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Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways
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....
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10461936/ https://www.ncbi.nlm.nih.gov/pubmed/37352472 http://dx.doi.org/10.14309/ctg.0000000000000611 |
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author | van Toledo, David E. F. W. M. IJspeert, Joep E.G. Boersma, Hannah Musler, Alex R. Bleijenberg, Arne G. C. Dekker, Evelien van Noesel, Carel J. M. |
author_facet | van Toledo, David E. F. W. M. IJspeert, Joep E.G. Boersma, Hannah Musler, Alex R. Bleijenberg, Arne G. C. Dekker, Evelien van Noesel, Carel J. M. |
author_sort | van Toledo, David E. F. W. M. |
collection | PubMed |
description | 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 BRAF(V600E) mutated CRCs, indicating serrated pathway CRCs (sCRCs). CRCs lacking BRAF(V600E) most likely inferred a classical adenoma-carcinoma origin (aCRCs). We assessed patient, polyp, and CRC characteristics and stratified for BRAF(V600E) mutation status. RESULTS: Thirty-five patients with SPS harbored a total of 43 CRCs. Twenty-one CRCs (48.8%) carried a BRAF(V600E) 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 BRAF(V600E) 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 BRAF(wt)-CRCs, a higher ratio of the median number of conventional adenomas versus serrated polyps was found (4 vs 13) than patients with BRAF(V600E)-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. |
format | Online Article Text |
id | pubmed-10461936 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Wolters Kluwer |
record_format | MEDLINE/PubMed |
spelling | pubmed-104619362023-08-29 Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways van Toledo, David E. F. W. M. IJspeert, Joep E.G. Boersma, Hannah Musler, Alex R. Bleijenberg, Arne G. C. Dekker, Evelien van Noesel, Carel J. M. Clin Transl Gastroenterol Article 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 BRAF(V600E) mutated CRCs, indicating serrated pathway CRCs (sCRCs). CRCs lacking BRAF(V600E) most likely inferred a classical adenoma-carcinoma origin (aCRCs). We assessed patient, polyp, and CRC characteristics and stratified for BRAF(V600E) mutation status. RESULTS: Thirty-five patients with SPS harbored a total of 43 CRCs. Twenty-one CRCs (48.8%) carried a BRAF(V600E) 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 BRAF(V600E) 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 BRAF(wt)-CRCs, a higher ratio of the median number of conventional adenomas versus serrated polyps was found (4 vs 13) than patients with BRAF(V600E)-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. Wolters Kluwer 2023-06-26 /pmc/articles/PMC10461936/ /pubmed/37352472 http://dx.doi.org/10.14309/ctg.0000000000000611 Text en © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND) (https://creativecommons.org/licenses/by-nc-nd/4.0/) , where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. |
spellingShingle | Article van Toledo, David E. F. W. M. IJspeert, Joep E.G. Boersma, Hannah Musler, Alex R. Bleijenberg, Arne G. C. Dekker, Evelien van Noesel, Carel J. M. Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways |
title | Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways |
title_full | Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways |
title_fullStr | Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways |
title_full_unstemmed | Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways |
title_short | Polyps and Colorectal Cancer in Serrated Polyposis Syndrome: Contribution of the Classical Adenoma-Carcinoma and Serrated Neoplasia Pathways |
title_sort | polyps and colorectal cancer in serrated polyposis syndrome: contribution of the classical adenoma-carcinoma and serrated neoplasia pathways |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10461936/ https://www.ncbi.nlm.nih.gov/pubmed/37352472 http://dx.doi.org/10.14309/ctg.0000000000000611 |
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