Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenes MYCN, MET, WNT2, and ERBB2
Identifieur interne : 000594 ( Main/Corpus ); précédent : 000593; suivant : 000595Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenes MYCN, MET, WNT2, and ERBB2
Auteurs : Michelle Nessling ; Sabina Solinas Oldo ; Klaus K. Wilgenbus ; Franz Borchard ; Peter LichterSource :
- Genes, Chromosomes and Cancer [ 1045-2257 ] ; 1998-12.
Abstract
Gastric adenocarcinoma is a malignant tumor with a high incidence and a low survival rate. In order to identify genetic alterations associated with this tumor, we screened 23 gastric adenocarcinomas for recurrent chromosomal imbalances by using comparative genomic hybridization (CGH). The most common gains of chromosomal material were found on chromosome arms 20q (10 cases), 16p (7 cases), and 1q (4 cases) and on chromosome 11 (4 cases). Losses were observed on chromosome arms 4q, 5q, 9p, and 21q (3 cases each). Four tumors exhibited high‐level amplifications localized on chromosome regions 2p23–p24, 7q31–q32, 8p21–p22, 10q25–q26, 11q13, 17q11–q21, and 20q. Based on the position of these amplifications, candidate (onco)genes were selected and subsequently tested by Southern blot analysis of the respective tumors. Of the seven tested candidates, MYCN, MET, WNT2, and ERBB2 were found to participate in the amplicons of the respective tumor samples. Of these four presumably activated oncogenes, two, MYCN and WNT2, were previously not assumed to play a pathogenic role in stomach cancer. Among the other regions of imbalance, gain of 20q seems particularly interesting, because it is found in almost half of the analyzed cases and is highly amplified. Our data allowed us to narrow the relevant region down to the commonly gained bands 20q12–q13.1. This and other imbalanced regions provide a basis for searching new putative oncogenes and tumor suppressor genes involved in the development or progression of gastric adenocarcinoma. Genes Chromosomes Cancer 23:307–316, 1998. © 1998 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/(SICI)1098-2264(199812)23:4<307::AID-GCC5>3.0.CO;2-#
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In order to identify genetic alterations associated with this tumor, we screened 23 gastric adenocarcinomas for recurrent chromosomal imbalances by using comparative genomic hybridization (CGH). The most common gains of chromosomal material were found on chromosome arms 20q (10 cases), 16p (7 cases), and 1q (4 cases) and on chromosome 11 (4 cases). Losses were observed on chromosome arms 4q, 5q, 9p, and 21q (3 cases each). Four tumors exhibited high‐level amplifications localized on chromosome regions 2p23–p24, 7q31–q32, 8p21–p22, 10q25–q26, 11q13, 17q11–q21, and 20q. Based on the position of these amplifications, candidate (onco)genes were selected and subsequently tested by Southern blot analysis of the respective tumors. Of the seven tested candidates, MYCN, MET, WNT2, and ERBB2 were found to participate in the amplicons of the respective tumor samples. Of these four presumably activated oncogenes, two, MYCN and WNT2, were previously not assumed to play a pathogenic role in stomach cancer. Among the other regions of imbalance, gain of 20q seems particularly interesting, because it is found in almost half of the analyzed cases and is highly amplified. Our data allowed us to narrow the relevant region down to the commonly gained bands 20q12–q13.1. This and other imbalanced regions provide a basis for searching new putative oncogenes and tumor suppressor genes involved in the development or progression of gastric adenocarcinoma. 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Our data allowed us to narrow the relevant region down to the commonly gained bands 20q12–q13.1. This and other imbalanced regions provide a basis for searching new putative oncogenes and tumor suppressor genes involved in the development or progression of gastric adenocarcinoma. 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Of these four presumably activated oncogenes, two, MYCN and WNT2, were previously not assumed to play a pathogenic role in stomach cancer. Among the other regions of imbalance, gain of 20q seems particularly interesting, because it is found in almost half of the analyzed cases and is highly amplified. Our data allowed us to narrow the relevant region down to the commonly gained bands 20q12–q13.1. This and other imbalanced regions provide a basis for searching new putative oncogenes and tumor suppressor genes involved in the development or progression of gastric adenocarcinoma. Genes Chromosomes Cancer 23:307–316, 1998. © 1998 Wiley‐Liss, Inc.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-01-23">Received</change><change when="1998-05-13">Registration</change><change when="1998-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/B793CC990A99449AA9F0A1F5188C67489C289C34/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1098-2264</doi><issn type="print">1045-2257</issn><issn type="electronic">1098-2264</issn><idGroup><id type="product" value="GCC"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="GENES, CHROMOSOMES AND CANCER">Genes, Chromosomes and Cancer</title><title type="short">Genes Chromosom. 