Increased estrogen receptor and epidermal growth factor receptor gene product co-expression in surgically resected gastric adenocarcinomas
Background Evidence exists that estrogens influence the action of epidermal growth factor (EGF) and its receptor (EGF‐R) at multiple levels. Estrogen and antiestrogen action on gastric and other gastrointestinal malignancies has been evaluated by several groups with conflicting results, and EGF‐R ha...
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| Veröffentlicht in: | Journal of surgical oncology 1996-11, Vol.63 (3), p.166-171 |
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| container_title | Journal of surgical oncology |
| container_volume | 63 |
| creator | Koullias, George J. Kouraklis, Gregorios P. Raftopoulos, Ioannis S. Davaris, Panagiotis S. Papadopoulos, Stefanos Ap Golematis, Basil Ch |
| description | Background
Evidence exists that estrogens influence the action of epidermal growth factor (EGF) and its receptor (EGF‐R) at multiple levels. Estrogen and antiestrogen action on gastric and other gastrointestinal malignancies has been evaluated by several groups with conflicting results, and EGF‐R has been implicated in the current growth factor‐mediated models for gastric cancer progression.
Methods
ERs and EGF‐Rs were detected immunohistochemically in a total of 53 advanced gastric carcinomas using monoclonal antibodies (mAbs) to human ERs and EGF‐Rs.
Results
ERs were expressed in 30 (56%) and EGF‐Rs in 20 (38%) of the gastric tumors. ER(+) gastric tumors were closely associated with the intestinal type (P < 0.01), whereas EGF‐R(+) tumors were significantly correlated with poor differentiation status and ER(+) expression (P < 0.01). Of EGF‐R(+) tumors, 85% were also ER(+). EGF‐R and ER co‐expression was demonstrated in 17 tumors (32% of the group). These cases were significantly corelated with poor differentiation and large tumor size upon resection (P < 0.05).
Conclusions
ER and EGF‐R co‐expression indicates that a functional interaction between estrogens and EGF may exist in gastric cancer and that when such an interaction becomes operative, it may lead to dedifferentiation and increased tumor growth. © 1996 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/(SICI)1096-9098(199611)63:3<166::AID-JSO6>3.0.CO;2-B |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78579066</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>754880130</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4596-81e8e7b7dad48c822c00cb15e0566f6a36eded202ce91803585866fb24284f1a3</originalsourceid><addsrcrecordid>eNqFkcGO0zAQhiMEWsrCIyDlgGD3kDKOE8cpK6RtCktRRZFaxHHkOpNiSJNip9rtK_DUOLQqBxCcrPH88_v3fEFwxWDIAOKXF4tpMb1kkIsoh1xesDwXjF0KPuJXTIjR6Ho6id4v5uI1H8KwmL-Ko_G9YHAauB8MvE0cJVkOD4NHzn0FAO-RnAVnMk8SEDAIfkwbbUk5KkNynW3X1ISWNG271oaq8bdbU5LdqDpc2_a2-xJWSve9k8hPULi1bbnTXajbiO62lpwzbROaJnQ7uzZa1fXeTzjSnX9orfxLRoeqpKbVymrTtBvlHgcPKlU7enI8z4NPb98si3fRbH4zLa5nkU5S_zXJSFK2ykpVJlLLONYAesVSglSISiguqKQyhlhTziTwVKbSN1ZxEsukYoqfB88Pvj70953_NW6M01TXqqF25zCTqd-YEF744t_CNJESGAevXB6U2rbOWapwa81G2T0ywB4mYg8TezbYs8EDTBQcOXqYiB4m9jB9DVjMMcaxt316DLBbbag8mR7p-f6zY185v-PKqkYbd5LFKWQJZ7_T3Zqa9n9E-0-yvwT7VXvb6GBrXEd3J1tlv6HIeJbi5w83-JFP5GwxnuCS_wRjrNiO</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>754880130</pqid></control><display><type>article</type><title>Increased estrogen receptor and epidermal growth factor receptor gene product co-expression in surgically resected gastric adenocarcinomas</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Koullias, George J. ; Kouraklis, Gregorios P. ; Raftopoulos, Ioannis S. ; Davaris, Panagiotis S. ; Papadopoulos, Stefanos Ap ; Golematis, Basil Ch</creator><creatorcontrib>Koullias, George J. ; Kouraklis, Gregorios P. ; Raftopoulos, Ioannis S. ; Davaris, Panagiotis S. ; Papadopoulos, Stefanos Ap ; Golematis, Basil Ch</creatorcontrib><description>Background
Evidence exists that estrogens influence the action of epidermal growth factor (EGF) and its receptor (EGF‐R) at multiple levels. Estrogen and antiestrogen action on gastric and other gastrointestinal malignancies has been evaluated by several groups with conflicting results, and EGF‐R has been implicated in the current growth factor‐mediated models for gastric cancer progression.
