Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays
Identifieur interne : 002341 ( Istex/Corpus ); précédent : 002340; suivant : 002342Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays
Auteurs : Yee Leng Yap ; Maria P. Wong ; Xue Wu Zhang ; David Hernandez ; Robin Gras ; David K. Smith ; Antoine DanchinSource :
- Nucleic Acids Research [ 0305-1048 ] ; 2005.
Abstract
Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. A total of 3442 genes, called the set M AD, were found to be either up- or down-regulated by at least 2-fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside M AD. Terms that were overrepresented in M AD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in M AD were grouped into likely co-regulated gene sets. Highly conserved sequences in the 5 kb region upstream of the genes in these sets were identified with the motif discovery tool, MoDEL. Potential oncogenic transcription factors and their corresponding binding sites were identified in these conserved regions using the TRANSFAC 8.3 database. Several of the transcription factors identified in this study have been shown elsewhere to be involved in oncogenic processes. This study searched beyond phenotypic gene expression profiles in cancer cells, in order to identify the more important regulatory transcription factors that caused these aberrations in gene expression.
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DOI: 10.1093/nar/gki188
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Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely@hkusua.hku.hk</mods:affiliation></affiliation></author><author><name sortKey="Wong, Maria P" sort="Wong, Maria P" uniqKey="Wong M" first="Maria P." last="Wong">Maria P. Wong</name><affiliation><mods:affiliation>Department of Pathology, The University of Hong Kong Pokfulam, Hong Kong, China</mods:affiliation></affiliation></author><author><name sortKey="Zhang, Xue Wu" sort="Zhang, Xue Wu" uniqKey="Zhang X" first="Xue Wu" last="Zhang">Xue Wu Zhang</name><affiliation><mods:affiliation>HKU-Pasteur Research Centre Dexter H.C. 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Smith</name><affiliation><mods:affiliation>Department of Biochemistry, The University of Hong Kong Pokfulam, Hong Kong, China</mods:affiliation></affiliation></author><author><name sortKey="Danchin, Antoine" sort="Danchin, Antoine" uniqKey="Danchin A" first="Antoine" last="Danchin">Antoine Danchin</name><affiliation><mods:affiliation>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0BFC1DB5DBE0149707002F146869EB08D51A995C</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1093/nar/gki188</idno><idno type="url">https://api.istex.fr/document/0BFC1DB5DBE0149707002F146869EB08D51A995C/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002341</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002341</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays</title><author><name sortKey="Yap, Yee Leng" sort="Yap, Yee Leng" uniqKey="Yap Y" first="Yee Leng" last="Yap">Yee Leng Yap</name><affiliation><mods:affiliation>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</mods:affiliation></affiliation><affiliation><mods:affiliation>To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely@hkusua.hku.hk</mods:affiliation></affiliation></author><author><name sortKey="Wong, Maria P" sort="Wong, Maria P" uniqKey="Wong M" first="Maria P." last="Wong">Maria P. Wong</name><affiliation><mods:affiliation>Department of Pathology, The University of Hong Kong Pokfulam, Hong Kong, China</mods:affiliation></affiliation></author><author><name sortKey="Zhang, Xue Wu" sort="Zhang, Xue Wu" uniqKey="Zhang X" first="Xue Wu" last="Zhang">Xue Wu Zhang</name><affiliation><mods:affiliation>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</mods:affiliation></affiliation></author><author><name sortKey="Hernandez, David" sort="Hernandez, David" uniqKey="Hernandez D" first="David" last="Hernandez">David Hernandez</name><affiliation><mods:affiliation>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Gras, Robin" sort="Gras, Robin" uniqKey="Gras R" first="Robin" last="Gras">Robin Gras</name><affiliation><mods:affiliation>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Smith, David K" sort="Smith, David K" uniqKey="Smith D" first="David K." last="Smith">David K. Smith</name><affiliation><mods:affiliation>Department of Biochemistry, The University of Hong Kong Pokfulam, Hong Kong, China</mods:affiliation></affiliation></author><author><name sortKey="Danchin, Antoine" sort="Danchin, Antoine" uniqKey="Danchin A" first="Antoine" last="Danchin">Antoine Danchin</name><affiliation><mods:affiliation>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Nucleic Acids Research</title><title level="j" type="abbrev">Nucl. Acids Res.