Loading…
Germline variant testing in serrated polyposis syndrome
Background and Aim Serrated polyposis syndrome (SPS) is now known to be the commonest polyposis syndrome. Previous analyses for germline variants have shown no consistent positive findings. To exclude other polyposis syndromes, 2019 British Society of Gastroenterology (BSG) guidelines advise gene pa...
Saved in:
| Published in: | Journal of gastroenterology and hepatology 2022-05, Vol.37 (5), p.861-869 |
|---|---|
| Main Authors: | , , , , , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c4431-cc01fcc0e4cf1e8d495cf620fd6dfdc40f130d7479a2cb6025c21e5091df25a53 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c4431-cc01fcc0e4cf1e8d495cf620fd6dfdc40f130d7479a2cb6025c21e5091df25a53 |
| container_end_page | 869 |
| container_issue | 5 |
| container_start_page | 861 |
| container_title | Journal of gastroenterology and hepatology |
| container_volume | 37 |
| creator | Murphy, Aisling Solomons, Joyce Risby, Peter Gabriel, Jessica Bedenham, Tina Johnson, Michael Atkinson, Nathan Bailey, Adam A Bird‐Lieberman, Elizabeth Leedham, Simon J East, James E Biswas, Sujata |
| description | Background and Aim
Serrated polyposis syndrome (SPS) is now known to be the commonest polyposis syndrome. Previous analyses for germline variants have shown no consistent positive findings. To exclude other polyposis syndromes, 2019 British Society of Gastroenterology (BSG) guidelines advise gene panel testing if the patient is under 50 years, there are multiple affected individuals within a family, or there is dysplasia within any of the polyps.
Methods
A database of SPS patients was established at the Oxford University Hospitals NHS Foundation Trust. Patients were referred for genetic assessment based on personal and family history and patient preference. The majority were tested for a hereditary colorectal cancer panel including MUTYH, APC, PTEN, SMAD4, BMPR1A, STK11, NTLH1, POLD1, POLE, GREM1 (40‐kb duplication), PMS2, and Lynch syndrome mismatch repair genes.
Results
One hundred and seventy‐three patients were diagnosed with SPS based on World Health Organization 2019 criteria between February 2010 and December 2020. The mean age of diagnosis was 54.2 ± 16.8 years. Seventy‐three patients underwent genetic testing and 15/73 (20.5%) were found to have germline variants, of which 7/73 (9.6%) had a pathogenic variant (MUTYH n = 2, SMAD4 n = 1, CHEK2 n = 2, POLD1 n = 1, and RNF43 n = 1). Only 60% (9/15) of these patients would have been recommended for gene panel testing according to current BSG guidelines.
Conclusions
A total of 20.5% of SPS patients tested were affected by heterozygous germline variants, including previously unreported associations with CHEK2 and POLD1. This led to a change in management in seven patients (9.6%). Current recommendations may miss SPS associated with germline variants, which is more common than previously anticipated. |
| doi_str_mv | 10.1111/jgh.15791 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9305167</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2626223411</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4431-cc01fcc0e4cf1e8d495cf620fd6dfdc40f130d7479a2cb6025c21e5091df25a53</originalsourceid><addsrcrecordid>eNp1kUtLAzEYRYMoWqsL_4AMuNHF2Hx5zHQ2gohWpeBG1yHmUVNmkppMlf57o1VRwQSSRQ6H7-YidAD4FPIazWdPp8DrBjbQABjDJdSs2kQDPAZeNhSaHbSb0hxjzHDNt9EO5UDGNaEDVE9M7FrnTfEio5O-L3qTeudnhfNFMjHK3uhiEdrVIiSXirTyOobO7KEtK9tk9j_vIXq4ury_uC6nd5Obi_NpqRijUCqFwebDMGXBjDVruLIVwVZX2mrFsAWKdc3qRhL1WGHCFQHDcQPaEi45HaKztXexfOyMVsb3UbZiEV0n40oE6cTvF--exCy8iIZiDlWdBcefghielzmb6FxSpm2lN2GZBKnyJpQBZPToDzoPy-hzvExVQHkzzqGG6GRNqRhSisZ-DwNYvNchch3io47MHv6c_pv8-v8MjNbAq2vN6n-TuJ1cr5VvoL-U0w</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2661359844</pqid></control><display><type>article</type><title>Germline variant testing in serrated polyposis syndrome</title><source>Wiley-Blackwell Journals</source><creator>Murphy, Aisling ; Solomons, Joyce ; Risby, Peter ; Gabriel, Jessica ; Bedenham, Tina ; Johnson, Michael ; Atkinson, Nathan ; Bailey, Adam A ; Bird‐Lieberman, Elizabeth ; Leedham, Simon J ; East, James E ; Biswas, Sujata</creator><creatorcontrib>Murphy, Aisling ; Solomons, Joyce ; Risby, Peter ; Gabriel, Jessica ; Bedenham, Tina ; Johnson, Michael ; Atkinson, Nathan ; Bailey, Adam A ; Bird‐Lieberman, Elizabeth ; Leedham, Simon J ; East, James E ; Biswas, Sujata</creatorcontrib><description>Background and Aim
