Microsatellite instability in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus: a retrospective study
To analyze the loss of mismatch repair (MMR) system protein expression in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus (BE). This study retrospectively analyzed the data from 70 patients with pathohistological diagnosis of BE or esophageal adenocarcinoma (EAC) treated at the Cli...
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| Veröffentlicht in: | Croatian medical journal 2018-06, Vol.59 (3), p.100-107 |
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| creator | Pulanic, Roland Jakic-Razumovic, Jasminka Brcic, Iva Markos, Pave Brcic, Luka |
| description | To analyze the loss of mismatch repair (MMR) system protein expression in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus (BE).
This study retrospectively analyzed the data from 70 patients with pathohistological diagnosis of BE or esophageal adenocarcinoma (EAC) treated at the Clinical Department of Pathology and Cytology, University Hospital Center Zagreb, from January 2009 to January 2011. Patients were divided into three groups: BE without dysplasia (22 patients), BE with dysplasia (37 patients), and EAC (11 patients). Immunohistochemical expression of MutL homologue 1 (MLH1), MutS homologue 2 (MSH2), postmeiotic segregation increased 2 (PMS2), and MutS homologue 6 (MSH6) of DNA MMR system was measured and compared with tumor protein p53 expression.
A total of 81.8% and 81.8% patients with EAC, 32.4% and 35.1% patients with dysplasia, and 50% and 54.5% patients without dysplasia had loss of MLH1 and PMS2 expression, respectively. Patients with EAC and patients with dysplasia did not have loss of MSH2 and MSH6 expression, and 18.2% patients without dysplasia had loss of MSH2 and MSH6 expression. There was a strong positive correlation between MLH1 and PMS2 expression (Spearman ρ 0.97; P |
| doi_str_mv | 10.3325/cmj.2018.59.100 |
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This study retrospectively analyzed the data from 70 patients with pathohistological diagnosis of BE or esophageal adenocarcinoma (EAC) treated at the Clinical Department of Pathology and Cytology, University Hospital Center Zagreb, from January 2009 to January 2011. Patients were divided into three groups: BE without dysplasia (22 patients), BE with dysplasia (37 patients), and EAC (11 patients). Immunohistochemical expression of MutL homologue 1 (MLH1), MutS homologue 2 (MSH2), postmeiotic segregation increased 2 (PMS2), and MutS homologue 6 (MSH6) of DNA MMR system was measured and compared with tumor protein p53 expression.
A total of 81.8% and 81.8% patients with EAC, 32.4% and 35.1% patients with dysplasia, and 50% and 54.5% patients without dysplasia had loss of MLH1 and PMS2 expression, respectively. Patients with EAC and patients with dysplasia did not have loss of MSH2 and MSH6 expression, and 18.2% patients without dysplasia had loss of MSH2 and MSH6 expression. There was a strong positive correlation between MLH1 and PMS2 expression (Spearman ρ 0.97; P<0.001) and between MSH2 and MSH6 expression (Spearman ρ 0.90, P<0.001) in the entire sample and in all BE groups. No significant correlations of MLH1 and PMS2 with p53 expression were found, except in dysplasia group (φ 0.402, P=0.030 for MSH1; φ 0.371, P=0.042 for PMS2).
Although we demonstrated considerable loss of MLH1 and PMS2 expression in BE-associated carcinoma sequence, due to the retrospective study design and low number of patients we cannot conclude that MLH1 and PMS2 can be used as biomarkers for patient surveillance and therapy-making decisions. Oxford Centre for Evidence-based Medicine level of evidence: 3.</description><identifier>ISSN: 0353-9504</identifier><identifier>EISSN: 1332-8166</identifier><identifier>DOI: 10.3325/cmj.2018.59.100</identifier><identifier>PMID: 29972732</identifier><language>eng</language><publisher>Croatia: Sveuciliste U Zagrebu</publisher><subject>Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; Adult ; Aged ; Barrett esophagus ; Barrett Esophagus - metabolism ; Barrett Esophagus - pathology ; Biological markers ; Biomarkers, Tumor - metabolism ; Clinical Science ; DNA Mismatch Repair ; DNA-Binding Proteins - metabolism ; Esophageal Neoplasms - metabolism ; Esophageal Neoplasms - pathology ; Female ; Gene expression ; Genetic aspects ; Humans ; Immunoenzyme Techniques ; Male ; Metaplasia ; Microsatellite Instability ; Middle Aged ; Mismatch Repair Endonuclease PMS2 - metabolism ; MutL Protein Homolog 1 - metabolism ; MutS Homolog 2 Protein - metabolism ; Neoplasm Proteins - metabolism ; Retrospective Studies ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Croatian medical journal, 2018-06, Vol.59 (3), p.100-107</ispartof><rights>COPYRIGHT 2018 Sveuciliste U Zagrebu</rights><rights>Copyright © 2018 by the Croatian Medical Journal. All rights reserved. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6045894/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6045894/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29972732$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pulanic, Roland</creatorcontrib><creatorcontrib>Jakic-Razumovic, Jasminka</creatorcontrib><creatorcontrib>Brcic, Iva</creatorcontrib><creatorcontrib>Markos, Pave</creatorcontrib><creatorcontrib>Brcic, Luka</creatorcontrib><title>Microsatellite instability in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus: a retrospective study</title><title>Croatian medical journal</title><addtitle>Croat Med J</addtitle><description>To analyze the loss of mismatch repair (MMR) system protein expression in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus (BE).
