Profiling of gene expression changes caused by p53 gain‐of‐function mutant alleles in prostate cancer cells
Identifieur interne : 002358 ( Istex/Curation ); précédent : 002357; suivant : 002359Profiling of gene expression changes caused by p53 gain‐of‐function mutant alleles in prostate cancer cells
Auteurs : Clifford G. Tepper [États-Unis] ; Jeffrey P. Gregg [États-Unis] ; Xu-Bao Shi [États-Unis] ; Ruth L. Vinall [États-Unis] ; Colin A. Baron [États-Unis] ; Philip E. Ryan [États-Unis] ; Pierre-Yves Desprez [États-Unis] ; Hsing-Jien Kung [États-Unis] ; Ralph W. Devere White [États-Unis]Source :
- The Prostate [ 0270-4137 ] ; 2005-12-01.
English descriptors
- Teeft :
- Allele, Androgen, Androgen ablation, Androgen deprivation, Androgen independence, Androgen receptor, Assay, Basal, Basic davis cancer center, Binding protein, Cancer center support grant, Cdna, Cdna synthesis, Cell biol, Cell growth, Cell line, Cell lines, Cell lysates, Comparison analysis, Constitutive expression, Davis schoolof medicine, Differentially, Disease association, Duplex, Empty bars, Epper, Expression data, Expression level, Expression signature, Gain insight, Gene, Gene alterations, Gene expression, Gene expression changes, Gene expression signature, Gene mutation, Gene name, Genechip arrays, Grant number, Grant sponsor, Growth arrest, Growth inhibition, Human genome, Human prostate carcinoma, Invitrogen life technologies, Lncap, Lncap cells, Lncap cells transfected, Lncap prostate cancer cells, Lncap sublines, Luciferase, Melanoma antigen family, Metastatic, Microarray, Microarray analysis, Microarray gene expression, Microarray results, Model system, Mutant, Mutant alleles, Mutation, Mutational inactivation, Natl cancer inst, Nucleotide positions sense, Oligonucleotide arrays, Oncogene, Overexpressed genes, Overexpression, Pathway, Primary tumors, Proc natl acad, Progression, Proliferation, Promoter, Promoter activity, Prostate, Prostate cancer, Prostate epithelial cells, Protein expression, Proximal promoter region, Reagent, Receptor, Renilla luciferase activities, Reporter assays, Ribosomal protein, Rnai experiments, Signal detection, Simultaneous expression analysis, Sirna, Sirnas, Solute carrier family, Stable expression, Sublines, Suppressor, Target genes, Transcription, Transfected, Tumor development, Tumor phenotype, Tumor progression, Tumor suppressor, Tumor suppressor gene, Unique expression, Wang, Wild type, Wong.
Abstract
BACKGROUND: Tumor suppressor p53 mutations are associated with the transition of prostate cancer to metastatic, hormone‐refractory disease and stable expression of p53 gain‐of‐function (p53GOF) alleles support growth of LNCaP in androgen‐depleted medium. In this study, we performed gene expression profiling of four LNCaP‐p53GOF sublines to test the hypothesis that different p53GOF mutants mediated androgen independence via modulation of a common set of genes. METHODS: Expression profiling was performed using Affymetrix HG‐U95Av2 arrays followed by hierarchical clustering to identify expression patterns associated with particular molecular alterations. p53GOF‐mediated regulation of Id‐1 expression was validated by RT‐PCR and dual‐luciferase reporter assays. RNA interference was used to investigate the effects of Id‐1 and Id‐3 suppression. RESULTS: LNCaP‐p53GOF sublines possessed a molecular signature consisting of 95 differentially regulated genes that could be segregated into two clusters of transcripts induced (n = 50) and repressed (n = 45) by p53GOF expression. To begin validating these genes as effectors of the p53 mutants, we evaluated one of the overexpressed genes, Id‐1. RT‐PCR confirmed the microarray results and revealed elevated Id‐1 levels in LNCaP‐p53‐P151S (loss‐of‐function only mutant), thereby implicating p53 mutational inactivation, but not gain‐of‐function, as a basis for Id‐1 deregulation. Reporter assays demonstrated enhanced Id‐1 promoter activity in an LNCaP‐p53GOF subline. The contribution of Id‐1 to p53GOF‐mediated biology was demonstrated by the ability of RNAi‐mediated gene silencing to decrease both basal and androgen‐independent proliferation. CONCLUSIONS: While different p53GOF mutants result in overall distinct expression profiles, they share a common set of differentially‐expressed genes that can be used to signify their presence and provide insight into mechanisms underlying androgen independence. © 2005 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/pros.20308
