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  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/bf01753886.

Title:
Oncogene-induced basement membrane invasiveness in human mammary epithelial cells | Clinical & Experimental Metastasis
Description:
Expression of the intermediate filament protein vimentin, and loss of the cellular adhesion protein uvomorulin (E-cadherin) have been associated with increased invasiveness of established human breast cancer cell linesin vitro andin vivo. In the current study, we have further examined these relationships in oncogenically transformed human mammary epithelial cells. A normal human mammary epithelial strain, termed 184, was previously immortalized with benzo[a]pyrene, and two distinct sublines were derived (A1N4 and 184B5). These sublines were infected with retroviral vectors containing a single or two oncogenes of the nuclear, cytoplasmic, and plasma membrane-associated type (v-ras H, v-ras Ki, v -mos, SV40T and c -myc). All infectants have been previously shown to exhibit some aspects of phenotypic transformation. In the current study, cellular invasiveness was determinedin vitro using Matrigel, a reconstituted basement membrane extract. Lineage-specific differences were observed with respect to low constitutive invasiveness and invasive changes after infection withras, despite similarras-induced transformation of each line. Major effects on cellular invasiveness were observed after infection of the cells with two different oncogenes (v-ras H + SV40T and v -ras H + v -mos). In contrast, the effects of single oncogenes were only modest or negligible. All oncogenic infectants demonstrated increased attachment to laminin, but altered secretion of the 72 kDa and 92 kDa gelatinases was not associated with any aspect of malignant progression. Each of the two highly invasive double oncogene transformants were vimentinpositive and uvomorulin-negative, a phenotype indicative of the epithelial-mesenchymal transition (EMT) previously associated with invasiveness of established human breast cancer cell lines. Weakly invasive untransformed mammary epithelial cells in this study were positive for both vimentin and uvomorulin, suggesting that uvomorulin may over-ride the otherwise vimentin-associated invasiveness.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Telecommunications

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 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {πŸ’Έ}

We find it hard to spot revenue streams.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {πŸ”}

google, scholar, human, cancer, cell, breast, cells, epithelial, mammary, res, metastasis, type, invasive, article, expression, basement, thompson, liotta, collagenase, membrane, invasiveness, vimentin, invasion, tumor, usa, normal, growth, metastatic, stampfer, vitro, pathol, research, sommers, dickson, cellular, adhesion, oncogenes, laminin, malignant, natl, privacy, cookies, content, torri, lippman, uvomorulin, increased, transformation, potential, receptor,

Topics {βœ’οΈ}

c-erbb2/neu oncogeneinduced metastasis critical etv4/twist1/vimentin axis epithelial-mesenchymal transition month download article/chapter increased basement membrane-invasiveness node-negative breast cancers nih/3t3 cells transfected mcf-7 cells transfected matrigel-basedin vitro assays basement membrane invasion v-ras ki human breast carcinomas basement membrane invasiveness rat mammary cells cancer-derived extracellular vesicles basement membrane complexes cell surface properties luminal epithelial cells extracellular matrix-degrading potential human carcinoma cells human mammary gland neoplastic breast epithelium normal human macrophages gerontology research center similarras-induced transformation full article pdf lobular breast carcinomas privacy choices/manage cookies cell adhesion molecules human tumor dna related subjects v-ras hormone-responsive variants stetler-stevensen wg cell growth differ breast carcinoma progression rapidin vitro assay ki67 proliferation antigen natl cancer inst tumor cell migration cancer metastasis rev specific adult tissues malignant breast disease molec cell endocr basement membrane stetler-stevenson wg malignant breast tissue expl cell res low constitutive invasiveness clin expl metastasis

