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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
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We are analyzing https://link.springer.com/article/10.1186/bcr416.

Title:
E-cadherin and loss of heterozygosity at chromosome 16 in breast carcinogenesis: different genetic pathways in ductal and lobular breast cancer? | Breast Cancer Research
Description:
Loss of heterozygosity at the long arm of chromosome 16 is one of the most frequent genetic events in breast cancer. In the search for tumour suppressor genes that are the target of loss of heterozygosity at 16q, the E-cadherin gene CDH1 was unveiled by the identification of truncating mutations in the retained copy. However, only lobular tumours showed E-cadherin mutations. Whereas investigations are still devoted to finding the target genes in the more frequent ductal breast cancers, other studies suspect the E-cadherin gene to also be the target in this tumour type. The present article discusses the plausibility of those two lines of thought.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Health & Fitness
  • Education
  • Science

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}

We can't figure out the monetization strategy.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {πŸ”}

ecadherin, breast, cancer, pubmed, lobular, loh, google, scholar, article, carcinoma, cas, ductal, tumour, loss, gene, cdh, van, situ, genetic, mutations, tumours, expression, heterozygosity, cletonjansen, gastric, genes, dcis, lcis, chromosome, suppressor, central, data, target, carcinomas, protein, inactivation, cornelisse, frequent, mutation, cells, model, invasive, role, vos, human, roy, function, cellular, event, progression,

Topics {βœ’οΈ}

suppresses beta-catenin–lef/tcf-dependent transcription anne-marie cleton-jansen e-cadherin invasion-suppressor gene high-throughput screening methods de leeuw wj e-cadherin mutation status detectable e-cadherin mutation germline e-cadherin gene regulate e-cadherin transcription article cleton-jansen e-cadherin gene expression e-cadherin protein expression e-cadherin germline mutations somatic e-cadherin mutations e-cadherin gene cdh1 absent e-cadherin protein e-cadherin plasma membrane decreased e-cadherin expression de leeuw wjf dr cbj vos e-cadherin staining tumour suppressor gene present article discusses privacy choices/manage cookies e-cadherin gene cleton-jansen a mutation detection method de herreros ag e-cadherin expression human e-cadherin tumour suppressor genes references vleminckx e-cadherin molecules anchor e-cadherin e-cadherin activity detect e-cadherin breast cancer progression e-cad-herin central role breast tumors stratified diffuse gastric cancer invasion suppressor function epithelial tumour cells lobular tumour cells invasion suppressor role e-cadherin inactivation european economic area integrin-linked kinase [6] comparative genomic hybridisation rate-limiting factor

Questions {❓}

  • Beavon IR: Regulation of E-cadherin: does hypoxia initiate the metastatic cascade?
  • E-cadherin and loss of heterozygosity at chromosome 16 in breast carcinogenesis: different genetic pathways in ductal and lobular breast cancer?
  • E-cadherin and loss of heterozygosity at chromosome 16 in breast carcinogenesis: different genetic pathways in ductal and lobular breast cancer?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:E-cadherin and loss of heterozygosity at chromosome 16 in breast carcinogenesis: different genetic pathways in ductal and lobular breast cancer?
         description:Loss of heterozygosity at the long arm of chromosome 16 is one of the most frequent genetic events in breast cancer. In the search for tumour suppressor genes that are the target of loss of heterozygosity at 16q, the E-cadherin gene CDH1 was unveiled by the identification of truncating mutations in the retained copy. However, only lobular tumours showed E-cadherin mutations. Whereas investigations are still devoted to finding the target genes in the more frequent ductal breast cancers, other studies suspect the E-cadherin gene to also be the target in this tumour type. The present article discusses the plausibility of those two lines of thought.
         datePublished:2001-12-31T00:00:00Z
         dateModified:2001-12-31T00:00:00Z
         pageStart:1
         pageEnd:4
         sameAs:https://doi.org/10.1186/bcr416
         keywords:
            hereditary cancer
            loss of heterozygosity
            mutation
            tumour progression
            tumour suppressor genes
            Cancer Research
            Oncology
            Surgical Oncology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fbcr416/MediaObjects/13058_2001_Article_420_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fbcr416/MediaObjects/13058_2001_Article_420_HTML.jpg
         isPartOf:
            name:Breast Cancer Research
            issn:
               1465-542X
            volumeNumber:4
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Anne-Marie Cleton-Jansen
               affiliation:
                     name:Leiden University Medical Centre
                     address:
                        name:Departments of Pathology and Human and Clinical Genetics, Leiden University Medical Centre, Leiden, The Netherlands
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:E-cadherin and loss of heterozygosity at chromosome 16 in breast carcinogenesis: different genetic pathways in ductal and lobular breast cancer?
      description:Loss of heterozygosity at the long arm of chromosome 16 is one of the most frequent genetic events in breast cancer. In the search for tumour suppressor genes that are the target of loss of heterozygosity at 16q, the E-cadherin gene CDH1 was unveiled by the identification of truncating mutations in the retained copy. However, only lobular tumours showed E-cadherin mutations. Whereas investigations are still devoted to finding the target genes in the more frequent ductal breast cancers, other studies suspect the E-cadherin gene to also be the target in this tumour type. The present article discusses the plausibility of those two lines of thought.
      datePublished:2001-12-31T00:00:00Z
      dateModified:2001-12-31T00:00:00Z
      pageStart:1
      pageEnd:4
      sameAs:https://doi.org/10.1186/bcr416
      keywords:
         hereditary cancer
         loss of heterozygosity
         mutation
         tumour progression
         tumour suppressor genes
         Cancer Research
         Oncology
         Surgical Oncology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fbcr416/MediaObjects/13058_2001_Article_420_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fbcr416/MediaObjects/13058_2001_Article_420_HTML.jpg
      isPartOf:
         name:Breast Cancer Research
         issn:
            1465-542X
         volumeNumber:4
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Anne-Marie Cleton-Jansen
            affiliation:
                  name:Leiden University Medical Centre
                  address:
                     name:Departments of Pathology and Human and Clinical Genetics, Leiden University Medical Centre, Leiden, The Netherlands
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Breast Cancer Research
      issn:
         1465-542X
      volumeNumber:4
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Leiden University Medical Centre
      address:
         name:Departments of Pathology and Human and Clinical Genetics, Leiden University Medical Centre, Leiden, The Netherlands
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Anne-Marie Cleton-Jansen
      affiliation:
            name:Leiden University Medical Centre
            address:
               name:Departments of Pathology and Human and Clinical Genetics, Leiden University Medical Centre, Leiden, The Netherlands
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Departments of Pathology and Human and Clinical Genetics, Leiden University Medical Centre, Leiden, The Netherlands

External Links {πŸ”—}(110)

Analytics and Tracking {πŸ“Š}

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3.9s.