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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s10585-010-9367-3.

Title:
A systems view of epithelial–mesenchymal transition signaling states | Clinical & Experimental Metastasis
Description:
Epithelial–mesenchymal transition (EMT) is an important contributor to the invasion and metastasis of epithelial-derived cancers. While considerable effort has focused in the regulators involved in the transition process, we have focused on consequences of EMT to prosurvival signaling. Changes in distinct metastable and ‘epigentically-fixed’ EMT states were measured by correlation of protein, phosphoprotein, phosphopeptide and RNA transcript abundance. The assembly of 1167 modulated components into functional systems or machines simplified biological understanding and increased prediction confidence highlighting four functional groups: cell adhesion and migration, metabolism, transcription nodes and proliferation/survival networks. A coordinate metabolic reduction in a cluster of 17 free-radical stress pathway components was observed and correlated with reduced glycolytic and increased oxidative phosphorylation enzyme capacity, consistent with reduced cell cycling and reduced need for macromolecular biosynthesis in the mesenchymal state. An attenuation of EGFR autophosphorylation and a switch from autocrine to paracrine-competent EGFR signaling was implicated in the enablement of tumor cell chemotaxis. A similar attenuation of IGF1R, MET and RON signaling with EMT was observed. In contrast, EMT increased prosurvival autocrine IL11/IL6-JAK2-STAT signaling, autocrine fibronectin-integrin α5β1 activation, autocrine Axl/Tyro3/PDGFR/FGFR RTK signaling and autocrine TGFβR signaling. A relatively uniform loss of polarity and cell–cell junction linkages to actin cytoskeleton and intermediate filaments was measured at a systems level. A more heterogeneous gain of ECM remodeling and associated with invasion and migration was observed. Correlation to stem cell, EMT, invasion and metastasis datasets revealed the greatest similarity with normal and cancerous breast stem cell populations, CD49fhi/EpCAM-/lo and CD44hi/CD24lo, respectively.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

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 can't tell how the site generates income.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

emt, cell, google, scholar, pubmed, cells, cas, cancer, epithelial, mesenchymal, tumor, increased, signaling, models, transition, supplementary, protein, phosphorylation, state, egfr, networks, observed, components, activation, fig, metastable, snail, tgfβ, proteins, res, states, data, autocrine, table, expression, phenotype, mesenchymallike, zeb, survival, receptor, abundance, loss, growth, factor, resistance, genes, systems, rna, nsclc, lines,

Topics {✒️}

included autocrine il11/il6-gp130/jak2/stat tgf-beta-induced epithelial-mesenchymal transition time-lapse live-cell imaging itraq 2d-lc-ms/ms ras-induced raf-mek-erk activation proteomic lc-ms/ms analysis autocrine il6st-jak-stat signaling block nfe2l2/l3-mediated increases itraq-2dlc-ms/ms colony-stimulating factor-1 receptor jak/stat signaling pathways il11/il6-jak/stat fibronectin-mediated α5β1-integrin activation large-scale transcriptional profiling �epigenetically-fixed’ nsclc lines post-transcriptional rna processing pure spindle-cell carcinomas control n1/control n2 reactive oxygen species epithelial-derived carcinoma cells article download pdf epigenetically-fixed chromatin states growth factor receptor active multi-directional communication egf-mediated directional chemotaxis pro-inflammatory cytokine pge2 tumor micro-environment play �epigentically-fixed’ emt states receptor tyrosine kinases restores cell–cell junctions weaken cell–cell junctions serine-threonine kinases pak1 epigenically-fixed emt states large-scale microarray analysis �epigenetically-fixed’ emt state epithelial-derived tumor cells elevated sdf-1/cxcl12 secretion hepatocyte growth factor cell cycle kinases integrin/cadherin switching allowing mesenchymal transition-induced regulator lc-tandem ms lacked e-cadherin expression fixed-state mesenchymal lines notably glutathione s-transferase induce epithelial-mesenchymal transition forms cell–cell junctions cell–cell junction linkages epithelial cell–cell junctions h358/doxzeb1 cells show

