Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways.

Autor:	van Toledo DEFWM; Department of Gastroenterology and Hepatology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.; Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, the Netherlands.; Cancer Center Amsterdam, Amsterdam, the Netherlands., IJspeert JEG; Department of Gastroenterology and Hepatology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.; Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, the Netherlands.; Cancer Center Amsterdam, Amsterdam, the Netherlands., Boersma H; Department of Gastroenterology and Hepatology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands., Musler AR; Amsterdam University Medical Centers, University of Amsterdam, Department of Pathology, Amsterdam, the Netherlands., Bleijenberg AGC; Department of Gastroenterology and Hepatology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.; Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, the Netherlands.; Cancer Center Amsterdam, Amsterdam, the Netherlands., Dekker E; Department of Gastroenterology and Hepatology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.; Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, the Netherlands.; Cancer Center Amsterdam, Amsterdam, the Netherlands., van Noesel CJM; Amsterdam University Medical Centers, University of Amsterdam, Department of Pathology, Amsterdam, the Netherlands.
Jazyk:	angličtina
Zdroj:	Clinical and translational gastroenterology [Clin Transl Gastroenterol] 2023 Aug 01; Vol. 14 (8), pp. e00611. Date of Electronic Publication: 2023 Aug 01.
DOI:	10.14309/ctg.0000000000000611
Abstrakt:	Introduction: Patients with serrated polyposis syndrome (SPS) have an increased risk to develop colorectal cancer (CRC). Due to an abundance of serrated polyps, these CRCs are assumed to arise mainly through the serrated neoplasia pathway rather than through the classical adenoma-carcinoma pathway. We aimed to evaluate the pathogenetic routes of CRCs in patients with SPS. Methods: We collected endoscopy and pathology data on CRCs and polyps of patients with SPS under treatment in our center. Our primary end point was the proportion of BRAFV600E mutated CRCs, indicating serrated pathway CRCs (sCRCs). CRCs lacking BRAFV600E most likely inferred a classical adenoma-carcinoma origin (aCRCs). We assessed patient, polyp, and CRC characteristics and stratified for BRAFV600E mutation status. Results: Thirty-five patients with SPS harbored a total of 43 CRCs. Twenty-one CRCs (48.8%) carried a BRAFV600E mutation, 10 of which lacked MLH1 staining and 17 (81%) were located in the proximal colon. Twenty-two CRCs (51.1%) did not carry a BRAFV600E mutation and were MLH1 proficient. Of these 22 putatively aCRCs, 17 (77.3%) were located distally and one-third (36.4%) harbored a pathogenic KRAS or NRAS mutation. In patients with BRAFwt -CRCs, a higher ratio of the median number of conventional adenomas versus serrated polyps was found (4 vs 13) than patients with BRAFV600E -CRCs (1 vs 14). Discussion: Our study indicates that in patients with SPS, the ratio of sCRCs:aCRCs on average is 50:50. This elevated sCRC:aCRC ratio in patients with SPS, when compared with non-SPS patients, correlates well with the differences in the ratios of the numbers of sessile serrated lesions and conventional adenomas in patients with SPS and non-SPS patients, respectively. (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)
Databáze:	MEDLINE
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