This study retrospectively analyzed the data from 70 patients with pathohistological diagnosis of BE or esophageal adenocarcinoma (EAC) treated at the Clinical Department of Pathology and Cytology, University Hospital Center Zagreb, from January 2009 to January 2011. Patients were divided into three groups: BE without dysplasia (22 patients), BE with dysplasia (37 patients), and EAC (11 patients). Immunohistochemical expression of MutL homologue 1 (MLH1), MutS homologue 2 (MSH2), postmeiotic segregation increased 2 (PMS2), and MutS homologue 6 (MSH6) of DNA MMR system was measured and compared with tumor protein p53 expression.
A total of 81.8% and 81.8% patients with EAC, 32.4% and 35.1% patients with dysplasia, and 50% and 54.5% patients without dysplasia had loss of MLH1 and PMS2 expression, respectively. Patients with EAC and patients with dysplasia did not have loss of MSH2 and MSH6 expression, and 18.2% patients without dysplasia had loss of MSH2 and MSH6 expression. There was a strong positive correlation between MLH1 and PMS2 expression (Spearman ρ 0.97; P<0.001) and between MSH2 and MSH6 expression (Spearman ρ 0.90, P<0.001) in the entire sample and in all BE groups. No significant correlations of MLH1 and PMS2 with p53 expression were found, except in dysplasia group (φ 0.402, P=0.030 for MSH1; φ 0.371, P=0.042 for PMS2).
Although we demonstrated considerable loss of MLH1 and PMS2 expression in BE-associated carcinoma sequence, due to the retrospective study design and low number of patients we cannot conclude that MLH1 and PMS2 can be used as biomarkers for patient surveillance and therapy-making decisions. Oxford Centre for Evidence-based Medicine level of evidence: 3.</description><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>Adult</subject><subject>Aged</subject><subject>Barrett esophagus</subject><subject>Barrett Esophagus - metabolism</subject><subject>Barrett Esophagus - pathology</subject><subject>Biological markers</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Clinical Science</subject><subject>DNA Mismatch Repair</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Esophageal Neoplasms - metabolism</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Male</subject><subject>Metaplasia</subject><subject>Microsatellite Instability</subject><subject>Middle Aged</subject><subject>Mismatch Repair Endonuclease PMS2 - metabolism</subject><subject>MutL Protein Homolog 1 - metabolism</subject><subject>MutS Homolog 2 Protein - metabolism</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Retrospective Studies</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0353-9504</issn><issn>1332-8166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1v1DAQxS0EokvhzA1FQkJcsvV3Yg6VSsWXVMQFztbEmey6SuIQOyvtf4-jXar25PHzz288foS8ZXQrBFdXbrjfcsrqrTJbRukzsmFZL2um9XOyoUKJ0igqL8irGO8p5VRK_ZJccGMqXgm-IYef3s0hQsK-9wkLP8YEjc_1MdfFgAmmHqKHsj3GcwUtjsHB7PwYBigi_l1wdFiErvgM84wpFRjDtIfdEj8VUGQlt5jQJX_AIqalPb4mLzroI745r5fkz9cvv2-_l3e_vv24vbkrnRA6ldA4phAV143SShvVsqZzmHfCmBpdS5G2Ncim4rKRoKVymXJ103YU6qYSl-T65DstzYCtwzHN0Ntp9gPMRxvA26cno9_bXThYTaWqjcwGH88Gc8hjxmQHH13-LBgxLNFyqmVVc85YRt-f0B30aP3YhezoVtzeKGmYqrheDT88ovYIfdrH0C_JhzE-Ba9O4JpPnLF7eDWjdg3f5vDtGr5VJms033j3eNgH_n_a4h8zjq5g</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Pulanic, Roland</creator><creator>Jakic-Razumovic, Jasminka</creator><creator>Brcic, Iva</creator><creator>Markos, Pave</creator><creator>Brcic, Luka</creator><general>Sveuciliste U Zagrebu</general><general>Croatian Medical Schools</general><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180601</creationdate><title>Microsatellite instability in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus: a retrospective study</title><author>Pulanic, Roland ; Jakic-Razumovic, Jasminka ; Brcic, Iva ; Markos, Pave ; Brcic, Luka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c336t-abc15ee526b565695d1bfce6b53998ecd0e0d8a4b724b4a645c569c8bdf0a8b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>Adult</topic><topic>Aged</topic><topic>Barrett esophagus</topic><topic>Barrett Esophagus - metabolism</topic><topic>Barrett Esophagus - pathology</topic><topic>Biological markers</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Clinical Science</topic><topic>DNA