Questions {❓}

  • Another question that arises from these findings is what is promoting cell survival and preventing anoikis or senescence, in the absence of EGFR family, IGF1R, Met and Ron signaling, important survival networks for normal epithelium?
  • Blaukovitsch M et al (2006) Sarcomatoid carcinomas of the lung—are these histogenetically heterogeneous tumors?
  • Peinado H, Olmeda D, Cano A (2007) Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?
  • Trachootham D, Alexandre J, Huang P (2009) Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:A systems view of epithelial–mesenchymal transition signaling states
         description:Epithelial–mesenchymal transition (EMT) is an important contributor to the invasion and metastasis of epithelial-derived cancers. While considerable effort has focused in the regulators involved in the transition process, we have focused on consequences of EMT to prosurvival signaling. Changes in distinct metastable and ‘epigentically-fixed’ EMT states were measured by correlation of protein, phosphoprotein, phosphopeptide and RNA transcript abundance. The assembly of 1167 modulated components into functional systems or machines simplified biological understanding and increased prediction confidence highlighting four functional groups: cell adhesion and migration, metabolism, transcription nodes and proliferation/survival networks. A coordinate metabolic reduction in a cluster of 17 free-radical stress pathway components was observed and correlated with reduced glycolytic and increased oxidative phosphorylation enzyme capacity, consistent with reduced cell cycling and reduced need for macromolecular biosynthesis in the mesenchymal state. An attenuation of EGFR autophosphorylation and a switch from autocrine to paracrine-competent EGFR signaling was implicated in the enablement of tumor cell chemotaxis. A similar attenuation of IGF1R, MET and RON signaling with EMT was observed. In contrast, EMT increased prosurvival autocrine IL11/IL6-JAK2-STAT signaling, autocrine fibronectin-integrin Îą5β1 activation, autocrine Axl/Tyro3/PDGFR/FGFR RTK signaling and autocrine TGFβR signaling. A relatively uniform loss of polarity and cell–cell junction linkages to actin cytoskeleton and intermediate filaments was measured at a systems level. A more heterogeneous gain of ECM remodeling and associated with invasion and migration was observed. Correlation to stem cell, EMT, invasion and metastasis datasets revealed the greatest similarity with normal and cancerous breast stem cell populations, CD49fhi/EpCAM-/lo and CD44hi/CD24lo, respectively.
         datePublished:2010-12-31T00:00:00Z
         dateModified:2010-12-31T00:00:00Z
         pageStart:137
         pageEnd:155
         license:https://creativecommons.org/licenses/by-nc/2.0
         sameAs:https://doi.org/10.1007/s10585-010-9367-3
         keywords:
            Cell polarity
            Drug resistance
            Epithelial mesenchymal transition
            EMT
            Non-small cell lung cancer
            Phosphorylation
            Snail
            Systems biology
            TGF beta
            Zeb1
            Kinase
            Cancer Research
            Biomedicine
            general
            Oncology
            Hematology
            Surgical Oncology
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ScholarlyArticle:
      headline:A systems view of epithelial–mesenchymal transition signaling states
      description:Epithelial–mesenchymal transition (EMT) is an important contributor to the invasion and metastasis of epithelial-derived cancers. While considerable effort has focused in the regulators involved in the transition process, we have focused on consequences of EMT to prosurvival signaling. Changes in distinct metastable and ‘epigentically-fixed’ EMT states were measured by correlation of protein, phosphoprotein, phosphopeptide and RNA transcript abundance. The assembly of 1167 modulated components into functional systems or machines simplified biological understanding and increased prediction confidence highlighting four functional groups: cell adhesion and migration, metabolism, transcription nodes and proliferation/survival networks. A coordinate metabolic reduction in a cluster of 17 free-radical stress pathway components was observed and correlated with reduced glycolytic and increased oxidative phosphorylation enzyme capacity, consistent with reduced cell cycling and reduced need for macromolecular biosynthesis in the mesenchymal state. An attenuation of EGFR autophosphorylation and a switch from autocrine to paracrine-competent EGFR signaling was implicated in the enablement of tumor cell chemotaxis. A similar attenuation of IGF1R, MET and RON signaling with EMT was observed. In contrast, EMT increased prosurvival autocrine IL11/IL6-JAK2-STAT signaling, autocrine fibronectin-integrin Îą5β1 activation, autocrine Axl/Tyro3/PDGFR/FGFR RTK signaling and autocrine TGFβR signaling. A relatively uniform loss of polarity and cell–cell junction linkages to actin cytoskeleton and intermediate filaments was measured at a systems level. A more heterogeneous gain of ECM remodeling and associated with invasion and migration was observed. Correlation to stem cell, EMT, invasion and metastasis datasets revealed the greatest similarity with normal and cancerous breast stem cell populations, CD49fhi/EpCAM-/lo and CD44hi/CD24lo, respectively.
      datePublished:2010-12-31T00:00:00Z
      dateModified:2010-12-31T00:00:00Z
      pageStart:137
      pageEnd:155
      license:https://creativecommons.org/licenses/by-nc/2.0
      sameAs:https://doi.org/10.1007/s10585-010-9367-3
      keywords:
         Cell polarity
         Drug resistance
         Epithelial mesenchymal transition
         EMT
         Non-small cell lung cancer
         Phosphorylation
         Snail
         Systems biology
         TGF beta
         Zeb1
         Kinase
         Cancer Research