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Tepper</name><affiliation wicri:level="2"><mods:affiliation>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: cgtepper@ucdavis.edu</mods:affiliation><country wicri:rule="url">États-Unis</country></affiliation><affiliation wicri:level="2"><mods:affiliation>Correspondence address: University of California Davis Medical Center, Research III, Room 2200A, 4645 2nd Avenue, Sacramento, CA 95817.</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Correspondence address: University of California Davis Medical Center, Research III, Room 2200A, 4645 2nd Avenue, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Gregg, Jeffrey P" sort="Gregg, Jeffrey P" uniqKey="Gregg J" first="Jeffrey P." last="Gregg">Jeffrey P. 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Ryan</name><affiliation wicri:level="2"><mods:affiliation>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Desprez, Pierre Ves" sort="Desprez, Pierre Ves" uniqKey="Desprez P" first="Pierre-Yves" last="Desprez">Pierre-Yves Desprez</name><affiliation wicri:level="2"><mods:affiliation>Geraldine Brush Cancer Research Institute, California Pacific Medical Center, San Francisco, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Geraldine Brush Cancer Research Institute, California Pacific Medical Center, San Francisco</wicri:cityArea></affiliation></author><author><name sortKey="Kung, Hsing Ien" sort="Kung, Hsing Ien" uniqKey="Kung H" first="Hsing-Jien" last="Kung">Hsing-Jien Kung</name><affiliation wicri:level="2"><mods:affiliation>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Devere White, Ralph W" sort="Devere White, Ralph W" uniqKey="Devere White R" first="Ralph W." last="Devere White">Ralph W. Devere White</name><affiliation wicri:level="2"><mods:affiliation>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:D186DC9C2947358AF2A8EDA1495760BBF52E9C79</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1002/pros.20308</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-HKHT7DCX-8/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002358</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002358</idno><idno type="wicri:Area/Istex/Curation">002358</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Profiling of gene expression changes caused by p53 gain‐of‐function mutant alleles in prostate cancer cells</title><author><name sortKey="Tepper, Clifford G" sort="Tepper, Clifford G" uniqKey="Tepper C" first="Clifford G." last="Tepper">Clifford G. Tepper</name><affiliation wicri:level="2"><mods:affiliation>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: cgtepper@ucdavis.edu</mods:affiliation><country wicri:rule="url">États-Unis</country></affiliation><affiliation wicri:level="2"><mods:affiliation>Correspondence address: University of California Davis Medical Center, Research III, Room 2200A, 4645 2nd Avenue, Sacramento, CA 95817.</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Correspondence address: University of California Davis Medical Center, Research III, Room 2200A, 4645 2nd Avenue, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Gregg, Jeffrey P" sort="Gregg, Jeffrey P" uniqKey="Gregg J" first="Jeffrey P." last="Gregg">Jeffrey P. Gregg</name><affiliation wicri:level="2"><mods:affiliation>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Shi, Xu Ao" sort="Shi, Xu Ao" uniqKey="Shi X" first="Xu-Bao" last="Shi">Xu-Bao Shi</name><affiliation wicri:level="2"><mods:affiliation>Department of Urology, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Urology, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Vinall, Ruth L" sort="Vinall, Ruth L" uniqKey="Vinall R" first="Ruth L." last="Vinall">Ruth L. Vinall</name><affiliation wicri:level="2"><mods:affiliation>Department of Urology, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Urology, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Baron, Colin A" sort="Baron, Colin A" uniqKey="Baron C" first="Colin A." last="Baron">Colin A. Baron</name><affiliation wicri:level="2"><mods:affiliation>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Ryan, Philip E" sort="Ryan, Philip E" uniqKey="Ryan P" first="Philip E." last="Ryan">Philip E. Ryan</name><affiliation wicri:level="2"><mods:affiliation>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Desprez, Pierre Ves" sort="Desprez, Pierre Ves" uniqKey="Desprez P" first="Pierre-Yves" last="Desprez">Pierre-Yves Desprez</name><affiliation wicri:level="2"><mods:affiliation>Geraldine Brush Cancer Research Institute, California Pacific Medical Center, San Francisco, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Geraldine Brush Cancer Research Institute, California Pacific Medical Center, San Francisco</wicri:cityArea></affiliation></author><author><name sortKey="Kung, Hsing Ien" sort="Kung, Hsing Ien" uniqKey="Kung H" first="Hsing-Jien" last="Kung">Hsing-Jien Kung</name><affiliation wicri:level="2"><mods:affiliation>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author><author><name sortKey="Devere White, Ralph W" sort="Devere White, Ralph W" uniqKey="Devere White R" first="Ralph W." last="Devere White">Ralph W. Devere White</name><affiliation wicri:level="2"><mods:affiliation>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento, California</mods:affiliation><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Division of Basic Sciences, UC Davis Cancer Center, Sacramento</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The Prostate</title><title level="j" type="alt">PROSTATE, THE</title><idno type="ISSN">0270-4137</idno><idno type="eISSN">1097-0045</idno><imprint><biblScope unit="vol">65</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="375">375</biblScope><biblScope unit="page" to="389">389</biblScope><biblScope unit="page-count">15</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-12-01">2005-12-01</date></imprint><idno