Here's how DOI.ORG makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

DOI . ORG {}

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

We began analyzing https://link.springer.com/article/10.1023/A:1024031731269, but it redirected us to https://link.springer.com/article/10.1023/A:1024031731269. The analysis below is for the second page.

Title[redir]:
Progesterone Receptors A and B Differentially Affect the Growth of Estrogen-Dependent Human Breast Tumor Xenografts | Breast Cancer Research and Treatment
Description:
Sixty to seventy percent of all primary human breast cancers are estrogen-dependent and express both estrogen (ER) and progesterone receptors (PR). Whereas expression of the two naturally occurring PR isoforms, PR-A and PR-B, is close to equimolar in normal human tissues, the ratio of the two receptors varies extensively in tumors. This is important since the two PR are functionally distinct and have differential repressor effects on ER. The PR isoform content may, therefore, affect the outcome of endocrine therapies targeted at ER. Study of PR isoforms is difficult because the two receptors are co-expressed in cells under estradiol stimulation. We have engineered four sets of T47D human breast cancer cells that, independent of estrogen: (i) express only PR-A; (ii) express only PR-B; (iii) are PR-negative; or (iv) contain both PR isoforms. Each of these cell lines was grown into solid tumors in nude mice in a strictly 17Ξ²-estradiol-dependent manner. Results show, first, that PR-A expressing cells grow into tumors that are approximately half the size of PR-B expressing tumors, and second, that the reduced growth of PR-A tumors occurs in the absence of PR ligand. Tamoxifen treatment preferentially inhibited the growth of PR-A tumors, whereas PR-B tumors were unaffected. Thus, PR are not just passive markers of functional ER; the prevalence of PR-A or PR-B may differentially influence tumor phenotype.

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of doi.org 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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {πŸ’Έ}

We don't see any clear sign of profit-making.

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. Doi.org might be cashing in, but we can't detect the method they're using.

Keywords {πŸ”}

breast, google, scholar, cancer, progesterone, human, receptor, receptors, horwitz, article, cell, estrogen, isoforms, cells, res, biol, growth, pra, tumors, access, characterization, chem, content, sartorius, expression, prb, mol, privacy, cookies, function, research, tumor, mice, hormone, endocrinol, usa, steroid, information, publish, search, affect, xenografts, shen, cancers, differential, study, open, tung, takimoto, regulation,

Topics {βœ’οΈ}

strictly 17Ξ²-estradiol-dependent manner hormone-dependent breast cancers month download article/chapter improved relapse-free survival antiprogestin-occupied b-receptors high progesterone-receptor levels progesterone receptor-mediated transcription unique n-terminal segment single steroid-binding subunit cyclin-dependent kinase inhibitors endocrine therapies targeted steroid hormone receptors human breast cancer small breast carcinomas human progesterone receptor human estrogen receptor related subjects specific progesterone receptors clinicopathologic tumor parameters primary breast cancer estrogen receptors alpha privacy choices/manage cookies full article pdf rabbit progesterone receptor unoccupied progesterone receptor receptors varies extensively oestrogen receptor-Ξ± ligand binding specificity malignant breast disease progesterone receptor isoforms differential repressor effects receptor signaling pathways estrogen receptor beta expressing cells grow hormonal prevention tumorigenic cell lines ligand-independent activation promoter-specific repressor normal human tissues differential cofactor binding european economic area limiting factor mediates transcript tissue distribution responses illustrate interactions o'malley bw induce sexual behavior van golen kl differential gene regulation check access instant access