         Biomedicine
         general
         Oncology
         Hematology
         Surgical Oncology
      image:
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         name:Clinical & Experimental Metastasis
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            1573-7276
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         volumeNumber:28
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer Netherlands
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Stuart Thomson
            affiliation:
                  name:Translational Research, OSI Pharmaceuticals Inc
                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Filippo Petti
            affiliation:
                  name:Translational Research, OSI Pharmaceuticals Inc
                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
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                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
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                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:James Bean
            affiliation:
                  name:Translational Research, OSI Pharmaceuticals Inc
                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Melissa Monaghan
            affiliation:
                  name:Translational Research, OSI Pharmaceuticals Inc
                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
                  type:Organization
            type:Person
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                  name:AB Sciex
                  address:
                     name:AB Sciex, Foster City, USA
                     type:PostalAddress
                  type:Organization
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            name:Gretchen M. Argast
            affiliation:
                  name:Translational Research, OSI Pharmaceuticals Inc
                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:David M. Epstein
            affiliation:
                  name:Translational Research, OSI Pharmaceuticals Inc
                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:John D. Haley
            affiliation:
                  name:Translational Research, OSI Pharmaceuticals Inc
                  address:
                     name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
                     type:PostalAddress
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      name:Clinical & Experimental Metastasis
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      volumeNumber:28
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         name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
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      name:Translational Research, OSI Pharmaceuticals Inc
      address:
         name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
         type:PostalAddress
      name:AB Sciex
      address:
         name:AB Sciex, Foster City, USA
         type:PostalAddress
      name:Translational Research, OSI Pharmaceuticals Inc
      address:
         name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
         type:PostalAddress
      name:Translational Research, OSI Pharmaceuticals Inc
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         name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
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      name:Stuart Thomson
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            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
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      name:Filippo Petti
      affiliation:
            name:Translational Research, OSI Pharmaceuticals Inc
            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
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      name:Izabela Sujka-Kwok
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            name:Translational Research, OSI Pharmaceuticals Inc
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               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
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      name:Peter Mercado
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            name:Translational Research, OSI Pharmaceuticals Inc
            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
            type:Organization
      name:James Bean
      affiliation:
            name:Translational Research, OSI Pharmaceuticals Inc
            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
            type:Organization
      name:Melissa Monaghan
      affiliation:
            name:Translational Research, OSI Pharmaceuticals Inc
            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
            type:Organization
      name:Sean L. Seymour
      affiliation:
            name:AB Sciex
            address:
               name:AB Sciex, Foster City, USA
               type:PostalAddress
            type:Organization
      name:Gretchen M. Argast
      affiliation:
            name:Translational Research, OSI Pharmaceuticals Inc
            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
            type:Organization
      name:David M. Epstein
      affiliation:
            name:Translational Research, OSI Pharmaceuticals Inc
            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
            type:Organization
      name:John D. Haley
      affiliation:
            name:Translational Research, OSI Pharmaceuticals Inc
            address:
               name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:AB Sciex, Foster City, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA
      name:Translational Research, OSI Pharmaceuticals Inc, Farmingdale, USA

External Links {🔗}(255)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

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