type="ISSN">0270-4137</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0270-4137</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Allele</term><term>Androgen</term><term>Androgen ablation</term><term>Androgen deprivation</term><term>Androgen independence</term><term>Androgen receptor</term><term>Assay</term><term>Basal</term><term>Basic davis cancer center</term><term>Binding protein</term><term>Cancer center support grant</term><term>Cdna</term><term>Cdna synthesis</term><term>Cell biol</term><term>Cell growth</term><term>Cell line</term><term>Cell lines</term><term>Cell lysates</term><term>Comparison analysis</term><term>Constitutive expression</term><term>Davis schoolof medicine</term><term>Differentially</term><term>Disease association</term><term>Duplex</term><term>Empty bars</term><term>Epper</term><term>Expression data</term><term>Expression level</term><term>Expression signature</term><term>Gain insight</term><term>Gene</term><term>Gene alterations</term><term>Gene expression</term><term>Gene expression changes</term><term>Gene expression signature</term><term>Gene mutation</term><term>Gene name</term><term>Genechip arrays</term><term>Grant number</term><term>Grant sponsor</term><term>Growth arrest</term><term>Growth inhibition</term><term>Human genome</term><term>Human prostate carcinoma</term><term>Invitrogen life technologies</term><term>Lncap</term><term>Lncap cells</term><term>Lncap cells transfected</term><term>Lncap prostate cancer cells</term><term>Lncap sublines</term><term>Luciferase</term><term>Melanoma antigen family</term><term>Metastatic</term><term>Microarray</term><term>Microarray analysis</term><term>Microarray gene expression</term><term>Microarray results</term><term>Model system</term><term>Mutant</term><term>Mutant alleles</term><term>Mutation</term><term>Mutational inactivation</term><term>Natl cancer inst</term><term>Nucleotide positions sense</term><term>Oligonucleotide arrays</term><term>Oncogene</term><term>Overexpressed genes</term><term>Overexpression</term><term>Pathway</term><term>Primary tumors</term><term>Proc natl acad</term><term>Progression</term><term>Proliferation</term><term>Promoter</term><term>Promoter activity</term><term>Prostate</term><term>Prostate cancer</term><term>Prostate epithelial cells</term><term>Protein expression</term><term>Proximal promoter region</term><term>Reagent</term><term>Receptor</term><term>Renilla luciferase activities</term><term>Reporter assays</term><term>Ribosomal protein</term><term>Rnai experiments</term><term>Signal detection</term><term>Simultaneous expression analysis</term><term>Sirna</term><term>Sirnas</term><term>Solute carrier family</term><term>Stable expression</term><term>Sublines</term><term>Suppressor</term><term>Target genes</term><term>Transcription</term><term>Transfected</term><term>Tumor development</term><term>Tumor phenotype</term><term>Tumor progression</term><term>Tumor suppressor</term><term>Tumor suppressor gene</term><term>Unique expression</term><term>Wang</term><term>Wild type</term><term>Wong</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">BACKGROUND: Tumor suppressor p53 mutations are associated with the transition of prostate cancer to metastatic, hormone‐refractory disease and stable expression of p53 gain‐of‐function (p53GOF) alleles support growth of LNCaP in androgen‐depleted medium. In this study, we performed gene expression profiling of four LNCaP‐p53GOF sublines to test the hypothesis that different p53GOF mutants mediated androgen independence via modulation of a common set of genes. METHODS: Expression profiling was performed using Affymetrix HG‐U95Av2 arrays followed by hierarchical clustering to identify expression patterns associated with particular molecular alterations. p53GOF‐mediated regulation of Id‐1 expression was validated by RT‐PCR and dual‐luciferase reporter assays. RNA interference was used to investigate the effects of Id‐1 and Id‐3 suppression. RESULTS: LNCaP‐p53GOF sublines possessed a molecular signature consisting of 95 differentially regulated genes that could be segregated into two clusters of transcripts induced (n = 50) and repressed (n = 45) by p53GOF expression. To begin validating these genes as effectors of the p53 mutants, we evaluated one of the overexpressed genes, Id‐1. RT‐PCR confirmed the microarray results and revealed elevated Id‐1 levels in LNCaP‐p53‐P151S (loss‐of‐function only mutant), thereby implicating p53 mutational inactivation, but not gain‐of‐function, as a basis for Id‐1 deregulation. Reporter assays demonstrated enhanced Id‐1 promoter activity in an LNCaP‐p53GOF subline. The contribution of Id‐1 to p53GOF‐mediated biology was demonstrated by the ability of RNAi‐mediated gene silencing to decrease both basal and androgen‐independent proliferation. CONCLUSIONS: While different p53GOF mutants result in overall distinct expression profiles, they share a common set of differentially‐expressed genes that can be used to signify their presence and provide insight into mechanisms underlying androgen independence. © 2005 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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