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Article: Normalization and analysis of cDNA microarrays using within-array replications applied to neuroblastoma cell response to a cytokine

TitleNormalization and analysis of cDNA microarrays using within-array replications applied to neuroblastoma cell response to a cytokine
Authors
Issue Date2004
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2004, v. 101 n. 5, p. 1135-1140 How to Cite?
AbstractThe quantitative comparison of two or more microarrays can reveal, for example, the distinct patterns of gene expression that define different cellular phenotypes or the genes that are induced in the cellular response to certain stimulations. Normalization of the measured intensities is a prerequisite of such comparisons. However, a fundamental problem in cDNA microarray analysis is the lack of a common standard to compare the expression levels of different samples. Several normalization protocols have been proposed to overcome the variabilities inherent in this technology. We have developed a normalization procedure based on within-array replications via a semilinear in-slide model, which adjusts objectively experimental variations without making critical biological assumptions. The significant analysis of gene expressions is based on a weighted t statistic, which accounts for the heteroscedasticity of the observed log ratios of expressions, and a balanced sign permutation test. We illustrated the use of the techniques in a comparison of the expression profiles of neuroblastoma cells that were stimulated with a growth factor, macrophage migration inhibitory factor (MIF). The analysis of expression changes at mRNA levels showed that approximately 99 genes were up-regulated and 24 were reduced significantly (P <0.001) in MIF-stimulated neuroblastoma cells. The regulated genes included several oncogenes, growth-related genes, tumor metastatic genes, and immuno-related genes. The findings provide clues as to the molecular mechanisms of MIF-mediated tumor progression and supply therapeutic targets for neuroblastoma treatment.
Persistent Identifierhttp://hdl.handle.net/10722/49342
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFan, Jen_HK
dc.contributor.authorTam, Pen_HK
dc.contributor.authorVande Woude, Gen_HK
dc.contributor.authorRen, Yen_HK
dc.date.accessioned2008-06-12T06:39:54Z-
dc.date.available2008-06-12T06:39:54Z-
dc.date.issued2004en_HK
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2004, v. 101 n. 5, p. 1135-1140en_US
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49342-
dc.description.abstractThe quantitative comparison of two or more microarrays can reveal, for example, the distinct patterns of gene expression that define different cellular phenotypes or the genes that are induced in the cellular response to certain stimulations. Normalization of the measured intensities is a prerequisite of such comparisons. However, a fundamental problem in cDNA microarray analysis is the lack of a common standard to compare the expression levels of different samples. Several normalization protocols have been proposed to overcome the variabilities inherent in this technology. We have developed a normalization procedure based on within-array replications via a semilinear in-slide model, which adjusts objectively experimental variations without making critical biological assumptions. The significant analysis of gene expressions is based on a weighted t statistic, which accounts for the heteroscedasticity of the observed log ratios of expressions, and a balanced sign permutation test. We illustrated the use of the techniques in a comparison of the expression profiles of neuroblastoma cells that were stimulated with a growth factor, macrophage migration inhibitory factor (MIF). The analysis of expression changes at mRNA levels showed that approximately 99 genes were up-regulated and 24 were reduced significantly (P <0.001) in MIF-stimulated neuroblastoma cells. The regulated genes included several oncogenes, growth-related genes, tumor metastatic genes, and immuno-related genes. The findings provide clues as to the molecular mechanisms of MIF-mediated tumor progression and supply therapeutic targets for neuroblastoma treatment.en_HK
dc.format.extent386 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_HK
dc.relation.ispartofProceedings Of The National Academy Of Sciences Of The United States Of Americaen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsNational Academy of Sciences Proceedings. Copyright © National Academy of Sciences.en_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors - pharmacologyen_HK
dc.subject.meshNeuroblastoma - genetics - pathologyen_HK
dc.subject.meshOligonucleotide Array Sequence Analysisen_HK
dc.subject.meshHumansen_HK
dc.titleNormalization and analysis of cDNA microarrays using within-array replications applied to neuroblastoma cell response to a cytokineen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0027-8424&volume=101&issue=5&spage=1135&epage=1140&date=2004&atitle=Normalization+and+analysis+of+cDNA+microarrays+using+within-array+replications+applied+to+neuroblastoma+cell+response+to+a+cytokineen_HK
dc.identifier.emailTam, P: paultam@hkucc.hku.hken_HK
dc.identifier.emailRen, Y: yren@hkucc.hku.hken_HK
dc.identifier.authorityTam, PKH=rp00060en_US
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1073/pnas.0307557100en_HK
dc.identifier.pmid14739336-
dc.identifier.pmcidPMC337019en_HK
dc.identifier.scopuseid_2-s2.0-0842321044en_US
dc.identifier.hkuros85912-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0842321044&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume101en_US
dc.identifier.issue5en_US
dc.identifier.spage1135en_US
dc.identifier.epage1140en_US
dc.identifier.isiWOS:000188796800009-

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