HER3 Expression Is a Marker of Tumor Progression in Premalignant Lesions of the Gastroesophageal Junction
Overexpression of receptor tyrosine kinases (RTK), including members of the HER family, has prognostic and therapeutic significance in invasive esophagogastric carcinoma. RTK expression in premalignant gastroesophageal lesions has not been extensively explored. Formalin-fixed paraffin-embedded tissu...
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| description | Overexpression of receptor tyrosine kinases (RTK), including members of the HER family, has prognostic and therapeutic significance in invasive esophagogastric carcinoma. RTK expression in premalignant gastroesophageal lesions has not been extensively explored. Formalin-fixed paraffin-embedded tissue samples of esophageal biopsy specimens from 73 patients with Barrett's esophagus with either low-grade dysplasia (LGD) (n = 32) or high-grade dysplasia (HGD) (n = 59) were analyzed for HER1, HER2, HER3 and CMET expression by immunohistochemistry (IHC). Immunophenotype was correlated with histologic and clinical features. High-grade dysplasia (HGD) was associated with overexpression of HER1 (20.7% vs. 3.1%, p = 0.023), HER2 (5.3% vs. 0.0%, p = 0.187) and HER3 (47.4% vs. 9.4%, p |
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RTK expression in premalignant gastroesophageal lesions has not been extensively explored. Formalin-fixed paraffin-embedded tissue samples of esophageal biopsy specimens from 73 patients with Barrett's esophagus with either low-grade dysplasia (LGD) (n = 32) or high-grade dysplasia (HGD) (n = 59) were analyzed for HER1, HER2, HER3 and CMET expression by immunohistochemistry (IHC). Immunophenotype was correlated with histologic and clinical features. High-grade dysplasia (HGD) was associated with overexpression of HER1 (20.7% vs. 3.1%, p = 0.023), HER2 (5.3% vs. 0.0%, p = 0.187) and HER3 (47.4% vs. 9.4%, p<0.001) compared to low-grade dysplasia (LGD). There was a significant association of HER2 (20.0% vs. 2.1%, p = 0.022) and HER3 (80.0% vs. 40.4%, p = 0.023) overexpression in HGD lesions associated with foci of invasive carcinoma compared to those without invasive foci. Overexpression of CMET was observed in 42.9% of specimens, was increasingly observed with HGD compared to LGD (58.3% vs. 36.7%, p = 0.200), and was most often co-expressed with HER3 (62.5% of HER3-positive specimens vs. 38.2% of HER3-negative specimens, p = 0.212). In summary, HER3 is frequently overexpressed in high-grade dysplastic lesions of the gastroesophageal junction and may be a marker of invasive progression. These data provide rationale for targeting HER2 and HER3 pathways in an early disease setting to prevent disease progression.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0161781</identifier><identifier>PMID: 27559738</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Aged ; Alcohol ; Barrett Esophagus - metabolism ; Barrett Esophagus - pathology ; Biology and Life Sciences ; Biomarkers ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Biopsy ; Breast cancer ; Carcinoma - metabolism ; Carcinoma - pathology ; Chemotherapy ; Cloning ; Dendritic cells ; Dysplasia ; Endoscopy ; ErbB-2 protein ; Esophageal cancer ; Esophageal Neoplasms - metabolism ; Esophageal Neoplasms - pathology ; Esophagogastric junction ; Esophagogastric Junction - metabolism ; Esophagogastric Junction - pathology ; Esophagus ; Female ; Genetic aspects ; Growth factors ; Humans ; Immunohistochemistry ; Invasiveness ; Kinases ; Laboratories ; Lesions ; Male ; Medicine and Health Sciences ; Middle Aged ; Paraffin ; Pathology ; Patients ; Physiological aspects ; Protein kinases ; Receptor, ErbB-2 - genetics ; Receptor, ErbB-2 - metabolism ; Receptor, ErbB-3 - genetics ; Receptor, ErbB-3 - metabolism ; Research and Analysis Methods ; Surgery ; Surveillance ; Tyrosine</subject><ispartof>PloS one, 2016-08, Vol.11 (8), p.e0161781-e0161781</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Ecker et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Ecker et al 2016 Ecker et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-e97c4ea4a4b783fc0b7a273c82f189b3634ce1087f2e2b4f96a26dd0abbe6a2b3</citedby><cites>FETCH-LOGICAL-c725t-e97c4ea4a4b783fc0b7a273c82f189b3634ce1087f2e2b4f96a26dd0abbe6a2b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4999185/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4999185/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27559738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Mukaisho, Ken-ichi</contributor><creatorcontrib>Ecker, Brett L</creatorcontrib><creatorcontrib>Taylor, Laura</creatorcontrib><creatorcontrib>Zhang, Paul