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  4. Monthly Traffic Estimate
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We are analyzing https://link.springer.com/article/10.1186/gb-2006-7-4-r28.

Title:
Genes regulated by estrogen in breast tumor cells in vitro are similarly regulated in vivoin tumor xenografts and human breast tumors | Genome Biology
Description:
Background Estrogen plays a central role in breast cancer pathogenesis. Although many studies have characterized the estrogen regulation of genes using in vitro cell culture models by global mRNA expression profiling, it is not clear whether these genes are similarly regulated in vivo or how they might be coordinately expressed in primary human tumors. Results We generated DNA microarray-based gene expression profiles from three estrogen receptor α (ERα)-positive breast cancer cell lines stimulated by 17β-estradiol (E2) in vitro over a time course, as well as from MCF-7 cells grown as xenografts in ovariectomized athymic nude mice with E2 supplementation and after its withdrawal. When the patterns of genes regulated by E2 in vitro were compared to those obtained from xenografts, we found a remarkable overlap (over 40%) of genes regulated by E2 in both contexts. These patterns were compared to those obtained from published clinical data sets. We show that, as a group, E2-regulated genes from our preclinical models were co-expressed with ERα in a panel of ERα+ breast tumor mRNA profiles, when corrections were made for patient age, as well as with progesterone receptor. Furthermore, the E2-regulated genes were significantly enriched for transcriptional targets of the myc oncogene and were found to be coordinately expressed with Myc in human tumors. Conclusion Our results provide significant validation of a widely used in vitro model of estrogen signaling as being pathologically relevant to breast cancers in vivo.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Photography

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

genes, expression, erα, breast, gene, tumors, estrogen, cluster, vitro, myc, cancer, tumor, dataset, figure, pubmed, cell, article, data, google, scholar, mrna, transcripts, human, vivo, cells, significant, enrichment, hours, datasets, cas, patterns, induced, profiles, correlated, profile, clusters, compared, patients, eregulated, set, high, regulated, observed, age, targets, analysis, results, time, found, xenograft,

Topics {✒️}

estrogen-induced/activator protein-1-dependent genes estrogen-receptor-negative breast cancers estrogen-receptor-positive breast cancers cross-species gene-expression analysis pgc-1alpha-responsive genes involved article download pdf article number r28 family-wise error rate phenol red-free imem dna-chip analyzer software term search results conditional myc-estrogen receptor erα-positive cell lines yellow-blue color scale sustained-released e2 pellets gene ontology consortium e2-treated breast cells age-corrected mrna expression remaining e2-inducible genes sustained-release e2 pellets e2-regulated gene signatures age-corrected er expression estrogen-regulated gene clusters authors’ original file er+/pr- breast tumors e2-induced mrna expression e2-induced gene signature estrogen receptor signaling e2-regulated gene clusters v-myb homolog considered erα-negative tumors integrated data-mining platform privacy choices/manage cookies cell cycle-related genes van de vijver identify erα-regulated genes estrogen transcription network multiple gene testing additional data files saldanha aj real-time pcr analysis estrogen-regulated gene cluster 'er/age low' group genes showing e2-regulation 'er/age low' groups transcriptional programs activated progesterone receptor valley biomedical products erα+ breast cancers identified transcription networks