Serrated polyposis syndrome (SPS) is now known to be the commonest polyposis syndrome. Previous analyses for germline variants have shown no consistent positive findings. To exclude other polyposis syndromes, 2019 British Society of Gastroenterology (BSG) guidelines advise gene panel testing if the patient is under 50 years, there are multiple affected individuals within a family, or there is dysplasia within any of the polyps.
Methods
A database of SPS patients was established at the Oxford University Hospitals NHS Foundation Trust. Patients were referred for genetic assessment based on personal and family history and patient preference. The majority were tested for a hereditary colorectal cancer panel including MUTYH, APC, PTEN, SMAD4, BMPR1A, STK11, NTLH1, POLD1, POLE, GREM1 (40‐kb duplication), PMS2, and Lynch syndrome mismatch repair genes.
Results
One hundred and seventy‐three patients were diagnosed with SPS based on World Health Organization 2019 criteria between February 2010 and December 2020. The mean age of diagnosis was 54.2 ± 16.8 years. Seventy‐three patients underwent genetic testing and 15/73 (20.5%) were found to have germline variants, of which 7/73 (9.6%) had a pathogenic variant (MUTYH n = 2, SMAD4 n = 1, CHEK2 n = 2, POLD1 n = 1, and RNF43 n = 1). Only 60% (9/15) of these patients would have been recommended for gene panel testing according to current BSG guidelines.
Conclusions
A total of 20.5% of SPS patients tested were affected by heterozygous germline variants, including previously unreported associations with CHEK2 and POLD1. This led to a change in management in seven patients (9.6%). Current recommendations may miss SPS associated with germline variants, which is more common than previously anticipated.</description><identifier>ISSN: 0815-9319</identifier><identifier>EISSN: 1440-1746</identifier><identifier>DOI: 10.1111/jgh.15791</identifier><identifier>PMID: 35128723</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>Adenomatous polyposis coli ; Adenomatous Polyposis Coli - genetics ; Adult ; Aged ; colon ; Colorectal carcinoma ; Colorectal Neoplasms - diagnosis ; Colorectal Neoplasms, Hereditary Nonpolyposis - genetics ; Dysplasia ; Gastroenterology ; Genetic screening ; Genetic Testing ; genetics ; Germ Cells ; Germ-Line Mutation ; Humans ; Middle Aged ; Mismatch repair ; Original ‐ Gastroenterology (Clinical) ; Patients ; Polyposis ; Polyps ; PTEN protein ; Smad4 protein ; Syndrome</subject><ispartof>Journal of gastroenterology and hepatology, 2022-05, Vol.37 (5), p.861-869</ispartof><rights>2022 The Authors. Journal of Gastroenterology and Hepatology published by Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.</rights><rights>2022. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4431-cc01fcc0e4cf1e8d495cf620fd6dfdc40f130d7479a2cb6025c21e5091df25a53</citedby><cites>FETCH-LOGICAL-c4431-cc01fcc0e4cf1e8d495cf620fd6dfdc40f130d7479a2cb6025c21e5091df25a53</cites><orcidid>0000-0002-8371-2147 ; 0000-0002-0700-7286</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjgh.15791$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjgh.15791$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,315,786,790,891,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35128723$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Murphy, Aisling</creatorcontrib><creatorcontrib>Solomons, Joyce</creatorcontrib><creatorcontrib>Risby, Peter</creatorcontrib><creatorcontrib>Gabriel, Jessica</creatorcontrib><creatorcontrib>Bedenham, Tina</creatorcontrib><creatorcontrib>Johnson, Michael</creatorcontrib><creatorcontrib>Atkinson, Nathan</creatorcontrib><creatorcontrib>Bailey, Adam A</creatorcontrib><creatorcontrib>Bird‐Lieberman, Elizabeth</creatorcontrib><creatorcontrib>Leedham, Simon J</creatorcontrib><creatorcontrib>East, James E</creatorcontrib><creatorcontrib>Biswas, Sujata</creatorcontrib><title>Germline variant testing in serrated polyposis syndrome</title><title>Journal of gastroenterology and hepatology</title><addtitle>J Gastroenterol Hepatol</addtitle><description>Background and Aim