Methods
ERs and EGF‐Rs were detected immunohistochemically in a total of 53 advanced gastric carcinomas using monoclonal antibodies (mAbs) to human ERs and EGF‐Rs.
Results
ERs were expressed in 30 (56%) and EGF‐Rs in 20 (38%) of the gastric tumors. ER(+) gastric tumors were closely associated with the intestinal type (P < 0.01), whereas EGF‐R(+) tumors were significantly correlated with poor differentiation status and ER(+) expression (P < 0.01). Of EGF‐R(+) tumors, 85% were also ER(+). EGF‐R and ER co‐expression was demonstrated in 17 tumors (32% of the group). These cases were significantly corelated with poor differentiation and large tumor size upon resection (P < 0.05).
Conclusions
ER and EGF‐R co‐expression indicates that a functional interaction between estrogens and EGF may exist in gastric cancer and that when such an interaction becomes operative, it may lead to dedifferentiation and increased tumor growth. © 1996 Wiley‐Liss, Inc.</description><identifier>ISSN: 0022-4790</identifier><identifier>EISSN: 1096-9098</identifier><identifier>DOI: 10.1002/(SICI)1096-9098(199611)63:3<166::AID-JSO6>3.0.CO;2-B</identifier><identifier>PMID: 8944060</identifier><identifier>CODEN: JSONAU</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adenocarcinoma - chemistry ; Adenocarcinoma - surgery ; Adult ; Aged ; Antibodies, Monoclonal ; autocrine ; Biological and medical sciences ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; growth factors ; Humans ; Immunohistochemistry ; Male ; Medical sciences ; Middle Aged ; Receptor, Epidermal Growth Factor - analysis ; Receptor, Epidermal Growth Factor - immunology ; Receptors, Estrogen - analysis ; Receptors, Estrogen - immunology ; steroid receptors ; stomach ; Stomach Neoplasms - chemistry ; Stomach Neoplasms - surgery ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors ; Up-Regulation</subject><ispartof>Journal of surgical oncology, 1996-11, Vol.63 (3), p.166-171</ispartof><rights>Copyright © 1996 Wiley‐Liss, Inc.</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4596-81e8e7b7dad48c822c00cb15e0566f6a36eded202ce91803585866fb24284f1a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291096-9098%28199611%2963%3A3%3C166%3A%3AAID-JSO6%3E3.0.CO%3B2-B$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291096-9098%28199611%2963%3A3%3C166%3A%3AAID-JSO6%3E3.0.CO%3B2-B$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2507431$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8944060$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koullias, George J.</creatorcontrib><creatorcontrib>Kouraklis, Gregorios P.</creatorcontrib><creatorcontrib>Raftopoulos, Ioannis S.</creatorcontrib><creatorcontrib>Davaris, Panagiotis S.</creatorcontrib><creatorcontrib>Papadopoulos, Stefanos Ap</creatorcontrib><creatorcontrib>Golematis, Basil Ch</creatorcontrib><title>Increased estrogen receptor and epidermal growth factor receptor gene product co-expression in surgically resected gastric adenocarcinomas</title><title>Journal of surgical oncology</title><addtitle>J. Surg. Oncol</addtitle><description>Background
Evidence exists that estrogens influence the action of epidermal growth factor (EGF) and its receptor (EGF‐R) at multiple levels. Estrogen and antiestrogen action on gastric and other gastrointestinal malignancies has been evaluated by several groups with conflicting results, and EGF‐R has been implicated in the current growth factor‐mediated models for gastric cancer progression.
