Interobserver variability in the evaluation of mismatch repair protein immunostaining
Summary Immunohistochemical staining for mismatch repair proteins has during recent years been established as a routine analysis in many pathology laboratories with the aim to identify tumors linked to the hereditary nonpolyposis colorectal cancer syndrome. Despite widespread application, data on re...
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| creator | Klarskov, Louise, MD Ladelund, Steen Holck, Susanne, MD, PhD Roenlund, Karina, MD Lindebjerg, Jan, MD Elebro, Jacob, MD Halvarsson, Britta, MD, PhD von Salomé, Jenny, MSc Bernstein, Inge, MD, PhD Nilbert, Mef, MD, PhD |
| description | Summary Immunohistochemical staining for mismatch repair proteins has during recent years been established as a routine analysis in many pathology laboratories with the aim to identify tumors linked to the hereditary nonpolyposis colorectal cancer syndrome. Despite widespread application, data on reliability are lacking. We therefore evaluated interobserver variability among 6 pathologists, 3 experienced gastrointestinal pathologists and 3 residents. In total, 225 immunohistochemically stained colorectal cancers were evaluated as having normal, weak, loss of, or nonevaluable mismatch repair protein staining. Full consensus was achieved in 51% of the stainings for MLH1, 61% for PMS2, 83% for MSH2, and 45% for MSH6. Weak stainings were the main cause of reduced consensus, whereas contradictory evaluations with normal as well as loss of staining were reported in 2% to 6% of the tumors. Interobserver variability was considerable, though experienced pathologists and residents reached the same level of consensus. Because results from immunohistochemical mismatch repair protein stainings are used for decisions on mutation analysis and as an aid in the interpretation of gene variants of unknown significance in hereditary nonpolyposis colorectal cancer, the interobserver variability identified highlights the need for quality assessment programs, including guidelines for classification of different expression patterns. |
| doi_str_mv | 10.1016/j.humpath.2010.03.003 |
| format | Article |
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Despite widespread application, data on reliability are lacking. We therefore evaluated interobserver variability among 6 pathologists, 3 experienced gastrointestinal pathologists and 3 residents. In total, 225 immunohistochemically stained colorectal cancers were evaluated as having normal, weak, loss of, or nonevaluable mismatch repair protein staining. Full consensus was achieved in 51% of the stainings for MLH1, 61% for PMS2, 83% for MSH2, and 45% for MSH6. Weak stainings were the main cause of reduced consensus, whereas contradictory evaluations with normal as well as loss of staining were reported in 2% to 6% of the tumors. Interobserver variability was considerable, though experienced pathologists and residents reached the same level of consensus. Because results from immunohistochemical mismatch repair protein stainings are used for decisions on mutation analysis and as an aid in the interpretation of gene variants of unknown significance in hereditary nonpolyposis colorectal cancer, the interobserver variability identified highlights the need for quality assessment programs, including guidelines for classification of different expression patterns.</description><identifier>ISSN: 0046-8177</identifier><identifier>ISSN: 1532-8392</identifier><identifier>EISSN: 1532-8392</identifier><identifier>DOI: 10.1016/j.humpath.2010.03.003</identifier><identifier>PMID: 20573374</identifier><identifier>CODEN: HPCQA4</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Adenosine Triphosphatases - genetics ; Adenosine Triphosphatases - metabolism ; Adult ; Aged ; Aged, 80 and over ; Automation ; Biological and medical sciences ; Cancer and Oncology ; Cancer och onkologi ; Clinical Medicine ; Colorectal cancer ; Colorectal Neoplasms, Hereditary Nonpolyposis - genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis - metabolism ; DNA Mismatch Repair ; DNA Repair Enzymes - genetics ; DNA Repair Enzymes - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Genetic