Serrated polyposis syndrome (SPS) is now known to be the commonest polyposis syndrome. Previous analyses for germline variants have shown no consistent positive findings. To exclude other polyposis syndromes, 2019 British Society of Gastroenterology (BSG) guidelines advise gene panel testing if the patient is under 50 years, there are multiple affected individuals within a family, or there is dysplasia within any of the polyps.
Methods
A database of SPS patients was established at the Oxford University Hospitals NHS Foundation Trust. Patients were referred for genetic assessment based on personal and family history and patient preference. The majority were tested for a hereditary colorectal cancer panel including MUTYH, APC, PTEN, SMAD4, BMPR1A, STK11, NTLH1, POLD1, POLE, GREM1 (40‐kb duplication), PMS2, and Lynch syndrome mismatch repair genes.
Results
One hundred and seventy‐three patients were diagnosed with SPS based on World Health Organization 2019 criteria between February 2010 and December 2020. The mean age of diagnosis was 54.2 ± 16.8 years. Seventy‐three patients underwent genetic testing and 15/73 (20.5%) were found to have germline variants, of which 7/73 (9.6%) had a pathogenic variant (MUTYH n = 2, SMAD4 n = 1, CHEK2 n = 2, POLD1 n = 1, and RNF43 n = 1). Only 60% (9/15) of these patients would have been recommended for gene panel testing according to current BSG guidelines.
Conclusions
A total of 20.5% of SPS patients tested were affected by heterozygous germline variants, including previously unreported associations with CHEK2 and POLD1. This led to a change in management in seven patients (9.6%). Current recommendations may miss SPS associated with germline variants, which is more common than previously anticipated.</description><subject>Adenomatous polyposis coli</subject><subject>Adenomatous Polyposis Coli - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>colon</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - diagnosis</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</subject><subject>Dysplasia</subject><subject>Gastroenterology</subject><subject>Genetic screening</subject><subject>Genetic Testing</subject><subject>genetics</subject><subject>Germ Cells</subject><subject>Germ-Line Mutation</subject><subject>Humans</subject><subject>Middle Aged</subject><subject>Mismatch repair</subject><subject>Original ‐ Gastroenterology (Clinical)</subject><subject>Patients</subject><subject>Polyposis</subject><subject>Polyps</subject><subject>PTEN protein</subject><subject>Smad4 protein</subject><subject>Syndrome</subject><issn>0815-9319</issn><issn>1440-1746</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><recordid>eNp1kUtLAzEYRYMoWqsL_4AMuNHF2Hx5zHQ2gohWpeBG1yHmUVNmkppMlf57o1VRwQSSRQ6H7-YidAD4FPIazWdPp8DrBjbQABjDJdSs2kQDPAZeNhSaHbSb0hxjzHDNt9EO5UDGNaEDVE9M7FrnTfEio5O-L3qTeudnhfNFMjHK3uhiEdrVIiSXirTyOobO7KEtK9tk9j_vIXq4ury_uC6nd5Obi_NpqRijUCqFwebDMGXBjDVruLIVwVZX2mrFsAWKdc3qRhL1WGHCFQHDcQPaEi45HaKztXexfOyMVsb3UbZiEV0n40oE6cTvF--exCy8iIZiDlWdBcefghielzmb6FxSpm2lN2GZBKnyJpQBZPToDzoPy-hzvExVQHkzzqGG6GRNqRhSisZ-DwNYvNchch3io47MHv6c_pv8-v8MjNbAq2vN6n-TuJ1cr5VvoL-U0w</recordid><startdate>202205</startdate><enddate>202205</enddate><creator>Murphy, Aisling</creator><creator>Solomons, Joyce</creator><creator>Risby, Peter</creator><creator>Gabriel, Jessica</creator><creator>Bedenham, Tina</creator><creator>Johnson, Michael</creator><creator>Atkinson, Nathan</creator><creator>Bailey, Adam A</creator><creator>Bird‐Lieberman, Elizabeth</creator><creator>Leedham, Simon J</creator><creator>East, James E</creator><creator>Biswas, Sujata</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8371-2147</orcidid><orcidid>https://orcid.org/0000-0002-0700-7286</orcidid></search><sort><creationdate>202205</creationdate><title>Germline variant testing in serrated polyposis syndrome</title><author>Murphy, Aisling ; Solomons, Joyce ; Risby, Peter ; Gabriel, Jessica ; Bedenham, Tina ; Johnson, Michael ; Atkinson, Nathan ; Bailey, Adam A ; Bird‐Lieberman, Elizabeth ; Leedham, Simon J ; East, James E ; Biswas, Sujata</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4431-cc01fcc0e4cf1e8d495cf620fd6dfdc40f130d7479a2cb6025c21e5091df25a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenomatous polyposis coli</topic><topic>Adenomatous Polyposis Coli - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>colon</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - diagnosis</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</topic><topic>Dysplasia</topic><topic>Gastroenterology</topic><topic>Genetic screening</topic><topic>Genetic Testing</topic><topic>genetics</topic><topic>Germ Cells</topic><topic>Germ-Line Mutation</topic><topic>Humans</topic><topic>Middle Aged</topic><topic>Mismatch repair</topic><topic>Original ‐ Gastroenterology (Clinical)</topic><topic>Patients</topic><topic>Polyposis</topic><topic>Polyps</topic><topic>PTEN protein</topic><topic>Smad4 protein</topic><topic>Syndrome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Murphy, Aisling</creatorcontrib><creatorcontrib>Solomons, Joyce</creatorcontrib><creatorcontrib>Risby, Peter</creatorcontrib><creatorcontrib>Gabriel, Jessica</creatorcontrib><creatorcontrib>Bedenham, Tina</creatorcontrib><creatorcontrib>Johnson, Michael</creatorcontrib><creatorcontrib>Atkinson, Nathan</creatorcontrib><creatorcontrib>Bailey, Adam A</creatorcontrib><creatorcontrib>Bird‐Lieberman, Elizabeth</creatorcontrib><creatorcontrib>Leedham, Simon J</creatorcontrib><creatorcontrib>East, James E</creatorcontrib><creatorcontrib>Biswas, Sujata</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Online Library</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of gastroenterology and hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Murphy, Aisling</au><au>Solomons, Joyce</au><au>Risby, Peter</au><au>Gabriel, Jessica</au><au>Bedenham, Tina</au><au>Johnson, Michael</au><au>Atkinson, Nathan</au><au>Bailey, Adam A</au><au>Bird‐Lieberman, Elizabeth</au><au>Leedham, Simon J</au><au>East, James E</au><au>Biswas, Sujata</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Germline variant testing in serrated polyposis syndrome</atitle><jtitle>Journal of gastroenterology and hepatology</jtitle><addtitle>J Gastroenterol Hepatol</addtitle><date>2022-05</date><risdate>2022</risdate><volume>37</volume><issue>5</issue><spage>861</spage><epage>869</epage><pages>861-869</pages><issn>0815-9319</issn><eissn>1440-1746</eissn><notes>Author contribution</notes><notes>AM and SB conducted the research and wrote the first draft of the manuscript. JM, PR, JG, and TB edited the genetics aspects to the manuscript. MJ, NA, AB, EBL, SL, and JE edited the manuscript.</notes><notes>JEE and EBL are funded by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. The views expressed are those of the authors and not necessarily those of the National Health Service, the NIHR, or the Department of Health. SJL was supported by a Wellcome Trust Senior Clinical Research Fellowship (206314/Z/17/Z).</notes><notes>There are no conflict of interests.</notes><notes>Declaration of conflict of interest</notes><notes>Financial support</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>Author contribution: AM and SB conducted the research and wrote the first draft of the manuscript. JM, PR, JG, and TB edited the genetics aspects to the manuscript. MJ, NA, AB, EBL, SL, and JE edited the manuscript.</notes><notes>Financial support: JEE and EBL are funded by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. The views expressed are those of the authors and not necessarily those of the National Health Service, the NIHR, or the Department of Health. SJL was supported by a Wellcome Trust Senior Clinical Research Fellowship (206314/Z/17/Z).</notes><notes>Declaration of conflict of interest: There are no conflict of interests.</notes><abstract>Background and Aim
Serrated polyposis syndrome (SPS) is now known to be the commonest polyposis syndrome. Previous analyses for germline variants have shown no consistent positive findings. To exclude other polyposis syndromes, 2019 British Society of Gastroenterology (BSG) guidelines advise gene panel testing if the patient is under 50 years, there are multiple affected individuals within a family, or there is dysplasia within any of the polyps.