</title><idno type="ISSN">0305-1048</idno><idno type="eISSN">1362-4962</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2005">2005</date><biblScope unit="volume">33</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="409">409</biblScope><biblScope unit="page" to="421">421</biblScope></imprint><idno type="ISSN">0305-1048</idno></series><idno type="istex">0BFC1DB5DBE0149707002F146869EB08D51A995C</idno><idno type="DOI">10.1093/nar/gki188</idno><idno type="local">gki188</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0305-1048</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. A total of 3442 genes, called the set M AD, were found to be either up- or down-regulated by at least 2-fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside M AD. Terms that were overrepresented in M AD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in M AD were grouped into likely co-regulated gene sets. Highly conserved sequences in the 5 kb region upstream of the genes in these sets were identified with the motif discovery tool, MoDEL. Potential oncogenic transcription factors and their corresponding binding sites were identified in these conserved regions using the TRANSFAC 8.3 database. Several of the transcription factors identified in this study have been shown elsewhere to be involved in oncogenic processes. This study searched beyond phenotypic gene expression profiles in cancer cells, in order to identify the more important regulatory transcription factors that caused these aberrations in gene expression.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Yee Leng Yap</name><affiliations><json:string>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</json:string><json:string>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</json:string><json:string>To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely@hkusua.hku.hk</json:string></affiliations></json:item><json:item><name>Maria P. Wong</name><affiliations><json:string>Department of Pathology, The University of Hong Kong Pokfulam, Hong Kong, China</json:string></affiliations></json:item><json:item><name>Xue Wu Zhang</name><affiliations><json:string>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</json:string></affiliations></json:item><json:item><name>David Hernandez</name><affiliations><json:string>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</json:string></affiliations></json:item><json:item><name>Robin Gras</name><affiliations><json:string>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</json:string></affiliations></json:item><json:item><name>David K. Smith</name><affiliations><json:string>Department of Biochemistry, The University of Hong Kong Pokfulam, Hong Kong, China</json:string></affiliations></json:item><json:item><name>Antoine Danchin</name><affiliations><json:string>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>24</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>other</json:string></originalGenre><abstract>Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. A total of 3442 genes, called the set M AD, were found to be either up- or down-regulated by at least 2-fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside M AD. Terms that were overrepresented in M AD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in M AD were grouped into likely co-regulated gene sets. Highly conserved sequences in the 5 kb region upstream of the genes in these sets were identified with the motif discovery tool, MoDEL. Potential oncogenic transcription factors and their corresponding binding sites were identified in these conserved regions using the TRANSFAC 8.3 database. Several of the transcription factors identified in this study have been shown elsewhere to be involved in oncogenic processes. This study searched beyond phenotypic gene expression profiles in cancer cells, in order to identify the more important regulatory transcription factors that caused these aberrations in gene expression.</abstract><qualityIndicators><score>9.4</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612 x 794 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>1298</abstractCharCount><pdfWordCount>7183</pdfWordCount><pdfCharCount>58043</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>200</abstractWordCount></qualityIndicators><title>Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays</title><refBibs><json:item><author><json:item><name>D Hanahan</name></json:item><json:item><name>R,A Weinberg</name></json:item></author><host><volume>100</volume><pages><last>70</last><first>57</first></pages><author></author><title>Cell</title><publicationDate>2000</publicationDate></host><title>The hallmarks of cancer</title><publicationDate>2000</publicationDate></json:item><json:item><author><json:item><name>A Jemal</name></json:item><json:item><name>T Murray</name></json:item><json:item><name>A Samuels</name></json:item><json:item><name>A Ghafoor</name></json:item><json:item><name>E Ward</name></json:item><json:item><name>M,J Thun</name></json:item></author><host><volume>53</volume><pages><last>26</last><first>5</first></pages><author></author><title>CA Cancer J. 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The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use permissions, please contact journals.permissions@oupjournals.org.</p></availability><date>2005</date></publicationStmt><notesStmt><note>*To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely@hkusua.hku.hk</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays</title><author xml:id="author-1"><persName><forename type="first">Yee Leng</forename><surname>Yap</surname></persName><affiliation>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</affiliation><affiliation>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</affiliation><affiliation>To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely@hkusua.hku.hk</affiliation></author><author xml:id="author-2"><persName><forename type="first">Maria P.