counseling ; HNPCC ; Humans ; Immunohistochemistry ; Investigative techniques, diagnostic techniques (general aspects) ; Klinisk medicin ; Laboratories ; Lynch Syndrome ; Male ; Medical and Health Sciences ; Medical sciences ; Medicin och hälsovetenskap ; Middle Aged ; Mismatch Repair Endonuclease PMS2 ; MMR ; Mutation ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein - genetics ; MutS Homolog 2 Protein - metabolism ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Observer Variation ; Pathology ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Reliability ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors ; Young Adult</subject><ispartof>Human pathology, 2010-10, Vol.41 (10), p.1387-1396</ispartof><rights>Elsevier Inc.</rights><rights>2010 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c634t-69f8f08ef520a5bb1c6f37cf251be466b5666e2f7f7e753d9a5340f06801cede3</citedby><cites>FETCH-LOGICAL-c634t-69f8f08ef520a5bb1c6f37cf251be466b5666e2f7f7e753d9a5340f06801cede3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.humpath.2010.03.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,315,781,785,886,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23312156$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20573374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://lup.lub.lu.se/record/1727153$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:121383337$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Klarskov, Louise, MD</creatorcontrib><creatorcontrib>Ladelund, Steen</creatorcontrib><creatorcontrib>Holck, Susanne, MD, PhD</creatorcontrib><creatorcontrib>Roenlund, Karina, MD</creatorcontrib><creatorcontrib>Lindebjerg, Jan, MD</creatorcontrib><creatorcontrib>Elebro, Jacob, MD</creatorcontrib><creatorcontrib>Halvarsson, Britta, MD, PhD</creatorcontrib><creatorcontrib>von Salomé, Jenny, MSc</creatorcontrib><creatorcontrib>Bernstein, Inge, MD, PhD</creatorcontrib><creatorcontrib>Nilbert, Mef, MD, PhD</creatorcontrib><title>Interobserver variability in the evaluation of mismatch repair protein immunostaining</title><title>Human pathology</title><addtitle>Hum Pathol</addtitle><description>Summary Immunohistochemical staining for mismatch repair proteins has during recent years been established as a routine analysis in many pathology laboratories with the aim to identify tumors linked to the hereditary nonpolyposis colorectal cancer syndrome. Despite widespread application, data on reliability are lacking. We therefore evaluated interobserver variability among 6 pathologists, 3 experienced gastrointestinal pathologists and 3 residents. In total, 225 immunohistochemically stained colorectal cancers were evaluated as having normal, weak, loss of, or nonevaluable mismatch repair protein staining. Full consensus was achieved in 51% of the stainings for MLH1, 61% for PMS2, 83% for MSH2, and 45% for MSH6. Weak stainings were the main cause of reduced consensus, whereas contradictory evaluations with normal as well as loss of staining were reported in 2% to 6% of the tumors. Interobserver variability was considerable, though experienced pathologists and residents reached the same level of consensus. Because results from immunohistochemical mismatch repair protein stainings are used for decisions on mutation analysis and as an aid in the interpretation of gene variants of unknown significance in hereditary nonpolyposis colorectal cancer, the interobserver variability identified highlights the need for quality assessment programs, including guidelines for classification of different expression patterns.