Methods
A database of SPS patients was established at the Oxford University Hospitals NHS Foundation Trust. Patients were referred for genetic assessment based on personal and family history and patient preference. The majority were tested for a hereditary colorectal cancer panel including MUTYH, APC, PTEN, SMAD4, BMPR1A, STK11, NTLH1, POLD1, POLE, GREM1 (40‐kb duplication), PMS2, and Lynch syndrome mismatch repair genes.
Results
One hundred and seventy‐three patients were diagnosed with SPS based on World Health Organization 2019 criteria between February 2010 and December 2020. The mean age of diagnosis was 54.2 ± 16.8 years. Seventy‐three patients underwent genetic testing and 15/73 (20.5%) were found to have germline variants, of which 7/73 (9.6%) had a pathogenic variant (MUTYH n = 2, SMAD4 n = 1, CHEK2 n = 2, POLD1 n = 1, and RNF43 n = 1). Only 60% (9/15) of these patients would have been recommended for gene panel testing according to current BSG guidelines.
Conclusions
A total of 20.5% of SPS patients tested were affected by heterozygous germline variants, including previously unreported associations with CHEK2 and POLD1. This led to a change in management in seven patients (9.6%). Current recommendations may miss SPS associated with germline variants, which is more common than previously anticipated.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>35128723</pmid><doi>10.1111/jgh.15791</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8371-2147</orcidid><orcidid>https://orcid.org/0000-0002-0700-7286</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0815-9319 |
| ispartof | Journal of gastroenterology and hepatology, 2022-05, Vol.37 (5), p.861-869 |
| issn | 0815-9319 1440-1746 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9305167 |
| source | Wiley-Blackwell Journals |
| subjects | Adenomatous polyposis coli Adenomatous Polyposis Coli - genetics Adult Aged colon Colorectal carcinoma Colorectal Neoplasms - diagnosis Colorectal Neoplasms, Hereditary Nonpolyposis - genetics Dysplasia Gastroenterology Genetic screening Genetic Testing genetics Germ Cells Germ-Line Mutation Humans Middle Aged Mismatch repair Original ‐ Gastroenterology (Clinical) Patients Polyposis Polyps PTEN protein Smad4 protein Syndrome |
| title | Germline variant testing in serrated polyposis syndrome |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-21T20%3A27%3A18IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Germline%20variant%20testing%20in%20serrated%20polyposis%20syndrome&rft.jtitle=Journal%20of%20gastroenterology%20and%20hepatology&rft.au=Murphy,%20Aisling&rft.date=2022-05&rft.volume=37&rft.issue=5&rft.spage=861&rft.epage=869&rft.pages=861-869&rft.issn=0815-9319&rft.eissn=1440-1746&rft_id=info:doi/10.1111/jgh.15791&rft_dat=%3Cproquest_pubme%3E2626223411%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4431-cc01fcc0e4cf1e8d495cf620fd6dfdc40f130d7479a2cb6025c21e5091df25a53%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2661359844&rft_id=info:pmid/35128723&rfr_iscdi=true |