Loss of p16/CDKN2A tumor suppressor protein in gastric adenocarcinoma is associated with epstein-barr virus and anatomic location in the body of the stomach
Gastric adenocarcinomas (n = 125) were analyzed by immunohistochemistry for the presence of p16, the CDKN2A gene product. This protein was lost in 31 of 125 cases (25%), and loss was associated with location of the tumor in the body of the stomach ( P = .001). Loss of p16 was also associated with th...
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| Veröffentlicht in: | Human pathology 2000, Vol.31 (1), p.45-50 |
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| creator | Schneider, Barbara G. Gulley, Margaret L. Eagan, Phyllis Bravo, Juan Carlos Mera, Robertino Geradts, Joseph |
| description | Gastric adenocarcinomas (n = 125) were analyzed by immunohistochemistry for the presence of p16, the CDKN2A gene product. This protein was lost in 31 of 125 cases (25%), and loss was associated with location of the tumor in the body of the stomach (
P = .001). Loss of p16 was also associated with the presence of Epstein-Barr virus (EBV) in tumor cells as determined by in situ hybridization (
P = .022). This effect may relate to anatomic site, because EBV-associated tumors originate more frequently in the body of the stomach. When p16 status was evaluated for ethnic origin of the patient (non-Hispanic white, Hispanic, or black), a strong trend (
P = .057) was found for African-American patients to have fewer p16-negative tumors than other patients. This also may relate to anatomic location, because fewer tumors from black patients arose in the body of the stomach (
P = .022). No significant associations were detected between p16 status and histological subtype (intestinal
v diffuse), the presence of microsatellite instability, grade or stage of the tumor, or age, gender, or survival of the patient. In conclusion, p16 loss is quite common in gastric adenocarcinoma, and such loss is more common in EBV-infected tumors arising in the body of the stomach. |
| doi_str_mv | 10.1016/S0046-8177(00)80197-5 |
| format | Article |
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P = .001). Loss of p16 was also associated with the presence of Epstein-Barr virus (EBV) in tumor cells as determined by in situ hybridization (
P = .022). This effect may relate to anatomic site, because EBV-associated tumors originate more frequently in the body of the stomach. When p16 status was evaluated for ethnic origin of the patient (non-Hispanic white, Hispanic, or black), a strong trend (
P = .057) was found for African-American patients to have fewer p16-negative tumors than other patients. This also may relate to anatomic location, because fewer tumors from black patients arose in the body of the stomach (
P = .022). No significant associations were detected between p16 status and histological subtype (intestinal
v diffuse), the presence of microsatellite instability, grade or stage of the tumor, or age, gender, or survival of the patient. In conclusion, p16 loss is quite common in gastric adenocarcinoma, and such loss is more common in EBV-infected tumors arising in the body of the stomach.</description><identifier>ISSN: 0046-8177</identifier><identifier>EISSN: 1532-8392</identifier><identifier>DOI: 10.1016/S0046-8177(00)80197-5</identifier><identifier>PMID: 10665912</identifier><identifier>CODEN: HPCQA4</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; Adenocarcinoma - virology ; African American ; Biological and medical sciences ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; ethnicity ; Gastroenterology. Liver. Pancreas. Abdomen ; Herpesvirus 4, Human - isolation & purification ; Hispanic ; Humans ; Immunohistochemistry ; In Situ Hybridization ; Medical sciences ; microsatellite instability ; RNA, Viral - metabolism ; Stomach - pathology ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Stomach Neoplasms - virology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors</subject><ispartof>Human pathology, 2000, Vol.31 (1), p.45-50</ispartof><rights>2000 W.B. Saunders Company. All rights reserved</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-c2d9f30426077c56508141ad93048393092347bab93b8d2b2a40ad9cdb7ff0133</citedby><cites>FETCH-LOGICAL-c390t-c2d9f30426077c56508141ad93048393092347bab93b8d2b2a40ad9cdb7ff0133</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0046-8177(00)80197-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,4012,27910,27911,27912,45982</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1250393$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10665912$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schneider, Barbara G.