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Article: Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays

TitleConserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://nar.oxfordjournals.org/
Citation
Nucleic Acids Research, 2005, v. 33 n. 1, p. 409-421 How to Cite?
AbstractGene 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 MAD, 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 MAD. Terms that were overrepresented in MAD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in MAD 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. © Oxford University Press 2005; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/48964
ISSN
2015 Impact Factor: 9.202
2015 SCImago Journal Rankings: 7.458
PubMed Central ID
ISI Accession Number ID
References
Errata

 

DC FieldValueLanguage
dc.contributor.authorYap, YLen_HK
dc.contributor.authorWong, MPen_HK
dc.contributor.authorZhang, XWen_HK
dc.contributor.authorHernandez, Den_HK
dc.contributor.authorGras, Ren_HK
dc.contributor.authorSmith, DKen_HK
dc.contributor.authorDanchin, Aen_HK
dc.date.accessioned2008-06-12T06:30:54Z-
dc.date.available2008-06-12T06:30:54Z-
dc.date.issued2005en_HK
dc.identifier.citationNucleic Acids Research, 2005, v. 33 n. 1, p. 409-421en_HK
dc.identifier.issn0305-1048en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48964-
dc.description.abstractGene 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 MAD, 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 MAD. Terms that were overrepresented in MAD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in MAD 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. © Oxford University Press 2005; all rights reserved.en_HK
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dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://nar.oxfordjournals.org/en_HK
dc.relation.ispartofNucleic Acids Researchen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAdenocarcinoma - genetics - metabolismen_HK
dc.subject.meshLung Neoplasms - genetics - metabolismen_HK
dc.subject.meshTranscription Factors - metabolismen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshTumor Markers, Biological - metabolismen_HK
dc.titleConserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarraysen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0305-1048&volume=33&issue=1&spage=409&epage=421&date=2005&atitle=Conserved+transcription+factor+binding+sites+of+cancer+markers+derived+from+primary+lung+adenocarcinoma+microarraysen_HK
dc.identifier.emailWong, MP:mwpik@hkucc.hku.hken_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1093/nar/gki188en_HK
dc.identifier.pmid15653641-
dc.identifier.pmcidPMC546166en_HK
dc.identifier.scopuseid_2-s2.0-13744257107en_HK
dc.identifier.hkuros112262-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-13744257107&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume33en_HK
dc.identifier.issue1en_HK
dc.identifier.spage409en_HK
dc.identifier.epage421en_HK
dc.identifier.isiWOS:000226477000039-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.erratumdoi:10.1093/nar/gki558-
dc.identifier.citeulike10576954-

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