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Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays
We performed genome-wide analysis of copy-number changes and loss of heterozygosity (LOH) in Barrett's esophageal adenocarcinoma by single nucleotide polymorphism (SNP) microarrays to identify associated genomic alterations. DNA from 27 esophageal adenocarcinomas and 14 matching normal tissues...
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| Published in: | Laboratory investigation 2009-04, Vol.89 (4), p.385-397 |
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| creator | Wiech, Thorsten Nikolopoulos, Elisabeth Weis, Roland Langer, Rupert Bartholomé, Kilian Timmer, Jens Walch, Axel K Höfler, Heinz Werner, Martin |
| description | We performed genome-wide analysis of copy-number changes and loss of heterozygosity (LOH) in Barrett's esophageal adenocarcinoma by single nucleotide polymorphism (SNP) microarrays to identify associated genomic alterations. DNA from 27 esophageal adenocarcinomas and 14 matching normal tissues was subjected to SNP microarrays. The data were analyzed using dChipSNP software. Copy-number changes occurring in at least 25% of the cases and LOH occurring in at least 19% were regarded as relevant changes. As a validation, fluorescence in situ hybridization (FISH) of 8q24.21 (CMYC) and 8p23.1 (SOX7) was performed. Previously described genomic alterations in esophageal adenocarcinomas could be confirmed by SNP microarrays, such as amplification on 8q (CMYC, confirmed by FISH) and 20q13 or deletion/LOH on 3p (FHIT) and 9p (CDKN2A). Moreover, frequent gains were detected on 2p23.3, 7q11.22, 13q31.1, 14q32.31, 17q23.2 and 20q13.2 harboring several novel candidate genes. The highest copy numbers were seen on 8p23.1, the location of SOX7, which could be demonstrated to be involved in amplification by FISH. A nuclear overexpression of the transcription factor SOX7 could be detected by immunohistochemistry in two amplified tumors. Copy-number losses were seen on 18q21.32 and 20p11.21, harboring interesting candidate genes, such as CDH20 and CST4. Finally, a novel LOH region could be identified on 6p in at least 19% of the cases. In conclusion, SNP microarrays are a valuable tool to detect DNA copy-number changes and LOH at a high resolution. Using this technique, we identified several novel genes and DNA regions associated with esophageal adenocarcinoma. |
| doi_str_mv | 10.1038/labinvest.2008.67 |
| format | article |
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DNA from 27 esophageal adenocarcinomas and 14 matching normal tissues was subjected to SNP microarrays. The data were analyzed using dChipSNP software. Copy-number changes occurring in at least 25% of the cases and LOH occurring in at least 19% were regarded as relevant changes. As a validation, fluorescence in situ hybridization (FISH) of 8q24.21 (CMYC) and 8p23.1 (SOX7) was performed. Previously described genomic alterations in esophageal adenocarcinomas could be confirmed by SNP microarrays, such as amplification on 8q (CMYC, confirmed by FISH) and 20q13 or deletion/LOH on 3p (FHIT) and 9p (CDKN2A). Moreover, frequent gains were detected on 2p23.3, 7q11.22, 13q31.1, 14q32.31, 17q23.2 and 20q13.2 harboring several novel candidate genes. The highest copy numbers were seen on 8p23.1, the location of SOX7, which could be demonstrated to be involved in amplification by FISH. A nuclear overexpression of the transcription factor SOX7 could be detected by immunohistochemistry in two amplified tumors. Copy-number losses were seen on 18q21.32 and 20p11.21, harboring interesting candidate genes, such as CDH20 and CST4. Finally, a novel LOH region could be identified on 6p in at least 19% of the cases. In conclusion, SNP microarrays are a valuable tool to detect DNA copy-number changes and LOH at a high resolution. Using this technique, we identified several novel genes and DNA regions associated with esophageal adenocarcinoma.