Methods
ERs and EGF‐Rs were detected immunohistochemically in a total of 53 advanced gastric carcinomas using monoclonal antibodies (mAbs) to human ERs and EGF‐Rs.
Results
ERs were expressed in 30 (56%) and EGF‐Rs in 20 (38%) of the gastric tumors. ER(+) gastric tumors were closely associated with the intestinal type (P < 0.01), whereas EGF‐R(+) tumors were significantly correlated with poor differentiation status and ER(+) expression (P < 0.01). Of EGF‐R(+) tumors, 85% were also ER(+). EGF‐R and ER co‐expression was demonstrated in 17 tumors (32% of the group). These cases were significantly corelated with poor differentiation and large tumor size upon resection (P < 0.05).
Conclusions
ER and EGF‐R co‐expression indicates that a functional interaction between estrogens and EGF may exist in gastric cancer and that when such an interaction becomes operative, it may lead to dedifferentiation and increased tumor growth. © 1996 Wiley‐Liss, Inc.</description><subject>Adenocarcinoma - chemistry</subject><subject>Adenocarcinoma - surgery</subject><subject>Adult</subject><subject>Aged</subject><subject>Antibodies, Monoclonal</subject><subject>autocrine</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>growth factors</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Receptor, Epidermal Growth Factor - analysis</subject><subject>Receptor, Epidermal Growth Factor - immunology</subject><subject>Receptors, Estrogen - analysis</subject><subject>Receptors, Estrogen - immunology</subject><subject>steroid receptors</subject><subject>stomach</subject><subject>Stomach Neoplasms - chemistry</subject><subject>Stomach Neoplasms - surgery</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>0022-4790</issn><issn>1096-9098</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcGO0zAQhiMEWsrCIyDlgGD3kDKOE8cpK6RtCktRRZFaxHHkOpNiSJNip9rtK_DUOLQqBxCcrPH88_v3fEFwxWDIAOKXF4tpMb1kkIsoh1xesDwXjF0KPuJXTIjR6Ho6id4v5uI1H8KwmL-Ko_G9YHAauB8MvE0cJVkOD4NHzn0FAO-RnAVnMk8SEDAIfkwbbUk5KkNynW3X1ISWNG271oaq8bdbU5LdqDpc2_a2-xJWSve9k8hPULi1bbnTXajbiO62lpwzbROaJnQ7uzZa1fXeTzjSnX9orfxLRoeqpKbVymrTtBvlHgcPKlU7enI8z4NPb98si3fRbH4zLa5nkU5S_zXJSFK2ykpVJlLLONYAesVSglSISiguqKQyhlhTziTwVKbSN1ZxEsukYoqfB88Pvj70953_NW6M01TXqqF25zCTqd-YEF744t_CNJESGAevXB6U2rbOWapwa81G2T0ywB4mYg8TezbYs8EDTBQcOXqYiB4m9jB9DVjMMcaxt316DLBbbag8mR7p-f6zY185v-PKqkYbd5LFKWQJZ7_T3Zqa9n9E-0-yvwT7VXvb6GBrXEd3J1tlv6HIeJbi5w83-JFP5GwxnuCS_wRjrNiO</recordid><startdate>199611</startdate><enddate>199611</enddate><creator>Koullias, George J.</creator><creator>Kouraklis, Gregorios P.</creator><creator>Raftopoulos, Ioannis S.</creator><creator>Davaris, Panagiotis S.</creator><creator>Papadopoulos, Stefanos Ap</creator><creator>Golematis, Basil Ch</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><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>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>199611</creationdate><title>Increased estrogen receptor and epidermal growth factor receptor gene product co-expression in surgically resected gastric adenocarcinomas</title><author>Koullias, George J. ; Kouraklis, Gregorios P. ; Raftopoulos, Ioannis S. ; Davaris, Panagiotis S. ; Papadopoulos, Stefanos Ap ; Golematis, Basil Ch</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4596-81e8e7b7dad48c822c00cb15e0566f6a36eded202ce91803585866fb24284f1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adenocarcinoma - chemistry</topic><topic>Adenocarcinoma - surgery</topic><topic>Adult</topic><topic>Aged</topic><topic>Antibodies, Monoclonal</topic><topic>autocrine</topic><topic>Biological and medical sciences</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>growth factors</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Receptor, Epidermal Growth Factor - analysis</topic><topic>Receptor, Epidermal Growth Factor - immunology</topic><topic>Receptors, Estrogen - analysis</topic><topic>Receptors, Estrogen - immunology</topic><topic>steroid receptors</topic><topic>stomach</topic><topic>Stomach Neoplasms - chemistry</topic><topic>Stomach Neoplasms - surgery</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koullias, George J.