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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

We are analyzing https://link.springer.com/article/10.1007/bf00690601.

Title:
Modulation of tumor cell gene expression and phenotype by the organspecific metastatic environment | Cancer and Metastasis Reviews
Description:
Cancer and Metastasis Reviews - The mechanistic basis of a metastatic cell
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Business & Finance

Content Management System {πŸ“}

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 {πŸ“ˆ}

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 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

The income method remains a mystery to us.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {πŸ”}

google, scholar, cancer, human, growth, cell, cells, res, expression, factor, metastasis, receptor, gene, tumor, melanoma, epidermal, fidler, metastatic, resistance, natl, colon, radinsky, biol, multidrug, nature, murine, inst, carcinoma, mouse, article, regulation, hormone, fan, sci, receptors, usa, apoptosis, acad, vogelstein, pglycoprotein, organspecific, organ, differentiation, rev, nude, mice, bucana, clin, proc, function,

Topics {βœ’οΈ}

Ξ±-melanocyte-stimulating hormone receptors melanocyte-stimulating hormone receptor melanocyte-stimulating hormone responsive receptor-tyrosine kinases expression month download article/chapter develop organ-specific metastases increased mdr-1/p-glycoprotein expression wild-type human p53 organ-specific metastatic site antireceptor monoclonal antibodies paraffin-embedded surgical specimens distinct p-glycoprotein precursors epidermal growth factor tumour necrosis factor transforming growth factor p-glycoprotein predict response autocrine/paracrine growth factors mousemdr gene family privacy choices/manage cookies human colon carcinoma human colon carcinomas experimental metastasis correlates colon carcinoma cells gene expression signatures receptor proteintyrosine kinases wild type p53 wild-type p53 site specific metastasis site-specific metastasis tissue-specific manner brain tumour progression p53 mutant cells tgf-Ξ±-pe38 organ-specific modulation multidrug resistance gene cultured human melanocytes mutant p53 proteins mdr1 rna levels intracranial human glioma steadystatemdr gene expression metastasis reviews aims p53 gene occur human melanoma cells experimental lung metastases bone gla-protein msh receptor expression human cancer metastasis human multidrug resistance radiation-induced apoptosis multidrug-resistant cells

Questions {❓}

  • Dalton WS, Grogan TM: Does P-glycoprotein predict response to chemotherapy, and if so, is there a reliable way to detect it?
  • Kerbel RS, Kobayashi H, Graham CH: Intrinsic or acquired drug resistance and metastasis: Are they linked phenotypes?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Modulation of tumor cell gene expression and phenotype by the organspecific metastatic environment
         description:The mechanistic basis of a metastatic cell's ability to proliferate in the parenchyma of certain organs and develop organ-specific metastases is under intense investigation. Signals from paracrine or autocrine pathways, alone or in combination, may regulate tumor cell proliferation with the eventual outcome dependent on the net balance of stimulatory and inhibitory factors. This article summarizes recent reports from our laboratory and others demonstrating that the organ microenvironment can profoundly influence the pattern of gene expression and the biological phenotype of metastatic tumor cells, including induction of melanocyte stimulating hormone receptor and production of melanin, regulation of terminal differentiation and apoptosis, resistance to chemotherapy, and regulation of growth at the organ-specific metastatic site. These recent data from both murine and human tumor models support the concept that the microenvironment of different organs can influence the pattern of gene expression and hence the phenotype of tumor cells at different steps of the metastatic process. These findings have obvious implications for the therapy of neoplasms in general and metastases in particular.
         datePublished:
         dateModified:
         pageStart:323
         pageEnd:338
         sameAs:https://doi.org/10.1007/BF00690601
         keywords:
            gene expression
            organ-specific metastasis
            melanin production
            terminal differentiation and apoptosis
            multidrug resistance
            colon cancer
            Cancer Research
            Oncology
            Biomedicine
            general
         image:
         isPartOf:
            name:Cancer and Metastasis Reviews
            issn:
               1573-7233
               0167-7659
            volumeNumber:14
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               Periodical
               PublicationVolume
         publisher:
            name:Kluwer Academic Publishers
            logo:
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               type:ImageObject
            type:Organization
         author:
               name:Robert Radinsky
               affiliation:
                     name:The University of Texas M.D. Anderson Cancer Center
                     address:
                        name:The Department of Cell Biology, The University of Texas M.D. Anderson Cancer Center, Houston, USA
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ScholarlyArticle:
      headline:Modulation of tumor cell gene expression and phenotype by the organspecific metastatic environment
      description:The mechanistic basis of a metastatic cell's ability to proliferate in the parenchyma of certain organs and develop organ-specific metastases is under intense investigation. Signals from paracrine or autocrine pathways, alone or in combination, may regulate tumor cell proliferation with the eventual outcome dependent on the net balance of stimulatory and inhibitory factors. This article summarizes recent reports from our laboratory and others demonstrating that the organ microenvironment can profoundly influence the pattern of gene expression and the biological phenotype of metastatic tumor cells, including induction of melanocyte stimulating hormone receptor and production of melanin, regulation of terminal differentiation and apoptosis, resistance to chemotherapy, and regulation of growth at the organ-specific metastatic site. These recent data from both murine and human tumor models support the concept that the microenvironment of different organs can influence the pattern of gene expression and hence the phenotype of tumor cells at different steps of the metastatic process. These findings have obvious implications for the therapy of neoplasms in general and metastases in particular.
      datePublished:
      dateModified:
      pageStart:323
      pageEnd:338
      sameAs:https://doi.org/10.1007/BF00690601
      keywords:
         gene expression
         organ-specific metastasis
         melanin production
         terminal differentiation and apoptosis
         multidrug resistance
         colon cancer
         Cancer Research
         Oncology
         Biomedicine
         general
      image:
      isPartOf:
         name:Cancer and Metastasis Reviews
         issn:
            1573-7233
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         name:Kluwer Academic Publishers
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Robert Radinsky
            affiliation:
                  name:The University of Texas M.D. Anderson Cancer Center
                  address:
                     name:The Department of Cell Biology, The University of Texas M.D. Anderson Cancer Center, Houston, USA
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      name:Cancer and Metastasis Reviews
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         1573-7233
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      volumeNumber:14
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      name:Kluwer Academic Publishers
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:The University of Texas M.D. Anderson Cancer Center
      address:
         name:The Department of Cell Biology, The University of Texas M.D. Anderson Cancer Center, Houston, USA
         type:PostalAddress
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      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
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      name:Robert Radinsky
      affiliation:
            name:The University of Texas M.D. Anderson Cancer Center
            address:
               name:The Department of Cell Biology, The University of Texas M.D. Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:The Department of Cell Biology, The University of Texas M.D. Anderson Cancer Center, Houston, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {πŸ”—}(167)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • AOS
  • Clipboard.js
  • Prism.js

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