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Adenosine Triphosphatases - genetics</subject><subject>Adenosine Triphosphatases - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Automation</subject><subject>Biological and medical sciences</subject><subject>Cancer and Oncology</subject><subject>Cancer och onkologi</subject><subject>Clinical Medicine</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - metabolism</subject><subject>DNA Mismatch Repair</subject><subject>DNA Repair Enzymes - genetics</subject><subject>DNA Repair Enzymes - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genetic counseling</subject><subject>HNPCC</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Klinisk medicin</subject><subject>Laboratories</subject><subject>Lynch Syndrome</subject><subject>Male</subject><subject>Medical and Health Sciences</subject><subject>Medical sciences</subject><subject>Medicin och hälsovetenskap</subject><subject>Middle Aged</subject><subject>Mismatch Repair Endonuclease PMS2</subject><subject>MMR</subject><subject>Mutation</subject><subject>MutL Protein Homolog 1</subject><subject>MutS Homolog 2 Protein - genetics</subject><subject>MutS Homolog 2 Protein - metabolism</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Observer Variation</subject><subject>Pathology</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Reliability</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumors</subject><subject>Young Adult</subject><issn>0046-8177</issn><issn>1532-8392</issn><issn>1532-8392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkt2L1DAUxYso7rj6JygFEZ863jRN0r4osvixMOCD7nNIMzdOZvtl0o7Mf-8t092BhcWH0BJ-5yT35CTJawZrBkx-2K93UzuYcbfOgfaArwH4k2TFBM-zklf502QFUMisZEpdJC9i3AMwJgrxPLnIQSjOVbFKbq67EUNfRwwHDOnBBG9q3_jxmPouHXeY4sE0kxl936W9S1sfWzPaXRpwMD6kQ-hHJNK37dT1cTS-893vl8kzZ5qIr5bvZXLz9cuvq-_Z5se366vPm8xKXoyZrFzpoEQncjCirpmVjivrcsFqLKSshZQSc6ecQiX4tjKCF-BAlsAsbpFfJtnJN_7FYar1EHxrwlH3xutl65b-UAtBE0viq0d5mmR7Ft0JWc54ySkr0m4e1TbTQKumNWtqAWVlweiKMaML7lCXNldaWMcAc6hZJcju_cmOzv0zYRw1RWuxaUyH_RS1EqIAIStG5NsH5L6fQke5aga8KCslVUWUOFE29DEGdPcXZKDnxui9Xhqj58Zo4JoaQ7o3i_tUt7i9V91VhIB3C2CiNY0LprM-njnOKSMxZ_vpxCE9-MFj0NF67OidfEA76m3v_3uVjw8cbEN1okNv8YjxPLWOuQb9c6733G4G1GwoSv4PP-33-g</recordid><startdate>20101001</startdate><enddate>20101001</enddate><creator>Klarskov, Louise, MD</creator><creator>Ladelund, Steen</creator><creator>Holck, Susanne, MD, PhD</creator><creator>Roenlund, Karina, MD</creator><creator>Lindebjerg, Jan, MD</creator><creator>Elebro, Jacob, MD</creator><creator>Halvarsson, Britta, MD, PhD</creator><creator>von Salomé, Jenny, MSc</creator><creator>Bernstein, Inge, MD, PhD</creator><creator>Nilbert, Mef, MD, PhD</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</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>K9.</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D95</scope></search><sort><creationdate>20101001</creationdate><title>Interobserver variability in the evaluation of mismatch repair protein immunostaining</title><author>Klarskov, Louise, MD ; Ladelund, Steen ; Holck, Susanne, MD, PhD ; Roenlund, Karina, MD ; Lindebjerg, Jan, MD ; Elebro, Jacob, MD ; Halvarsson, Britta, MD, PhD ; von Salomé, Jenny, MSc ; Bernstein, Inge, MD, PhD ; Nilbert, Mef, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c634t-69f8f08ef520a5bb1c6f37cf251be466b5666e2f7f7e753d9a5340f06801cede3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Adenosine Triphosphatases - genetics</topic><topic>Adenosine Triphosphatases - metabolism</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Automation</topic><topic>Biological and medical sciences</topic><topic>Cancer and Oncology</topic><topic>Cancer och onkologi</topic><topic>Clinical Medicine</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - metabolism</topic><topic>DNA Mismatch Repair</topic><topic>DNA Repair Enzymes - genetics</topic><topic>DNA Repair Enzymes - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genetic counseling</topic><topic>HNPCC</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Klinisk medicin</topic><topic>Laboratories</topic><topic>Lynch Syndrome</topic><topic>Male</topic><topic>Medical and Health Sciences</topic><topic>Medical sciences</topic><topic>Medicin och hälsovetenskap</topic><topic>Middle Aged</topic><topic>Mismatch Repair Endonuclease PMS2</topic><topic>MMR</topic><topic>Mutation</topic><topic>MutL Protein Homolog 1</topic><topic>MutS Homolog 2 Protein - genetics</topic><topic>MutS Homolog 2 Protein - metabolism</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Observer