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Progesterone Receptors A and B Differentially Affect the Growth of Estrogen-Dependent Human Breast Tumor Xenografts
         description:Sixty to seventy percent of all primary human breast cancers are estrogen-dependent and express both estrogen (ER) and progesterone receptors (PR). Whereas expression of the two naturally occurring PR isoforms, PR-A and PR-B, is close to equimolar in normal human tissues, the ratio of the two receptors varies extensively in tumors. This is important since the two PR are functionally distinct and have differential repressor effects on ER. The PR isoform content may, therefore, affect the outcome of endocrine therapies targeted at ER. Study of PR isoforms is difficult because the two receptors are co-expressed in cells under estradiol stimulation. We have engineered four sets of T47D human breast cancer cells that, independent of estrogen: (i) express only PR-A; (ii) express only PR-B; (iii) are PR-negative; or (iv) contain both PR isoforms. Each of these cell lines was grown into solid tumors in nude mice in a strictly 17Ξ²-estradiol-dependent manner. Results show, first, that PR-A expressing cells grow into tumors that are approximately half the size of PR-B expressing tumors, and second, that the reduced growth of PR-A tumors occurs in the absence of PR ligand. Tamoxifen treatment preferentially inhibited the growth of PR-A tumors, whereas PR-B tumors were unaffected. Thus, PR are not just passive markers of functional ER; the prevalence of PR-A or PR-B may differentially influence tumor phenotype.
         datePublished:
         dateModified:
         pageStart:287
         pageEnd:299
         sameAs:https://doi.org/10.1023/A:1024031731269
         keywords:
            breast cancers
            estrogens
            ligand-independence
            progesterone receptors
            xenografts
            Oncology
         image:
         isPartOf:
            name:Breast Cancer Research and Treatment
            issn:
               1573-7217
               0167-6806
            volumeNumber:79
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Kluwer Academic Publishers
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Carol A. Sartorius
               affiliation:
                     name:University of Colorado Health Sciences Center
                     address:
                        name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Tianjie Shen
               affiliation:
                     name:University of Colorado Health Sciences Center
                     address:
                        name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Kathryn B. Horwitz
               affiliation:
                     name:University of Colorado Health Sciences Center
                     address:
                        name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
                        type:PostalAddress
                     type:Organization
                     name:University of Colorado Health Sciences Center
                     address:
                        name:Department of Pathology, University of Colorado Health Sciences Center, Denver, USA
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Progesterone Receptors A and B Differentially Affect the Growth of Estrogen-Dependent Human Breast Tumor Xenografts
      description:Sixty to seventy percent of all primary human breast cancers are estrogen-dependent and express both estrogen (ER) and progesterone receptors (PR). Whereas expression of the two naturally occurring PR isoforms, PR-A and PR-B, is close to equimolar in normal human tissues, the ratio of the two receptors varies extensively in tumors. This is important since the two PR are functionally distinct and have differential repressor effects on ER. The PR isoform content may, therefore, affect the outcome of endocrine therapies targeted at ER. Study of PR isoforms is difficult because the two receptors are co-expressed in cells under estradiol stimulation. We have engineered four sets of T47D human breast cancer cells that, independent of estrogen: (i) express only PR-A; (ii) express only PR-B; (iii) are PR-negative; or (iv) contain both PR isoforms. Each of these cell lines was grown into solid tumors in nude mice in a strictly 17Ξ²-estradiol-dependent manner. Results show, first, that PR-A expressing cells grow into tumors that are approximately half the size of PR-B expressing tumors, and second, that the reduced growth of PR-A tumors occurs in the absence of PR ligand. Tamoxifen treatment preferentially inhibited the growth of PR-A tumors, whereas PR-B tumors were unaffected. Thus, PR are not just passive markers of functional ER; the prevalence of PR-A or PR-B may differentially influence tumor phenotype.
      datePublished:
      dateModified:
      pageStart:287
      pageEnd:299
      sameAs:https://doi.org/10.1023/A:1024031731269
      keywords:
         breast cancers
         estrogens
         ligand-independence
         progesterone receptors
         xenografts
         Oncology
      image:
      isPartOf:
         name:Breast Cancer Research and Treatment
         issn:
            1573-7217
            0167-6806
         volumeNumber:79
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Kluwer Academic Publishers
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Carol A. Sartorius
            affiliation:
                  name:University of Colorado Health Sciences Center
                  address:
                     name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Tianjie Shen
            affiliation:
                  name:University of Colorado Health Sciences Center
                  address:
                     name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Kathryn B. Horwitz
            affiliation:
                  name:University of Colorado Health Sciences Center
                  address:
                     name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
                     type:PostalAddress
                  type:Organization
                  name:University of Colorado Health Sciences Center
                  address:
                     name:Department of Pathology, University of Colorado Health Sciences Center, Denver, USA
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Breast Cancer Research and Treatment
      issn:
         1573-7217
         0167-6806
      volumeNumber:79
Organization:
      name:Kluwer Academic Publishers
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Colorado Health Sciences Center
      address:
         name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
         type:PostalAddress
      name:University of Colorado Health Sciences Center
      address:
         name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
         type:PostalAddress
      name:University of Colorado Health Sciences Center
      address:
         name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
         type:PostalAddress
      name:University of Colorado Health Sciences Center
      address:
         name:Department of Pathology, University of Colorado Health Sciences Center, Denver, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Carol A. Sartorius
      affiliation:
            name:University of Colorado Health Sciences Center
            address:
               name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
               type:PostalAddress
            type:Organization
      name:Tianjie Shen
      affiliation:
            name:University of Colorado Health Sciences Center
            address:
               name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
               type:PostalAddress
            type:Organization
      name:Kathryn B. Horwitz
      affiliation:
            name:University of Colorado Health Sciences Center
            address:
               name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
               type:PostalAddress
            type:Organization
            name:University of Colorado Health Sciences Center
            address:
               name:Department of Pathology, University of Colorado Health Sciences Center, Denver, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
      name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
      name:Department of Medicine, University of Colorado Health Sciences Center, Denver, USA
      name:Department of Pathology, University of Colorado Health Sciences Center, Denver, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {πŸ”—}(111)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Clipboard.js
  • Prism.js

Emails and Hosting {βœ‰οΈ}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {πŸ“¦}

  • Crossref

4s.