</creatorcontrib><creatorcontrib>Kouraklis, Gregorios P.</creatorcontrib><creatorcontrib>Raftopoulos, Ioannis S.</creatorcontrib><creatorcontrib>Davaris, Panagiotis S.</creatorcontrib><creatorcontrib>Papadopoulos, Stefanos Ap</creatorcontrib><creatorcontrib>Golematis, Basil Ch</creatorcontrib><collection>Istex</collection><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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koullias, George J.</au><au>Kouraklis, Gregorios P.</au><au>Raftopoulos, Ioannis S.</au><au>Davaris, Panagiotis S.</au><au>Papadopoulos, Stefanos Ap</au><au>Golematis, Basil Ch</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased estrogen receptor and epidermal growth factor receptor gene product co-expression in surgically resected gastric adenocarcinomas</atitle><jtitle>Journal of surgical oncology</jtitle><addtitle>J. Surg. Oncol</addtitle><date>1996-11</date><risdate>1996</risdate><volume>63</volume><issue>3</issue><spage>166</spage><epage>171</epage><pages>166-171</pages><issn>0022-4790</issn><eissn>1096-9098</eissn><coden>JSONAU</coden><abstract>Background
Evidence exists that estrogens influence the action of epidermal growth factor (EGF) and its receptor (EGF‐R) at multiple levels. Estrogen and antiestrogen action on gastric and other gastrointestinal malignancies has been evaluated by several groups with conflicting results, and EGF‐R has been implicated in the current growth factor‐mediated models for gastric cancer progression.
Methods
ERs and EGF‐Rs were detected immunohistochemically in a total of 53 advanced gastric carcinomas using monoclonal antibodies (mAbs) to human ERs and EGF‐Rs.
Results
ERs were expressed in 30 (56%) and EGF‐Rs in 20 (38%) of the gastric tumors. ER(+) gastric tumors were closely associated with the intestinal type (P < 0.01), whereas EGF‐R(+) tumors were significantly correlated with poor differentiation status and ER(+) expression (P < 0.01). Of EGF‐R(+) tumors, 85% were also ER(+). EGF‐R and ER co‐expression was demonstrated in 17 tumors (32% of the group). These cases were significantly corelated with poor differentiation and large tumor size upon resection (P < 0.05).
Conclusions
ER and EGF‐R co‐expression indicates that a functional interaction between estrogens and EGF may exist in gastric cancer and that when such an interaction becomes operative, it may lead to dedifferentiation and increased tumor growth. © 1996 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8944060</pmid><doi>10.1002/(SICI)1096-9098(199611)63:3<166::AID-JSO6>3.0.CO;2-B</doi><tpages>6</tpages></addata></record> |
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| ispartof | Journal of surgical oncology, 1996-11, Vol.63 (3), p.166-171 |
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| source | MEDLINE; Access via Wiley Online Library |
| subjects | Adenocarcinoma - chemistry Adenocarcinoma - surgery Adult Aged Antibodies, Monoclonal autocrine Biological and medical sciences Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic growth factors Humans Immunohistochemistry Male Medical sciences Middle Aged Receptor, Epidermal Growth Factor - analysis Receptor, Epidermal Growth Factor - immunology Receptors, Estrogen - analysis Receptors, Estrogen - immunology steroid receptors stomach Stomach Neoplasms - chemistry Stomach Neoplasms - surgery Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors Up-Regulation |
| title | Increased estrogen receptor and epidermal growth factor receptor gene product co-expression in surgically resected gastric adenocarcinomas |
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