J</creatorcontrib><creatorcontrib>Furth, Emma E</creatorcontrib><creatorcontrib>Ginsberg, Gregory G</creatorcontrib><creatorcontrib>McMillan, Matthew T</creatorcontrib><creatorcontrib>Datta, Jashodeep</creatorcontrib><creatorcontrib>Czerniecki, Brian J</creatorcontrib><creatorcontrib>Roses, Robert E</creatorcontrib><title>HER3 Expression Is a Marker of Tumor Progression in Premalignant Lesions of the Gastroesophageal Junction</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Overexpression of receptor tyrosine kinases (RTK), including members of the HER family, has prognostic and therapeutic significance in invasive esophagogastric carcinoma. RTK expression in premalignant gastroesophageal lesions has not been extensively explored. Formalin-fixed paraffin-embedded tissue samples of esophageal biopsy specimens from 73 patients with Barrett's esophagus with either low-grade dysplasia (LGD) (n = 32) or high-grade dysplasia (HGD) (n = 59) were analyzed for HER1, HER2, HER3 and CMET expression by immunohistochemistry (IHC). Immunophenotype was correlated with histologic and clinical features. High-grade dysplasia (HGD) was associated with overexpression of HER1 (20.7% vs. 3.1%, p = 0.023), HER2 (5.3% vs. 0.0%, p = 0.187) and HER3 (47.4% vs. 9.4%, p<0.001) compared to low-grade dysplasia (LGD). There was a significant association of HER2 (20.0% vs. 2.1%, p = 0.022) and HER3 (80.0% vs. 40.4%, p = 0.023) overexpression in HGD lesions associated with foci of invasive carcinoma compared to those without invasive foci. Overexpression of CMET was observed in 42.9% of specimens, was increasingly observed with HGD compared to LGD (58.3% vs. 36.7%, p = 0.200), and was most often co-expressed with HER3 (62.5% of HER3-positive specimens vs. 38.2% of HER3-negative specimens, p = 0.212). In summary, HER3 is frequently overexpressed in high-grade dysplastic lesions of the gastroesophageal junction and may be a marker of invasive progression. These data provide rationale for targeting HER2 and HER3 pathways in an early disease setting to prevent disease progression.</description><subject>Aged</subject><subject>Alcohol</subject><subject>Barrett Esophagus - metabolism</subject><subject>Barrett Esophagus - pathology</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Biopsy</subject><subject>Breast cancer</subject><subject>Carcinoma - metabolism</subject><subject>Carcinoma - pathology</subject><subject>Chemotherapy</subject><subject>Cloning</subject><subject>Dendritic cells</subject><subject>Dysplasia</subject><subject>Endoscopy</subject><subject>ErbB-2 protein</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - metabolism</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophagogastric junction</subject><subject>Esophagogastric Junction - metabolism</subject><subject>Esophagogastric Junction - pathology</subject><subject>Esophagus</subject><subject>Female</subject><subject>Genetic aspects</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Invasiveness</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lesions</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Middle Aged</subject><subject>Paraffin</subject><subject>Pathology</subject><subject>Patients</subject><subject>Physiological aspects</subject><subject>Protein kinases</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Receptor, ErbB-3 - genetics</subject><subject>Receptor, ErbB-3 - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Surgery</subject><subject>Surveillance</subject><subject>Tyrosine</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBEQkJw0RJ_JLZvJk1T2YqKhsbg1jpxnNQjiYudoPHvcdp0atAuZl_YOX7OG_t8RNFrlMwRYejTre1dC_V8Y1s9T1CGGEdPomMkCJ5lOCFPD_ZH0Qvvb5MkJTzLnkdHmKWpYIQfR-ZycU3ixd3Gae-NbeOljyH-Cu6XdrEt45u-sS7-5my1B0wbPnUDtalaaLt4pQezH-BureML8J2z2tvNGioNdfylb1UXiJfRsxJqr1-N60n04_Pi5vxytrq6WJ6frWaK4bSbacEU1UCB5oyTUiU5A8yI4rhEXOQkI1RplHBWYo1zWooMcFYUCeS5DtucnERvd7qb2no5RslLxBFFaYZTHIjljigs3MqNMw24v9KCkVuDdZUE1xlVa0lEUVCkUcpSTgkUoEpMiSCEJyEHaNA6Hf_W540ulG47B_VEdHrSmrWs7B9JhRCIp0Hgwyjg7O9e-042xitd19Bq22_vLRBljPPHoDTjOIyAvvsPfTgQI1VBeKtpSxuuqAZReUaz8GhBt9T8ASrMQjdGheorTbBPHD5OHALT6buugt57ufx-_Xj26ueUfX_ArkNxdWtv636oLj8F6Q5UznrvdHmfD5TIoXn20ZBD88ixeYLbm8Nc3jvtu4X8A26uE3s</recordid><startdate>20160825</startdate><enddate>20160825</enddate><creator>Ecker, Brett L</creator><creator>Taylor, Laura</creator><creator>Zhang, Paul J</creator><creator>Furth, Emma E</creator><creator>Ginsberg, Gregory G</creator><creator>McMillan, Matthew T</creator><creator>Datta, Jashodeep</creator><creator>Czerniecki, Brian J</creator><creator>Roses, Robert E</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160825</creationdate><title>HER3 Expression Is a Marker of Tumor Progression