</creatorcontrib><creatorcontrib>Gulley, Margaret L.</creatorcontrib><creatorcontrib>Eagan, Phyllis</creatorcontrib><creatorcontrib>Bravo, Juan Carlos</creatorcontrib><creatorcontrib>Mera, Robertino</creatorcontrib><creatorcontrib>Geradts, Joseph</creatorcontrib><title>Loss of p16/CDKN2A tumor suppressor protein in gastric adenocarcinoma is associated with epstein-barr virus and anatomic location in the body of the stomach</title><title>Human pathology</title><addtitle>Hum Pathol</addtitle><description>Gastric adenocarcinomas (n = 125) were analyzed by immunohistochemistry for the presence of p16, the CDKN2A gene product. This protein was lost in 31 of 125 cases (25%), and loss was associated with location of the tumor in the body of the stomach (
P = .001). Loss of p16 was also associated with the presence of Epstein-Barr virus (EBV) in tumor cells as determined by in situ hybridization (
P = .022). This effect may relate to anatomic site, because EBV-associated tumors originate more frequently in the body of the stomach. When p16 status was evaluated for ethnic origin of the patient (non-Hispanic white, Hispanic, or black), a strong trend (
P = .057) was found for African-American patients to have fewer p16-negative tumors than other patients. This also may relate to anatomic location, because fewer tumors from black patients arose in the body of the stomach (
P = .022). No significant associations were detected between p16 status and histological subtype (intestinal
v diffuse), the presence of microsatellite instability, grade or stage of the tumor, or age, gender, or survival of the patient. In conclusion, p16 loss is quite common in gastric adenocarcinoma, and such loss is more common in EBV-infected tumors arising in the body of the stomach.</description><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>Adenocarcinoma - virology</subject><subject>African American</subject><subject>Biological and medical sciences</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>ethnicity</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Herpesvirus 4, Human - isolation & purification</subject><subject>Hispanic</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization</subject><subject>Medical sciences</subject><subject>microsatellite instability</subject><subject>RNA, Viral - metabolism</subject><subject>Stomach - pathology</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Stomach Neoplasms - virology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumors</subject><issn>0046-8177</issn><issn>1532-8392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxi0EokvhEUA-IASHwNiJk_iEquVPq67gAJwtx3ZYoyQOtlPUd-FhmeyuCjckWx7Zv288Mx8hTxm8ZsDqN18AqrpoWdO8BHjVApNNIe6RDRMlL9pS8vtkc4eckUcp_QBgTFTiITljUNdCMr4hv3chJRp6OmPO7bvrT_yC5mUMkaZlnqNLCcM5huz8RHF91ylHb6i2bgpGR-OnMGrqE9WIGq-zs_SXz3vq5rSKik7HSG98XBCZLG6dw4gZBpRnHw5Z897RLtjbtZA1Tohos39MHvR6SO7J6Twn3z68_7q9LHafP15tL3aFKSXkwnAr-xIqXkPTGFELaFnFtJV4h5MoQfKyajrdybJrLe-4rgBfje2avgdWlufkxTEvNvpzcSmr0SfjhkFPLixJNdC2jWQSQXEETcSxRderOfpRx1vFQK22qIMtap25AlAHW5RA3bPTB0s3OvuP6ugDAs9PgE5GD33Uk_HpL8cFYCOIvT1iDqdx411UyXg3GWd9dCYrG_x_KvkDbGWqtw</recordid><startdate>2000</startdate><enddate>2000</enddate><creator>Schneider, Barbara G.</creator><creator>Gulley, Margaret L.