Questions {❓}

  • Raymond WA and Leong AS-Y, 1989, Vimentin-a new prognostic parameter in breast carcinoma?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Oncogene-induced basement membrane invasiveness in human mammary epithelial cells
         description:Expression of the intermediate filament protein vimentin, and loss of the cellular adhesion protein uvomorulin (E-cadherin) have been associated with increased invasiveness of established human breast cancer cell linesin vitro andin vivo. In the current study, we have further examined these relationships in oncogenically transformed human mammary epithelial cells. A normal human mammary epithelial strain, termed 184, was previously immortalized with benzo[a]pyrene, and two distinct sublines were derived (A1N4 and 184B5). These sublines were infected with retroviral vectors containing a single or two oncogenes of the nuclear, cytoplasmic, and plasma membrane-associated type (v-ras H, v-ras Ki, v -mos, SV40T and c -myc). All infectants have been previously shown to exhibit some aspects of phenotypic transformation. In the current study, cellular invasiveness was determinedin vitro using Matrigel, a reconstituted basement membrane extract. Lineage-specific differences were observed with respect to low constitutive invasiveness and invasive changes after infection withras, despite similarras-induced transformation of each line. Major effects on cellular invasiveness were observed after infection of the cells with two different oncogenes (v-ras H + SV40T and v -ras H + v -mos). In contrast, the effects of single oncogenes were only modest or negligible. All oncogenic infectants demonstrated increased attachment to laminin, but altered secretion of the 72 kDa and 92 kDa gelatinases was not associated with any aspect of malignant progression. Each of the two highly invasive double oncogene transformants were vimentinpositive and uvomorulin-negative, a phenotype indicative of the epithelial-mesenchymal transition (EMT) previously associated with invasiveness of established human breast cancer cell lines. Weakly invasive untransformed mammary epithelial cells in this study were positive for both vimentin and uvomorulin, suggesting that uvomorulin may over-ride the otherwise vimentin-associated invasiveness.
         datePublished:
         dateModified:
         pageStart:181
         pageEnd:194
         sameAs:https://doi.org/10.1007/BF01753886
         keywords:
            basement membrane
            human breast cancer
            invasion
            oncogene
            uvomorulin
            vimentin
            Cancer Research
            Biomedicine
            general
            Oncology
            Hematology
            Surgical Oncology
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      headline:Oncogene-induced basement membrane invasiveness in human mammary epithelial cells
      description:Expression of the intermediate filament protein vimentin, and loss of the cellular adhesion protein uvomorulin (E-cadherin) have been associated with increased invasiveness of established human breast cancer cell linesin vitro andin vivo. In the current study, we have further examined these relationships in oncogenically transformed human mammary epithelial cells. A normal human mammary epithelial strain, termed 184, was previously immortalized with benzo[a]pyrene, and two distinct sublines were derived (A1N4 and 184B5). These sublines were infected with retroviral vectors containing a single or two oncogenes of the nuclear, cytoplasmic, and plasma membrane-associated type (v-ras H, v-ras Ki, v -mos, SV40T and c -myc). All infectants have been previously shown to exhibit some aspects of phenotypic transformation. In the current study, cellular invasiveness was determinedin vitro using Matrigel, a reconstituted basement membrane extract. Lineage-specific differences were observed with respect to low constitutive invasiveness and invasive changes after infection withras, despite similarras-induced transformation of each line. Major effects on cellular invasiveness were observed after infection of the cells with two different oncogenes (v-ras H + SV40T and v -ras H + v -mos). In contrast, the effects of single oncogenes were only modest or negligible. All oncogenic infectants demonstrated increased attachment to laminin, but altered secretion of the 72 kDa and 92 kDa gelatinases was not associated with any aspect of malignant progression. Each of the two highly invasive double oncogene transformants were vimentinpositive and uvomorulin-negative, a phenotype indicative of the epithelial-mesenchymal transition (EMT) previously associated with invasiveness of established human breast cancer cell lines. Weakly invasive untransformed mammary epithelial cells in this study were positive for both vimentin and uvomorulin, suggesting that uvomorulin may over-ride the otherwise vimentin-associated invasiveness.
      datePublished:
      dateModified:
      pageStart:181
      pageEnd:194
      sameAs:https://doi.org/10.1007/BF01753886
      keywords:
         basement membrane
         human breast cancer
         invasion
         oncogene
         uvomorulin
         vimentin
         Cancer Research
         Biomedicine
         general
         Oncology
         Hematology
         Surgical Oncology
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                  name:Vincent T. Lombardi Cancer Research Center
                  address:
                     name:Vincent T. Lombardi Cancer Research Center, USA