Questions {❓}

  • Sheikh MS, Garcia M, Pujol P, Fontana JA, Rochefort H: Why are estrogen-receptor-negative breast cancers more aggressive than the estrogen-receptor-positive breast cancers?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Genes regulated by estrogen in breast tumor cells in vitro are similarly regulated in vivoin tumor xenografts and human breast tumors
         description:Estrogen plays a central role in breast cancer pathogenesis. Although many studies have characterized the estrogen regulation of genes using in vitro cell culture models by global mRNA expression profiling, it is not clear whether these genes are similarly regulated in vivo or how they might be coordinately expressed in primary human tumors. We generated DNA microarray-based gene expression profiles from three estrogen receptor α (ERα)-positive breast cancer cell lines stimulated by 17β-estradiol (E2) in vitro over a time course, as well as from MCF-7 cells grown as xenografts in ovariectomized athymic nude mice with E2 supplementation and after its withdrawal. When the patterns of genes regulated by E2 in vitro were compared to those obtained from xenografts, we found a remarkable overlap (over 40%) of genes regulated by E2 in both contexts. These patterns were compared to those obtained from published clinical data sets. We show that, as a group, E2-regulated genes from our preclinical models were co-expressed with ERα in a panel of ERα+ breast tumor mRNA profiles, when corrections were made for patient age, as well as with progesterone receptor. Furthermore, the E2-regulated genes were significantly enriched for transcriptional targets of the myc oncogene and were found to be coordinately expressed with Myc in human tumors. Our results provide significant validation of a widely used in vitro model of estrogen signaling as being pathologically relevant to breast cancers in vivo.
         datePublished:2006-04-07T00:00:00Z
         dateModified:2006-04-07T00:00:00Z
         pageStart:1
         pageEnd:13
         license:http://creativecommons.org/licenses/by/2.0/
         sameAs:https://doi.org/10.1186/gb-2006-7-4-r28
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            Gene Ontology
            Additional Data File
            Progesterone Receptor Expression
            Estrogen Signaling
            Profile Dataset
            Animal Genetics and Genomics
            Human Genetics
            Plant Genetics and Genomics
            Microbial Genetics and Genomics
            Bioinformatics
            Evolutionary Biology
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               name:James M Rae
               affiliation:
                     name:University of Michigan Medical Center
                     address:
                        name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
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ScholarlyArticle:
      headline:Genes regulated by estrogen in breast tumor cells in vitro are similarly regulated in vivoin tumor xenografts and human breast tumors
      description:Estrogen plays a central role in breast cancer pathogenesis. Although many studies have characterized the estrogen regulation of genes using in vitro cell culture models by global mRNA expression profiling, it is not clear whether these genes are similarly regulated in vivo or how they might be coordinately expressed in primary human tumors. We generated DNA microarray-based gene expression profiles from three estrogen receptor α (ERα)-positive breast cancer cell lines stimulated by 17β-estradiol (E2) in vitro over a time course, as well as from MCF-7 cells grown as xenografts in ovariectomized athymic nude mice with E2 supplementation and after its withdrawal. When the patterns of genes regulated by E2 in vitro were compared to those obtained from xenografts, we found a remarkable overlap (over 40%) of genes regulated by E2 in both contexts. These patterns were compared to those obtained from published clinical data sets. We show that, as a group, E2-regulated genes from our preclinical models were co-expressed with ERα in a panel of ERα+ breast tumor mRNA profiles, when corrections were made for patient age, as well as with progesterone receptor. Furthermore, the E2-regulated genes were significantly enriched for transcriptional targets of the myc oncogene and were found to be coordinately expressed with Myc in human tumors. Our results provide significant validation of a widely used in vitro model of estrogen signaling as being pathologically relevant to breast cancers in vivo.
      datePublished:2006-04-07T00:00:00Z
      dateModified:2006-04-07T00:00:00Z
      pageStart:1
      pageEnd:13
      license:http://creativecommons.org/licenses/by/2.0/
      sameAs:https://doi.org/10.1186/gb-2006-7-4-r28
      keywords:
         Gene Ontology
         Additional Data File
         Progesterone Receptor Expression
         Estrogen Signaling
         Profile Dataset
         Animal Genetics and Genomics
         Human Genetics
         Plant Genetics and Genomics
         Microbial Genetics and Genomics
         Bioinformatics
         Evolutionary Biology
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            name:Chad J Creighton
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                     type:PostalAddress
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            name:Jose M Larios
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                     name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Rebecca S Miller
            affiliation:
                  name:University of Michigan Medical Center
                  address:
                     name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Michael D Johnson
            affiliation:
                  name:Georgetown University
                  address:
                     name:Department of Oncology, Georgetown University, Washington, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Arul M Chinnaiyan
            affiliation:
                  name:University of Michigan Medical Center
                  address:
                     name:Department of Pathology, University of Michigan Medical Center, Ann Arbor, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Marc E Lippman
            affiliation:
                  name:University of Michigan Medical Center
                  address:
                     name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:James M Rae
            affiliation:
                  name:University of Michigan Medical Center
                  address:
                     name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
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      name:University of Michigan Medical Center
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         type:PostalAddress
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         name:Department of Pathology, University of Michigan Medical Center, Ann Arbor, USA
         type:PostalAddress
      name:University of Michigan Medical Center
      address:
         name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
         type:PostalAddress
      name:University of Michigan Medical Center
      address:
         name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
         type:PostalAddress
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      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Chad J Creighton
      affiliation:
            name:University of Michigan Medical Center
            address:
               name:Bioinformatics Program, University of Michigan Medical Center, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:Kevin E Cordero
      affiliation:
            name:University of Michigan Medical Center
            address:
               name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:Jose M Larios
      affiliation:
            name:University of Michigan Medical Center
            address:
               name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:Rebecca S Miller
      affiliation:
            name:University of Michigan Medical Center
            address:
               name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:Michael D Johnson
      affiliation:
            name:Georgetown University
            address:
               name:Department of Oncology, Georgetown University, Washington, USA
               type:PostalAddress
            type:Organization
      name:Arul M Chinnaiyan
      affiliation:
            name:University of Michigan Medical Center
            address:
               name:Department of Pathology, University of Michigan Medical Center, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:Marc E Lippman
      affiliation:
            name:University of Michigan Medical Center
            address:
               name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:James M Rae
      affiliation:
            name:University of Michigan Medical Center
            address:
               name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Bioinformatics Program, University of Michigan Medical Center, Ann Arbor, USA
      name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
      name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
      name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
      name:Department of Oncology, Georgetown University, Washington, USA
      name:Department of Pathology, University of Michigan Medical Center, Ann Arbor, USA
      name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
      name:Division of Hematology Oncology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA

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