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In order to identify genetic alterations associated with this tumor, we screened 23 gastric adenocarcinomas for recurrent chromosomal imbalances by using comparative genomic hybridization (CGH). The most common gains of chromosomal material were found on chromosome arms 20q (10 cases), 16p (7 cases), and 1q (4 cases) and on chromosome 11 (4 cases). Losses were observed on chromosome arms 4q, 5q, 9p, and 21q (3 cases each). Four tumors exhibited high‐level amplifications localized on chromosome regions 2p23–p24, 7q31–q32, 8p21–p22, 10q25–q26, 11q13, 17q11–q21, and 20q. Based on the position of these amplifications, candidate (onco)genes were selected and subsequently tested by Southern blot analysis of the respective tumors. Of the seven tested candidates, <i>MYCN</i>, <i>MET</i>, <i>WNT2</i>, and <i>ERBB2</i> were found to participate in the amplicons of the respective tumor samples. Of these four presumably activated oncogenes, two, <i>MYCN</i> and <i>WNT2</i>, were previously not assumed to play a pathogenic role in stomach cancer. Among the other regions of imbalance, gain of 20q seems particularly interesting, because it is found in almost half of the analyzed cases and is highly amplified. Our data allowed us to narrow the relevant region down to the commonly gained bands 20q12–q13.1. This and other imbalanced regions provide a basis for searching new putative oncogenes and tumor suppressor genes involved in the development or progression of gastric adenocarcinoma. <i>Genes Chromosomes Cancer 23:307–316, 1998.</i> © 1998 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenes MYCN, MET, WNT2, and ERBB2</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>GASTRIC ADENOCARCINOMA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenes</title></titleInfo><name type="personal"><namePart type="given">Michelle</namePart><namePart type="family">Nessling</namePart><affiliation>Abteilung Organisation komplexer Genome, Deutsches Krebsforschungszentrum, Heidelberg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sabina</namePart><namePart type="family">Solinas‐Toldo</namePart><affiliation>Abteilung Organisation komplexer Genome, Deutsches Krebsforschungszentrum, Heidelberg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus K.</namePart><namePart type="family">Wilgenbus</namePart><affiliation>Boehringer Ingelheim Research and Development, Vienna, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Franz</namePart><namePart type="family">Borchard</namePart><affiliation>Institut für Pathologie, Heinrich‐Heine‐Universität, Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Lichter</namePart><affiliation>Abteilung Organisation komplexer Genome, Deutsches Krebsforschungszentrum, Heidelberg, Germany</affiliation><description>Correspondence: Deutsches Krebsforschungszentrum, Abt. Organisation komplexer Genome, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">1998-12</dateIssued><dateCaptured encoding="w3cdtf">1998-01-23</dateCaptured><dateValid encoding="w3cdtf">1998-05-13</dateValid><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">3</extent><extent unit="tables">1</extent><extent unit="references">63</extent><extent unit="words">6637</extent></physicalDescription><abstract lang="en">Gastric adenocarcinoma is a malignant tumor with a high incidence and a low survival rate. In order to identify genetic alterations associated with this tumor, we screened 23 gastric adenocarcinomas for recurrent chromosomal imbalances by using comparative genomic hybridization (CGH). The most common gains of chromosomal material were found on chromosome arms 20q (10 cases), 16p (7 cases), and 1q (4 cases) and on chromosome 11 (4 cases). Losses were observed on chromosome arms 4q, 5q, 9p, and 21q (3 cases each). Four tumors exhibited high‐level amplifications localized on chromosome regions 2p23–p24, 7q31–q32, 8p21–p22, 10q25–q26, 11q13, 17q11–q21, and 20q. Based on the position of these amplifications, candidate (onco)genes were selected and subsequently tested by Southern blot analysis of the respective tumors. Of the seven tested candidates, MYCN, MET, WNT2, and ERBB2 were found to participate in the amplicons of the respective tumor samples. Of these four presumably activated oncogenes, two, MYCN and WNT2, were previously not assumed to play a pathogenic role in stomach cancer. Among the other regions of imbalance, gain of 20q seems particularly interesting, because it is found in almost half of the analyzed cases and is highly amplified. Our data allowed us to narrow the relevant region down to the commonly gained bands 20q12–q13.1. This and other imbalanced regions provide a basis for searching new putative oncogenes and tumor suppressor genes involved in the development or progression of gastric adenocarcinoma. Genes Chromosomes Cancer 23:307–316, 1998. © 1998 Wiley‐Liss, Inc.</abstract><relatedItem type="host"><titleInfo><title>Genes, Chromosomes and Cancer</title></titleInfo><titleInfo type="abbreviated"><title>Genes Chromosom. Cancer</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1045-2257</identifier><identifier type="eISSN">1098-2264</identifier><identifier type="DOI">10.1002/(ISSN)1098-2264</identifier><identifier type="PublisherID">GCC</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>307</start><end>316</end><total>10</total></extent></part></relatedItem><identifier type="istex">B793CC990A99449AA9F0A1F5188C67489C289C34</identifier><identifier type="DOI">10.1002/(SICI)1098-2264(199812)23:4<307::AID-GCC5>3.0.CO;2-#</identifier><identifier type="ArticleID">GCC5</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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