                     type:PostalAddress
                  type:Organization
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            name:Connie L. Sommers
            affiliation:
                  name:Vincent T. Lombardi Cancer Research Center
                  address:
                     name:Vincent T. Lombardi Cancer Research Center, USA
                     type:PostalAddress
                  type:Organization
                  name:Georgetown University Medical Center
                  address:
                     name:Department of Cell Biology, Georgetown University Medical Center, NW Washington, DC, USA
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                  address:
                     name:Vincent T. Lombardi Cancer Research Center, USA
                     type:PostalAddress
                  type:Organization
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            name:George R. Martin
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                  name:National Institute of Dental Research
                  address:
                     name:Laboratory of Developmental Biology, National Institute of Dental Research
                     type:PostalAddress
                  type:Organization
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            name:Marc E. Lippman
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                  address:
                     name:Vincent T. Lombardi Cancer Research Center, USA
                     type:PostalAddress
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            name:Martha R. Stampfer
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                  name:Lawrence Berkeley Laboratory
                  address:
                     name:Lawrence Berkeley Laboratory, USA
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                  address:
                     name:Vincent T. Lombardi Cancer Research Center, USA
                     type:PostalAddress
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      volumeNumber:12
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         name:Laboratory of Developmental Biology, National Institute of Dental Research
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         name:Vincent T. Lombardi Cancer Research Center, USA
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      address:
         name:Lawrence Berkeley Laboratory, USA
         type:PostalAddress
      name:Vincent T. Lombardi Cancer Research Center
      address:
         name:Vincent T. Lombardi Cancer Research Center, USA
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      name:Jeffrey Torri
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            name:Vincent T. Lombardi Cancer Research Center
            address:
               name:Vincent T. Lombardi Cancer Research Center, USA
               type:PostalAddress
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      name:Marybeth Sabol
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            name:Vincent T. Lombardi Cancer Research Center
            address:
               name:Vincent T. Lombardi Cancer Research Center, USA
               type:PostalAddress
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      name:Connie L. Sommers
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            name:Vincent T. Lombardi Cancer Research Center
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               name:Vincent T. Lombardi Cancer Research Center, USA
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               name:Vincent T. Lombardi Cancer Research Center, USA
               type:PostalAddress
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            name:Lawrence Berkeley Laboratory
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               name:Lawrence Berkeley Laboratory, USA
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            address:
               name:Vincent T. Lombardi Cancer Research Center, USA
               type:PostalAddress
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            name:Georgetown University Medical Center
            address:
               name:Department of Cell Biology, Georgetown University Medical Center, NW Washington, DC, USA
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      name:Vincent T. Lombardi Cancer Research Center, USA
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      name:Department of Pathology, University Hospital, Uppsala, Sweden
      name:Vincent T. Lombardi Cancer Research Center, USA
      name:Vincent T. Lombardi Cancer Research Center, USA
      name:Vincent T. Lombardi Cancer Research Center, USA
      name:Department of Cell Biology, Georgetown University Medical Center, NW Washington, DC, USA
      name:Department of Cell Biology, Georgetown University Medical Center, NW Washington, DC, USA
      name:Vincent T. Lombardi Cancer Research Center, USA
      name:Laboratory of Developmental Biology, National Institute of Dental Research
      name:Vincent T. Lombardi Cancer Research Center, USA
      name:Lawrence Berkeley Laboratory, USA
      name:Vincent T. Lombardi Cancer Research Center, USA
      name:Department of Cell Biology, Georgetown University Medical Center, NW Washington, DC, USA
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External Links {πŸ”—}(113)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Clipboard.js
  • Prism.js

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