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.2008.67</identifier><identifier>PMID: 18663352</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adenocarcinoma - genetics ; Adult ; Aged ; Barrett Esophagus - genetics ; Barrett's adenocarcinoma ; Biological and medical sciences ; Biotechnology ; copy-number changes ; esophageal carcinoma ; Esophageal Neoplasms - genetics ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Dosage ; Genome-Wide Association Study ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; LOH ; Loss of Heterozygosity ; Male ; mapping array ; Medical sciences ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; SNP array</subject><ispartof>Laboratory investigation, 2009-04, Vol.89 (4), p.385-397</ispartof><rights>2009 United States & Canadian Academy of Pathology</rights><rights>2009 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-839c714b9d39635fcd86d6205aa913220f5ff6f3e7813fa592928880ef8707cf3</citedby><cites>FETCH-LOGICAL-c450t-839c714b9d39635fcd86d6205aa913220f5ff6f3e7813fa592928880ef8707cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,2744,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21315926$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18663352$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wiech, Thorsten</creatorcontrib><creatorcontrib>Nikolopoulos, Elisabeth</creatorcontrib><creatorcontrib>Weis, Roland</creatorcontrib><creatorcontrib>Langer, Rupert</creatorcontrib><creatorcontrib>Bartholomé, Kilian</creatorcontrib><creatorcontrib>Timmer, Jens</creatorcontrib><creatorcontrib>Walch, Axel K</creatorcontrib><creatorcontrib>Höfler, Heinz</creatorcontrib><creatorcontrib>Werner, Martin</creatorcontrib><title>Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><description>We performed genome-wide analysis of copy-number changes and loss of heterozygosity (LOH) in Barrett's esophageal adenocarcinoma by single nucleotide polymorphism (SNP) microarrays to identify associated genomic alterations. DNA from 27 esophageal adenocarcinomas and 14 matching normal tissues was subjected to SNP microarrays. The data were analyzed using dChipSNP software. Copy-number changes occurring in at least 25% of the cases and LOH occurring in at least 19% were regarded as relevant changes. As a validation, fluorescence in situ hybridization (FISH) of 8q24.21 (CMYC) and 8p23.1 (SOX7) was performed. Previously described genomic alterations in esophageal adenocarcinomas could be confirmed by SNP microarrays, such as amplification on 8q (CMYC, confirmed by FISH) and 20q13 or deletion/LOH on 3p (FHIT) and 9p (CDKN2A). Moreover, frequent gains were detected on 2p23.3, 7q11.22, 13q31.1, 14q32.31, 17q23.2 and 20q13.2 harboring several novel candidate genes. The highest copy numbers were seen on 8p23.1, the location of SOX7, which could be demonstrated to be involved in amplification by FISH. A nuclear overexpression of the transcription factor SOX7 could be detected by immunohistochemistry in two amplified tumors. Copy-number losses were seen on 18q21.32 and 20p11.21, harboring interesting candidate genes, such as CDH20 and CST4. Finally, a novel LOH region could be identified on 6p in at least 19% of the cases. In conclusion, SNP microarrays are a valuable tool to detect DNA copy-number changes and LOH at a high resolution. Using this technique, we identified several novel genes and DNA regions associated with esophageal adenocarcinoma.</description><subject>Adenocarcinoma - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Barrett Esophagus - genetics</subject><subject>Barrett's adenocarcinoma</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>copy-number changes</subject><subject>esophageal carcinoma</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Dosage</subject><subject>Genome-Wide Association Study</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>LOH</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>mapping array</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Polymorphism, Single Nucleotide</subject><subject>SNP array</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNp9kE1v1DAQhi1ERZfCD-CCLCTEKVt_bBxHnEoFpVKlXuBszTrj4iqxF9sp2n-Pw662Ny725XnfmXkIecfZmjOpL0fY-vCEuawFY3qtuhdkxVvJGiZZ95KsGBOyUVp25-R1zo-M8c1Gta_IOddKSdmKFck3GOKEzR8_IIUA4z77TKOjDxiweEthLJig-Bgy9YF-gZSwlE-ZwlCTFpL1tQDonH14oMszIg2zHTGWpXMXx_0U0-6XzxOtYdjnN-TMwZjx7fG_ID-_ff1x_b25u7-5vb66a-ymZaXRsrcd32z7QfZKts4OWg1KsBag51II5lrnlJPYaS4dtL3ohdaaodMd66yTF-TDoXeX4u-5ajKPcU71xmxqWui-7USF-AGyKeac0Jld8hOkveHMLJbNybJZLBvV1cz7Y_G8nXB4Thy1VuDjEYBsYXQJgvX5xAkueV1XPXMBypzwBJxGLhP_Dfx84LDqevKYTLYeg8XBJ7TFDNH_Z92_ueerkg</recordid><startdate>20090401</startdate><enddate>20090401</enddate><creator>Wiech, Thorsten</creator><creator>Nikolopoulos, Elisabeth</creator><creator>Weis, Roland</creator><creator>Langer, Rupert</creator><creator>Bartholomé, Kilian</creator><creator>Timmer, Jens</creator><creator>Walch, Axel