</creator><creator>Eagan, Phyllis</creator><creator>Bravo, Juan Carlos</creator><creator>Mera, Robertino</creator><creator>Geradts, Joseph</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>2000</creationdate><title>Loss of p16/CDKN2A tumor suppressor protein in gastric adenocarcinoma is associated with epstein-barr virus and anatomic location in the body of the stomach</title><author>Schneider, Barbara G. ; Gulley, Margaret L. ; Eagan, Phyllis ; Bravo, Juan Carlos ; Mera, Robertino ; Geradts, Joseph</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-c2d9f30426077c56508141ad93048393092347bab93b8d2b2a40ad9cdb7ff0133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>Adenocarcinoma - virology</topic><topic>African American</topic><topic>Biological and medical sciences</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>ethnicity</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Herpesvirus 4, Human - isolation & purification</topic><topic>Hispanic</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization</topic><topic>Medical sciences</topic><topic>microsatellite instability</topic><topic>RNA, Viral - metabolism</topic><topic>Stomach - pathology</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Stomach Neoplasms - virology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schneider, Barbara G.</creatorcontrib><creatorcontrib>Gulley, Margaret L.</creatorcontrib><creatorcontrib>Eagan, Phyllis</creatorcontrib><creatorcontrib>Bravo, Juan Carlos</creatorcontrib><creatorcontrib>Mera, Robertino</creatorcontrib><creatorcontrib>Geradts, Joseph</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>MEDLINE - Academic</collection><jtitle>Human pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schneider, Barbara G.</au><au>Gulley, Margaret L.</au><au>Eagan, Phyllis</au><au>Bravo, Juan Carlos</au><au>Mera, Robertino</au><au>Geradts, Joseph</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of p16/CDKN2A tumor suppressor protein in gastric adenocarcinoma is associated with epstein-barr virus and anatomic location in the body of the stomach</atitle><jtitle>Human pathology</jtitle><addtitle>Hum Pathol</addtitle><date>2000</date><risdate>2000</risdate><volume>31</volume><issue>1</issue><spage>45</spage><epage>50</epage><pages>45-50</pages><issn>0046-8177</issn><eissn>1532-8392</eissn><coden>HPCQA4</coden><abstract>Gastric adenocarcinomas (n = 125) were analyzed by immunohistochemistry for the presence of p16, the CDKN2A gene product. This protein was lost in 31 of 125 cases (25%), and loss was associated with location of the tumor in the body of the stomach (
P = .001). Loss of p16 was also associated with the presence of Epstein-Barr virus (EBV) in tumor cells as determined by in situ hybridization (
P = .022). This effect may relate to anatomic site, because EBV-associated tumors originate more frequently in the body of the stomach. When p16 status was evaluated for ethnic origin of the patient (non-Hispanic white, Hispanic, or black), a strong trend (
P = .057) was found for African-American patients to have fewer p16-negative tumors than other patients. This also may relate to anatomic location, because fewer tumors from black patients arose in the body of the stomach (
P = .022). No significant associations were detected between p16 status and histological subtype (intestinal
v diffuse), the presence of microsatellite instability, grade or stage of the tumor, or age, gender, or survival of the patient. In conclusion, p16 loss is quite common in gastric adenocarcinoma, and such loss is more common in EBV-infected tumors arising in the body of the stomach.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10665912</pmid><doi>10.1016/S0046-8177(00)80197-5</doi><tpages>6</tpages></addata></record> |
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| subjects | Adenocarcinoma - metabolism Adenocarcinoma - pathology Adenocarcinoma - virology African American Biological and medical sciences Cyclin-Dependent Kinase Inhibitor p16 - metabolism ethnicity Gastroenterology. Liver. Pancreas. Abdomen Herpesvirus 4, Human - isolation & purification Hispanic Humans Immunohistochemistry In Situ Hybridization Medical sciences microsatellite instability RNA, Viral - metabolism Stomach - pathology Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Stomach Neoplasms - virology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
| title | Loss of p16/CDKN2A tumor suppressor protein in gastric adenocarcinoma is associated with epstein-barr virus and anatomic location in the body of the stomach |
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