</forename><surname>Wong</surname></persName><affiliation>Department of Pathology, The University of Hong Kong Pokfulam, Hong Kong, China</affiliation></author><author xml:id="author-3"><persName><forename type="first">Xue Wu</forename><surname>Zhang</surname></persName><affiliation>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</affiliation></author><author xml:id="author-4"><persName><forename type="first">David</forename><surname>Hernandez</surname></persName><affiliation>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</affiliation></author><author xml:id="author-5"><persName><forename type="first">Robin</forename><surname>Gras</surname></persName><affiliation>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</affiliation></author><author xml:id="author-6"><persName><forename type="first">David K.</forename><surname>Smith</surname></persName><affiliation>Department of Biochemistry, The University of Hong Kong Pokfulam, Hong Kong, China</affiliation></author><author xml:id="author-7"><persName><forename type="first">Antoine</forename><surname>Danchin</surname></persName><affiliation>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</affiliation></author></analytic><monogr><title level="j">Nucleic Acids Research</title><title level="j" type="abbrev">Nucl. Acids Res.</title><idno type="pISSN">0305-1048</idno><idno type="eISSN">1362-4962</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2005"></date><biblScope unit="volume">33</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="409">409</biblScope><biblScope unit="page" to="421">421</biblScope></imprint></monogr><idno type="istex">0BFC1DB5DBE0149707002F146869EB08D51A995C</idno><idno type="DOI">10.1093/nar/gki188</idno><idno type="local">gki188</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. A total of 3442 genes, called the set M AD, were found to be either up- or down-regulated by at least 2-fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside M AD. Terms that were overrepresented in M AD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in M AD were grouped into likely co-regulated gene sets. Highly conserved sequences in the 5 kb region upstream of the genes in these sets were identified with the motif discovery tool, MoDEL. Potential oncogenic transcription factors and their corresponding binding sites were identified in these conserved regions using the TRANSFAC 8.3 database. Several of the transcription factors identified in this study have been shown elsewhere to be involved in oncogenic processes. This study searched beyond phenotypic gene expression profiles in cancer cells, in order to identify the more important regulatory transcription factors that caused these aberrations in gene expression.</p></abstract><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>24</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-12-22">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/0BFC1DB5DBE0149707002F146869EB08D51A995C/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="other"><front><journal-meta><journal-id journal-id-type="hwp">nar</journal-id><journal-id journal-id-type="nlm-ta">Nucleic Acids Res</journal-id><journal-id journal-id-type="publisher-id">nar</journal-id><journal-title>Nucleic Acids Research</journal-title><abbrev-journal-title abbrev-type="publisher">Nucl. Acids Res.</abbrev-journal-title><issn pub-type="ppub">0305-1048</issn><issn pub-type="epub">1362-4962</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">gki188</article-id><article-id pub-id-type="doi">10.1093/nar/gki188</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>24</subject></subj-group></article-categories><title-group><article-title>Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Yap</surname><given-names>Yee Leng</given-names></name><xref rid="AU1">1</xref><xref rid="AU2">2</xref><xref rid="COR1">*</xref></contrib><contrib contrib-type="author"><name><surname>Wong</surname><given-names>Maria P.</given-names></name><xref rid="AU3">3</xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Xue Wu</given-names></name><xref rid="AU1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hernandez</surname><given-names>David</given-names></name><xref rid="AU4">4</xref></contrib><contrib contrib-type="author"><name><surname>Gras</surname><given-names>Robin</given-names></name><xref rid="AU4">4</xref></contrib><contrib contrib-type="author"><name><surname>Smith</surname><given-names>David K.</given-names></name><xref rid="AU5">5</xref></contrib><contrib contrib-type="author"><name><surname>Danchin</surname><given-names>Antoine</given-names></name><xref rid="AU2">2</xref></contrib><aff id="AU1"><sup>1</sup> HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China </aff><aff id="AU2"><sup>2</sup> Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France </aff><aff id="AU3"><sup>3</sup> Department of Pathology, The University of Hong Kong Pokfulam, Hong Kong, China </aff><aff id="AU4"><sup>4</sup> Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland </aff><aff id="AU5"><sup>5</sup> Department of Biochemistry, The University of Hong Kong Pokfulam, Hong Kong, China </aff></contrib-group><author-notes><corresp id="COR1"><sup>*</sup>To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: <ext-link xlink:href="daniely@hkusua.hku.hk" ext-link-type="email">daniely@hkusua.hku.hk</ext-link></corresp></author-notes><pub-date pub-type="ppub"><year>2005</year></pub-date><volume>33</volume><issue>1</issue><fpage>409</fpage><lpage>421</lpage><history><date date-type="accepted"><day>12</day><month>12</month><year>2004</year></date><date date-type="received"><day>14</day><month>8</month><year>2004</year></date><date date-type="rev-recd"><day>02</day><month>11</month><year>2004</year></date></history><permissions><copyright-statement>© 2005, the authors <italic>Nucleic Acids Research, Vol. 33 No. 1</italic> © <italic>Oxford University Press 2005; all rights reserved</italic>