Mismatch Repair</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Esophageal Neoplasms - metabolism</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Male</topic><topic>Metaplasia</topic><topic>Microsatellite Instability</topic><topic>Middle Aged</topic><topic>Mismatch Repair Endonuclease PMS2 - metabolism</topic><topic>MutL Protein Homolog 1 - metabolism</topic><topic>MutS Homolog 2 Protein - metabolism</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Retrospective Studies</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pulanic, Roland</creatorcontrib><creatorcontrib>Jakic-Razumovic, Jasminka</creatorcontrib><creatorcontrib>Brcic, Iva</creatorcontrib><creatorcontrib>Markos, Pave</creatorcontrib><creatorcontrib>Brcic, Luka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Croatian medical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pulanic, Roland</au><au>Jakic-Razumovic, Jasminka</au><au>Brcic, Iva</au><au>Markos, Pave</au><au>Brcic, Luka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microsatellite instability in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus: a retrospective study</atitle><jtitle>Croatian medical journal</jtitle><addtitle>Croat Med J</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>59</volume><issue>3</issue><spage>100</spage><epage>107</epage><pages>100-107</pages><issn>0353-9504</issn><eissn>1332-8166</eissn><abstract>To analyze the loss of mismatch repair (MMR) system protein expression in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus (BE).
This study retrospectively analyzed the data from 70 patients with pathohistological diagnosis of BE or esophageal adenocarcinoma (EAC) treated at the Clinical Department of Pathology and Cytology, University Hospital Center Zagreb, from January 2009 to January 2011. Patients were divided into three groups: BE without dysplasia (22 patients), BE with dysplasia (37 patients), and EAC (11 patients). Immunohistochemical expression of MutL homologue 1 (MLH1), MutS homologue 2 (MSH2), postmeiotic segregation increased 2 (PMS2), and MutS homologue 6 (MSH6) of DNA MMR system was measured and compared with tumor protein p53 expression.
A total of 81.8% and 81.8% patients with EAC, 32.4% and 35.1% patients with dysplasia, and 50% and 54.5% patients without dysplasia had loss of MLH1 and PMS2 expression, respectively. Patients with EAC and patients with dysplasia did not have loss of MSH2 and MSH6 expression, and 18.2% patients without dysplasia had loss of MSH2 and MSH6 expression. There was a strong positive correlation between MLH1 and PMS2 expression (Spearman ρ 0.97; P<0.001) and between MSH2 and MSH6 expression (Spearman ρ 0.90, P<0.001) in the entire sample and in all BE groups. No significant correlations of MLH1 and PMS2 with p53 expression were found, except in dysplasia group (φ 0.402, P=0.030 for MSH1; φ 0.371, P=0.042 for PMS2).
Although we demonstrated considerable loss of MLH1 and PMS2 expression in BE-associated carcinoma sequence, due to the retrospective study design and low number of patients we cannot conclude that MLH1 and PMS2 can be used as biomarkers for patient surveillance and therapy-making decisions. Oxford Centre for Evidence-based Medicine level of evidence: 3.</abstract><cop>Croatia</cop><pub>Sveuciliste U Zagrebu</pub><pmid>29972732</pmid><doi>10.3325/cmj.2018.59.100</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - metabolism Adenocarcinoma - pathology Adult Aged Barrett esophagus Barrett Esophagus - metabolism Barrett Esophagus - pathology Biological markers Biomarkers, Tumor - metabolism Clinical Science DNA Mismatch Repair DNA-Binding Proteins - metabolism Esophageal Neoplasms - metabolism Esophageal Neoplasms - pathology Female Gene expression Genetic aspects Humans Immunoenzyme Techniques Male Metaplasia Microsatellite Instability Middle Aged Mismatch Repair Endonuclease PMS2 - metabolism MutL Protein Homolog 1 - metabolism MutS Homolog 2 Protein - metabolism Neoplasm Proteins - metabolism Retrospective Studies Tumor Suppressor Protein p53 - metabolism |
| title | Microsatellite instability in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus: a retrospective study |
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