Variation</topic><topic>Pathology</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Reliability</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klarskov, Louise, MD</creatorcontrib><creatorcontrib>Ladelund, Steen</creatorcontrib><creatorcontrib>Holck, Susanne, MD, PhD</creatorcontrib><creatorcontrib>Roenlund, Karina, MD</creatorcontrib><creatorcontrib>Lindebjerg, Jan, MD</creatorcontrib><creatorcontrib>Elebro, Jacob, MD</creatorcontrib><creatorcontrib>Halvarsson, Britta, MD, PhD</creatorcontrib><creatorcontrib>von Salomé, Jenny, MSc</creatorcontrib><creatorcontrib>Bernstein, Inge, MD, PhD</creatorcontrib><creatorcontrib>Nilbert, Mef, MD, PhD</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Lunds universitet</collection><jtitle>Human pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klarskov, Louise, MD</au><au>Ladelund, Steen</au><au>Holck, Susanne, MD, PhD</au><au>Roenlund, Karina, MD</au><au>Lindebjerg, Jan, MD</au><au>Elebro, Jacob, MD</au><au>Halvarsson, Britta, MD, PhD</au><au>von Salomé, Jenny, MSc</au><au>Bernstein, Inge, MD, PhD</au><au>Nilbert, Mef, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interobserver variability in the evaluation of mismatch repair protein immunostaining</atitle><jtitle>Human pathology</jtitle><addtitle>Hum Pathol</addtitle><date>2010-10-01</date><risdate>2010</risdate><volume>41</volume><issue>10</issue><spage>1387</spage><epage>1396</epage><pages>1387-1396</pages><issn>0046-8177</issn><issn>1532-8392</issn><eissn>1532-8392</eissn><coden>HPCQA4</coden><abstract>Summary Immunohistochemical staining for mismatch repair proteins has during recent years been established as a routine analysis in many pathology laboratories with the aim to identify tumors linked to the hereditary nonpolyposis colorectal cancer syndrome. Despite widespread application, data on reliability are lacking. We therefore evaluated interobserver variability among 6 pathologists, 3 experienced gastrointestinal pathologists and 3 residents. In total, 225 immunohistochemically stained colorectal cancers were evaluated as having normal, weak, loss of, or nonevaluable mismatch repair protein staining. Full consensus was achieved in 51% of the stainings for MLH1, 61% for PMS2, 83% for MSH2, and 45% for MSH6. Weak stainings were the main cause of reduced consensus, whereas contradictory evaluations with normal as well as loss of staining were reported in 2% to 6% of the tumors. Interobserver variability was considerable, though experienced pathologists and residents reached the same level of consensus. Because results from immunohistochemical mismatch repair protein stainings are used for decisions on mutation analysis and as an aid in the interpretation of gene variants of unknown significance in hereditary nonpolyposis colorectal cancer, the interobserver variability identified highlights the need for quality assessment programs, including guidelines for classification of different expression patterns.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>20573374</pmid><doi>10.1016/j.humpath.2010.03.003</doi><tpages>10</tpages></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Adenosine Triphosphatases - genetics Adenosine Triphosphatases - metabolism Adult Aged Aged, 80 and over Automation Biological and medical sciences Cancer and Oncology Cancer och onkologi Clinical Medicine Colorectal cancer Colorectal Neoplasms, Hereditary Nonpolyposis - genetics Colorectal Neoplasms, Hereditary Nonpolyposis - metabolism DNA Mismatch Repair DNA Repair Enzymes - genetics DNA Repair Enzymes - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Female Gastroenterology. Liver. Pancreas. Abdomen Genetic counseling HNPCC Humans Immunohistochemistry Investigative techniques, diagnostic techniques (general aspects) Klinisk medicin Laboratories Lynch Syndrome Male Medical and Health Sciences Medical sciences Medicin och hälsovetenskap Middle Aged Mismatch Repair Endonuclease PMS2 MMR Mutation MutL Protein Homolog 1 MutS Homolog 2 Protein - genetics MutS Homolog 2 Protein - metabolism Nuclear Proteins - genetics Nuclear Proteins - metabolism Observer Variation Pathology Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Reliability Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors Young Adult |
| title | Interobserver variability in the evaluation of mismatch repair protein immunostaining |
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