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use permissions, please contact <ext-link xlink:href="journals.permissions@oupjournals.org" ext-link-type="email">journals.permissions@oupjournals.org</ext-link>.</copyright-statement><copyright-year>2005</copyright-year><license license-type="open-access"><p></p></license></permissions><abstract xml:lang="en"><p>Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. A total of 3442 genes, called the set <italic>M</italic> <sub>AD</sub>, were found to be either up- or down-regulated by at least 2-fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside <italic>M</italic> <sub>AD</sub>. Terms that were overrepresented in <italic>M</italic> <sub>AD</sub> included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in <italic>M</italic> <sub>AD</sub> were grouped into likely co-regulated gene sets. Highly conserved sequences in the 5 kb region upstream of the genes in these sets were identified with the motif discovery tool, MoDEL. Potential oncogenic transcription factors and their corresponding binding sites were identified in these conserved regions using the TRANSFAC 8.3 database. Several of the transcription factors identified in this study have been shown elsewhere to be involved in oncogenic processes. This study searched beyond phenotypic gene expression profiles in cancer cells, in order to identify the more important regulatory transcription factors that caused these aberrations in gene expression.</p></abstract><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>409</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>research-article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays</title></titleInfo><name type="personal"><namePart type="given">Yee Leng</namePart><namePart type="family">Yap</namePart><affiliation>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</affiliation><affiliation>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</affiliation><affiliation>To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely@hkusua.hku.hk</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maria P.</namePart><namePart type="family">Wong</namePart><affiliation>Department of Pathology, The University of Hong Kong Pokfulam, Hong Kong, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xue Wu</namePart><namePart type="family">Zhang</namePart><affiliation>HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Hernandez</namePart><affiliation>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robin</namePart><namePart type="family">Gras</namePart><affiliation>Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David K.</namePart><namePart type="family">Smith</namePart><affiliation>Department of Biochemistry, The University of Hong Kong Pokfulam, Hong Kong, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Antoine</namePart><namePart type="family">Danchin</namePart><affiliation>Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="other" displayLabel="other"></genre><subject><genre>hwp-journal-coll</genre><topic>24</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2005</dateIssued><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. A total of 3442 genes, called the set M AD, were found to be either up- or down-regulated by at least 2-fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside M AD. Terms that were overrepresented in M AD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in M AD were grouped into likely co-regulated gene sets. Highly conserved sequences in the 5 kb region upstream of the genes in these sets were identified with the motif discovery tool, MoDEL. Potential oncogenic transcription factors and their corresponding binding sites were identified in these conserved regions using the TRANSFAC 8.3 database. Several of the transcription factors identified in this study have been shown elsewhere to be involved in oncogenic processes. This study searched beyond phenotypic gene expression profiles in cancer cells, in order to identify the more important regulatory transcription factors that caused these aberrations in gene expression.</abstract><note type="author-notes">*To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely@hkusua.hku.hk</note><relatedItem type="host"><titleInfo><title>Nucleic Acids Research</title></titleInfo><titleInfo type="abbreviated"><title>Nucl. Acids Res.</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0305-1048</identifier><identifier type="eISSN">1362-4962</identifier><identifier type="PublisherID">nar</identifier><identifier type="PublisherID-hwp">nar</identifier><identifier type="PublisherID-nlm-ta">Nucleic Acids Res</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>409</start><end>421</end></extent></part></relatedItem><identifier type="istex">0BFC1DB5DBE0149707002F146869EB08D51A995C</identifier><identifier type="DOI">10.1093/nar/gki188</identifier><identifier type="local">gki188</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2005, the authors Nucleic Acids Research, Vol. 33 No. 1 © Oxford University Press 2005; all rights reserved
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