in Premalignant Lesions of the Gastroesophageal Junction</title><author>Ecker, Brett L ; Taylor, Laura ; Zhang, Paul J ; Furth, Emma E ; Ginsberg, Gregory G ; McMillan, Matthew T ; Datta, Jashodeep ; Czerniecki, Brian J ; Roses, Robert E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-e97c4ea4a4b783fc0b7a273c82f189b3634ce1087f2e2b4f96a26dd0abbe6a2b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Alcohol</topic><topic>Barrett Esophagus - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ecker, Brett L</au><au>Taylor, Laura</au><au>Zhang, Paul J</au><au>Furth, Emma E</au><au>Ginsberg, Gregory G</au><au>McMillan, Matthew T</au><au>Datta, Jashodeep</au><au>Czerniecki, Brian J</au><au>Roses, Robert E</au><au>Mukaisho, Ken-ichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HER3 Expression Is a Marker of Tumor Progression in Premalignant Lesions of the Gastroesophageal Junction</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-08-25</date><risdate>2016</risdate><volume>11</volume><issue>8</issue><spage>e0161781</spage><epage>e0161781</epage><pages>e0161781-e0161781</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Overexpression of receptor tyrosine kinases (RTK), including members of the HER family, has prognostic and therapeutic significance in invasive esophagogastric carcinoma. RTK expression in premalignant gastroesophageal lesions has not been extensively explored. Formalin-fixed paraffin-embedded tissue samples of esophageal biopsy specimens from 73 patients with Barrett's esophagus with either low-grade dysplasia (LGD) (n = 32) or high-grade dysplasia (HGD) (n = 59) were analyzed for HER1, HER2, HER3 and CMET expression by immunohistochemistry (IHC). Immunophenotype was correlated with histologic and clinical features. High-grade dysplasia (HGD) was associated with overexpression of HER1 (20.7% vs. 3.1%, p = 0.023), HER2 (5.3% vs. 0.0%, p = 0.187) and HER3 (47.4% vs. 9.4%, p<0.001) compared to low-grade dysplasia (LGD). There was a significant association of HER2 (20.0% vs. 2.1%, p = 0.022) and HER3 (80.0% vs. 40.4%, p = 0.023) overexpression in HGD lesions associated with foci of invasive carcinoma compared to those without invasive foci. Overexpression of CMET was observed in 42.9% of specimens, was increasingly observed with HGD compared to LGD (58.3% vs. 36.7%, p = 0.200), and was most often co-expressed with HER3 (62.5% of HER3-positive specimens vs. 38.2% of HER3-negative specimens, p = 0.212). In summary, HER3 is frequently overexpressed in high-grade dysplastic lesions of the gastroesophageal junction and may be a marker of invasive progression. These data provide rationale for targeting HER2 and HER3 pathways in an early disease setting to prevent disease progression.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27559738</pmid><doi>10.1371/journal.pone.0161781</doi><tpages>e0161781</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1814156252 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Aged Alcohol Barrett Esophagus - metabolism Barrett Esophagus - pathology Biology and Life Sciences Biomarkers Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Biopsy Breast cancer Carcinoma - metabolism Carcinoma - pathology Chemotherapy Cloning Dendritic cells Dysplasia Endoscopy ErbB-2 protein Esophageal cancer Esophageal Neoplasms - metabolism Esophageal Neoplasms - pathology Esophagogastric junction Esophagogastric Junction - metabolism Esophagogastric Junction - pathology Esophagus Female Genetic aspects Growth factors Humans Immunohistochemistry Invasiveness Kinases Laboratories Lesions Male Medicine and Health Sciences Middle Aged Paraffin Pathology Patients Physiological aspects Protein kinases Receptor, ErbB-2 - genetics Receptor, ErbB-2 - metabolism Receptor, ErbB-3 - genetics Receptor, ErbB-3 - metabolism Research and Analysis Methods Surgery Surveillance Tyrosine |
| title | HER3 Expression Is a Marker of Tumor Progression in Premalignant Lesions of the Gastroesophageal Junction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-16T03%3A36%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=HER3%20Expression%20Is%20a%20Marker%20of%20Tumor%20Progression%20in%20Premalignant%20Lesions%20of%20the%20Gastroesophageal%20Junction&rft.jtitle=PloS%20one&rft.au=Ecker,%20Brett%20L&rft.date=2016-08-25&rft.volume=11&rft.issue=8&rft.spage=e0161781&rft.epage=e0161781&rft.pages=e0161781-e0161781&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0161781&rft_dat=%3Cgale_plos_%3EA461579452%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1814156252&rft_id=info:pmid/27559738&rft_galeid=A461579452&rft_doaj_id=oai_doaj_org_article_39dd41e1575843adacf2439338037112&rfr_iscdi=true |