K</creator><creator>Höfler, Heinz</creator><creator>Werner, Martin</creator><general>Elsevier Inc</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20090401</creationdate><title>Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays</title><author>Wiech, Thorsten ; Nikolopoulos, Elisabeth ; Weis, Roland ; Langer, Rupert ; Bartholomé, Kilian ; Timmer, Jens ; Walch, Axel K ; Höfler, Heinz ; Werner, Martin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-839c714b9d39635fcd86d6205aa913220f5ff6f3e7813fa592928880ef8707cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adenocarcinoma - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>Barrett Esophagus - genetics</topic><topic>Barrett's adenocarcinoma</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>copy-number changes</topic><topic>esophageal carcinoma</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Dosage</topic><topic>Genome-Wide Association Study</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>LOH</topic><topic>Loss of Heterozygosity</topic><topic>Male</topic><topic>mapping array</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Polymorphism, Single Nucleotide</topic><topic>SNP array</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wiech, Thorsten</creatorcontrib><creatorcontrib>Nikolopoulos, Elisabeth</creatorcontrib><creatorcontrib>Weis, Roland</creatorcontrib><creatorcontrib>Langer, Rupert</creatorcontrib><creatorcontrib>Bartholomé, Kilian</creatorcontrib><creatorcontrib>Timmer, Jens</creatorcontrib><creatorcontrib>Walch, Axel K</creatorcontrib><creatorcontrib>Höfler, Heinz</creatorcontrib><creatorcontrib>Werner, Martin</creatorcontrib><collection>ScienceDirect 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genome-wide analysis of copy-number changes and loss of heterozygosity (LOH) in Barrett's esophageal adenocarcinoma by single nucleotide polymorphism (SNP) microarrays to identify associated genomic alterations. DNA from 27 esophageal adenocarcinomas and 14 matching normal tissues was subjected to SNP microarrays. The data were analyzed using dChipSNP software. Copy-number changes occurring in at least 25% of the cases and LOH occurring in at least 19% were regarded as relevant changes. As a validation, fluorescence in situ hybridization (FISH) of 8q24.21 (CMYC) and 8p23.1 (SOX7) was performed. Previously described genomic alterations in esophageal adenocarcinomas could be confirmed by SNP microarrays, such as amplification on 8q (CMYC, confirmed by FISH) and 20q13 or deletion/LOH on 3p (FHIT) and 9p (CDKN2A). Moreover, frequent gains were detected on 2p23.3, 7q11.22, 13q31.1, 14q32.31, 17q23.2 and 20q13.2 harboring several novel candidate genes. The highest copy numbers were seen on 8p23.1, the location of SOX7, which could be demonstrated to be involved in amplification by FISH. A nuclear overexpression of the transcription factor SOX7 could be detected by immunohistochemistry in two amplified tumors. Copy-number losses were seen on 18q21.32 and 20p11.21, harboring interesting candidate genes, such as CDH20 and CST4. Finally, a novel LOH region could be identified on 6p in at least 19% of the cases. In conclusion, SNP microarrays are a valuable tool to detect DNA copy-number changes and LOH at a high resolution. Using this technique, we identified several novel genes and DNA regions associated with esophageal adenocarcinoma.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>18663352</pmid><doi>10.1038/labinvest.2008.67</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Laboratory investigation, 2009-04, Vol.89 (4), p.385-397 |
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| source | Nature_系列刊 |
| subjects | Adenocarcinoma - genetics Adult Aged Barrett Esophagus - genetics Barrett's adenocarcinoma Biological and medical sciences Biotechnology copy-number changes esophageal carcinoma Esophageal Neoplasms - genetics Female Fundamental and applied biological sciences. Psychology Gene Dosage Genome-Wide Association Study Humans Investigative techniques, diagnostic techniques (general aspects) LOH Loss of Heterozygosity Male mapping array Medical sciences Middle Aged Oligonucleotide Array Sequence Analysis Polymorphism, Single Nucleotide SNP array |
| title | Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays |
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