical practice. We performed a prospective study on 1427 patients who underwent colonoscopy at 2 medical centers and had at least 1 nonpedunculated polyp (5-20 mm). After polyp removal was considered complete macroscopically, biopsies were obtained from the resection margin. The main outcome was the percentage of incompletely resected neoplastic polyps (incomplete resection rate [IRR]) determined by the presence of neoplastic tissue in post-polypectomy biopsies. Associations between IRR and polyp size, morphology, histology, and endoscopist were assessed by regression analysis. Of 346 neoplastic polyps (269 patients; 84.0% men; mean age, 63.4 years) removed by 11 gastroenterologists, 10.1% were incompletely resected. IRR increased with polyp size and was significantly higher for large (10-20 mm) than small (5-9 mm) neoplastic polyps (17.3% vs 6.8%; relative risk = 2.1), and for sessile serrated adenomas/polyps than for conventional adenomas (31.0% vs 7.2%; relative risk = 3.7). The IRR for endoscopists with at least 20 polypectomies ranged from 6.5% to 22.7%; there was a 3.4-fold difference between the highest and lowest IRR after adjusting for size and sessile serrated histology. Neoplastic polyps are often incompletely resected, and the rate of incomplete resection varies broadly among endoscopists. Incomplete resection might contribute to the development of colon cancers after colonoscopy (interval cancers). Efforts are needed to ensure complete resection, especially of larger lesions. ClinicalTrials.gov Number: NCT01224444. Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved.
                Bookmark

                Author and article information

                Journal
                Clin Endosc
                Clin Endosc
                CE
                Clinical Endoscopy
                Korean Society of Gastrointestinal Endoscopy
                2234-2400
                2234-2443
                May 2019
                8 January 2019
                : 52
                : 3
                : 235-238
                Affiliations
                Department of Medicine, Indiana University School of Medicine, Richard L. Roudebush VA Medical Center, Indianapolis, IN, USA
                Author notes
                Correspondence: Charles J. Kahi Department of Medicine, Indiana University School of Medicine, Richard L. Roudebush VA Medical Center, 1481 West 10th street, Indianapolis, IN 46202, USA Tel: +1-317-988-3682, Fax: +1-317-988-5313, E-mail: ckahi2@ 123456iu.edu
                Article
                ce-2018-112
                10.5946/ce.2018.112
                6547343
                30625264
                Copyright © 2019 Korean Society of Gastrointestinal Endoscopy

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Review

                Radiology & Imaging

                colonoscopy, screening, colorectal neoplasms

                Comments

                Comment on this article