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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. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s10555-016-9650-0.

Title:
From transformation to metastasis: deconstructing the extracellular matrix in breast cancer | Cancer and Metastasis Reviews
Description:
The extracellular matrix (ECM) is a guiding force that regulates various developmental stages of the breast. In addition to providing structural support for the cells, it mediates epithelial-stromal communication and provides cues for cell survival, proliferation, and differentiation. Perturbations in ECM architecture profoundly influence breast tumor progression and metastasis. Understanding how a dysregulated ECM can facilitate malignant transformation is crucial to designing treatments to effectively target the tumor microenvironment. Here, we address the contribution of ECM mechanics to breast cancer progression, metastasis, and treatment resistance and discuss potential therapeutic strategies targeting the ECM.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Health & Fitness

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 7,626,932 visitors per month in the current month.

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

We see no obvious way the site makes money.

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 might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {πŸ”}

cancer, pubmed, google, scholar, article, breast, cas, doi, cell, journal, matrix, research, central, tumor, biology, nature, weaver, metastasis, extracellular, cells, collagen, mammary, ecm, progression, metastatic, clinical, reviews, gland, development, niche, expression, human, carcinoma, oncology, lysyl, valerie, treatment, keely, oxidase, access, stiffness, medicine, receptor, gene, american, erler, premetastatic, ucsf, usa, content,

Topics {βœ’οΈ}

integrin-regulated fak-src signaling tgf-Ξ² blockade improves tamoxifen-resistant breast carcinomas month download article/chapter integrin-linked kinase ilk mediates epithelial-stromal communication node-positive breast cancer fibroblast-derived matrix proteins matrix density-induced mechanoregulation lox/hypoxia axis reverses single-cell analysis reveals tumor-extracellular matrix interactions modulating cellular metabolism hypoxia-induced lysyl oxidase lysyl oxidase inhibitor tumour-stromal interactions full article pdf discoidin domain receptors promotes tumor progression elastin gene expression epithelial cell lines tumor-specific expression vegfr1-positive erler hypoxia-inducible factor 1 extracellular matrix modulates endothelial cell behavior privacy choices/manage cookies nih public access mechanics meets morphogenesis initial bone metastasis eukaryotic gene expression gene expression profiling focal adhesion kinase focal complex development myeloid progenitor cells epithelial transition breast tumor progression extracellular matrix collagen human breast carcinoma mammary tumor induction transgenic mouse model fak-erk linkage deletion decreases atherosclerosis human breast cancer hypoxia-induced metastasis stem-cell program organ-specific colonization tumor collagenous matrix extracellular matrix degradation extracellular matrix assembly

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:From transformation to metastasis: deconstructing the extracellular matrix in breast cancer
         description:The extracellular matrix (ECM) is a guiding force that regulates various developmental stages of the breast. In addition to providing structural support for the cells, it mediates epithelial-stromal communication and provides cues for cell survival, proliferation, and differentiation. Perturbations in ECM architecture profoundly influence breast tumor progression and metastasis. Understanding how a dysregulated ECM can facilitate malignant transformation is crucial to designing treatments to effectively target the tumor microenvironment. Here, we address the contribution of ECM mechanics to breast cancer progression, metastasis, and treatment resistance and discuss potential therapeutic strategies targeting the ECM.
         datePublished:2016-12-02T00:00:00Z
         dateModified:2016-12-02T00:00:00Z
         pageStart:655
         pageEnd:667
         sameAs:https://doi.org/10.1007/s10555-016-9650-0
         keywords:
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            Breast cancer
            Desmoplasia
            Mechanosignaling
            Metastasis
            Treatment resistance
            Cancer Research
            Oncology
            Biomedicine
            general
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            name:Cancer and Metastasis Reviews
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                        name:Department of Radiation Oncology, UCSF, San Francisco, USA
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                        name:UCSF Helen Diller Comprehensive Cancer Center, UCSF, San Francisco, USA
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      headline:From transformation to metastasis: deconstructing the extracellular matrix in breast cancer
      description:The extracellular matrix (ECM) is a guiding force that regulates various developmental stages of the breast. In addition to providing structural support for the cells, it mediates epithelial-stromal communication and provides cues for cell survival, proliferation, and differentiation. Perturbations in ECM architecture profoundly influence breast tumor progression and metastasis. Understanding how a dysregulated ECM can facilitate malignant transformation is crucial to designing treatments to effectively target the tumor microenvironment. Here, we address the contribution of ECM mechanics to breast cancer progression, metastasis, and treatment resistance and discuss potential therapeutic strategies targeting the ECM.
      datePublished:2016-12-02T00:00:00Z
      dateModified:2016-12-02T00:00:00Z
      pageStart:655
      pageEnd:667
      sameAs:https://doi.org/10.1007/s10555-016-9650-0
      keywords:
         Extracellular matrix (ECM)
         Breast cancer
         Desmoplasia
         Mechanosignaling
         Metastasis
         Treatment resistance
         Cancer Research
         Oncology
         Biomedicine
         general
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                     type:PostalAddress
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                     name:Center for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, USA
                     type:PostalAddress
                  type:Organization
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                     name:Center for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, USA
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                     name:Department of Anatomy, UCSF, San Francisco, USA
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                     name:Department of Bioengineering and Therapeutic Sciences, UCSF, San Francisco, USA
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                     name:Department of Radiation Oncology, UCSF, San Francisco, USA
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                  name:UCSF
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                     name:UCSF Helen Diller Comprehensive Cancer Center, UCSF, San Francisco, USA
                     type:PostalAddress
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                  address:
                     name:Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, UCSF, San Francisco, USA
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         name:Center for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, USA
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         name:Department of Anatomy, UCSF, San Francisco, USA
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      address:
         name:Department of Bioengineering and Therapeutic Sciences, UCSF, San Francisco, USA
         type:PostalAddress
      name:UCSF
      address:
         name:Department of Radiation Oncology, UCSF, San Francisco, USA
         type:PostalAddress
      name:UCSF
      address:
         name:UCSF Helen Diller Comprehensive Cancer Center, UCSF, San Francisco, USA
         type:PostalAddress
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      address:
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               type:PostalAddress
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      name:Michael W Pickup
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            address:
               name:Center for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, USA
               type:PostalAddress
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      name:Valerie M Weaver
      affiliation:
            name:UCSF
            address:
               name:Center for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, USA
               type:PostalAddress
            type:Organization
            name:UCSF
            address:
               name:Department of Anatomy, UCSF, San Francisco, USA
               type:PostalAddress
            type:Organization
            name:UCSF
            address:
               name:Department of Bioengineering and Therapeutic Sciences, UCSF, San Francisco, USA
               type:PostalAddress
            type:Organization
            name:UCSF
            address:
               name:Department of Radiation Oncology, UCSF, San Francisco, USA
               type:PostalAddress
            type:Organization
            name:UCSF
            address:
               name:UCSF Helen Diller Comprehensive Cancer Center, UCSF, San Francisco, USA
               type:PostalAddress
            type:Organization
            name:UCSF
            address:
               name:Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, UCSF, San Francisco, USA
               type:PostalAddress
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      name:Department of Anatomy, UCSF, San Francisco, USA
      name:Department of Bioengineering and Therapeutic Sciences, UCSF, San Francisco, USA
      name:Department of Radiation Oncology, UCSF, San Francisco, USA
      name:UCSF Helen Diller Comprehensive Cancer Center, UCSF, San Francisco, USA
      name:Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, UCSF, San Francisco, USA
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External Links {πŸ”—}(350)

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