Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenes MYCN, MET, WNT2, and ERBB2
Identifieur interne : 000C65 ( Main/Exploration ); précédent : 000C64; suivant : 000C66Mapping of chromosomal imbalances in gastric adenocarcinoma revealed amplified protooncogenes MYCN, MET, WNT2, and ERBB2
Auteurs : Michelle Nessling [Allemagne] ; Sabina Solinas Oldo [Allemagne] ; Klaus K. Wilgenbus [Autriche] ; Franz Borchard [Allemagne] ; Peter Lichter [Allemagne]Source :
- 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-#
Affiliations:
- Allemagne, Autriche
- Bade-Wurtemberg, District de Düsseldorf, District de Karlsruhe, Rhénanie-du-Nord-Westphalie, Vienne (Autriche)
- Düsseldorf, Heidelberg, Vienne (Autriche)
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Cancer</title><idno type="ISSN">1045-2257</idno><idno type="eISSN">1098-2264</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="1998-12">1998-12</date><biblScope unit="volume">23</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="307">307</biblScope><biblScope unit="page" to="316">316</biblScope></imprint><idno type="ISSN">1045-2257</idno></series><idno type="istex">B793CC990A99449AA9F0A1F5188C67489C289C34</idno><idno type="DOI">10.1002/(SICI)1098-2264(199812)23:4<307::AID-GCC5>3.0.CO;2-#</idno><idno type="ArticleID">GCC5</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1045-2257</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Autriche</li></country><region><li>Bade-Wurtemberg</li><li>District de Düsseldorf</li><li>District de Karlsruhe</li><li>Rhénanie-du-Nord-Westphalie</li><li>Vienne (Autriche)</li></region><settlement><li>Düsseldorf</li><li>Heidelberg</li><li>Vienne (Autriche)</li></settlement></list><tree><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Nessling, Michelle" sort="Nessling, Michelle" uniqKey="Nessling M" first="Michelle" last="Nessling">Michelle Nessling</name></region><name sortKey="Borchard, Franz" sort="Borchard, Franz" uniqKey="Borchard F" first="Franz" last="Borchard">Franz Borchard</name><name sortKey="Lichter, Peter" sort="Lichter, Peter" uniqKey="Lichter P" first="Peter" last="Lichter">Peter Lichter</name><name sortKey="Solinas Oldo, Sabina" sort="Solinas Oldo, Sabina" uniqKey="Solinas Oldo S" first="Sabina" last="Solinas Oldo">Sabina Solinas Oldo</name></country><country name="Autriche"><region name="Vienne (Autriche)"><name sortKey="Wilgenbus, Klaus K" sort="Wilgenbus, Klaus K" uniqKey="Wilgenbus K" first="Klaus K." last="Wilgenbus">Klaus K. 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