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/10.1007/s12672-017-0285-6, but it redirected us to https://link.springer.com/article/10.1007/s12672-017-0285-6. The analysis below is for the second page.

Title[redir]:
MMTV-PyMT and Derived Met-1 Mouse Mammary Tumor Cells as Models for Studying the Role of the Androgen Receptor in Triple-Negative Breast Cancer Progression | Discover Oncology
Description:
Triple-negative breast cancer (TNBC) has a faster rate of metastasis compared to other breast cancer subtypes, and no effective targeted therapies are currently FDA-approved. Recent data indicate that the androgen receptor (AR) promotes tumor survival and may serve as a potential therapeutic target in TNBC. Studies of AR in disease progression and the systemic effects of anti-androgens have been hindered by the lack of an AR-positive (AR+) immunocompetent preclinical model. In this study, we identified the transgenic MMTV-PyMT (mouse mammary tumor virus-polyoma middle tumor-antigen) mouse mammary gland carcinoma model of breast cancer and Met-1 cells derived from this model as tools to study the role of AR in breast cancer progression. AR protein expression was examined in late-stage primary tumors and lung metastases from MMTV-PyMT mice as well as in Met-1 cells by immunohistochemistry (IHC). Sensitivity of Met-1 cells to the AR agonist dihydrotestosterone (DHT) and anti-androgen therapy was examined using cell viability, migration/invasion, and anchorage-independent growth assays. Late-stage primary tumors and lung metastases from MMTV-PyMT mice and Met-1 cells expressed abundant nuclear AR protein, while negative for estrogen and progesterone receptors. Met-1 sensitivity to DHT and AR antagonists demonstrated a reliance on AR for survival, and AR antagonists inhibited invasion and anchorage-independent growth. These data suggest that the MMTV-PyMT model and Met-1 cells may serve as valuable tools for mechanistic studies of the role of AR in disease progression and how anti-androgens affect the tumor microenvironment.

Matching Content Categories {πŸ“š}

  • Science
  • Education
  • Health & Fitness

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?

πŸ™οΈ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 96,105,781 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {πŸ’Έ}

We can't tell how the site generates income.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Doi.org might be cashing in, but we can't detect the method they're using.

Keywords {πŸ”}

cells, cancer, breast, met, cell, pubmed, article, expression, google, scholar, mmtvpymt, androgen, receptor, usa, mouse, tumors, tumor, tnbc, model, metastatic, cas, human, jrk, data, primary, mammary, fig, media, progression, enza, antagonists, tissue, invasion, central, protein, metastases, metastasis, growth, university, fbs, dht, migration, response, lung, viability, enzalutamide, dmso, role, triplenegative, potential,

Topics {βœ’οΈ}

horseradish peroxidase-conjugated anti-rabbit health r01 ca187733-01a1 late-stage mmtv-pymt tumors triple-negative breast cancer effective targeted therapies anchorage-independent growth assays mmtv-pymt mammary tumor biotinylated goat anti-rabbit stem-cell program late-stage primary tumors biotinylated goat anti-rat anti-mouse igg antibodies mmtv-pymt mouse model akt-phosphorylation dependent upregulation end-stage metastases found providing mmtv-pymt tissue targeted therapies mda-mb-453 cell lines mmtv-pymt primary tumors androgen-dependent gene expression single-cell analysis reveals anchorage-independent growth anti-tumor immune response anti-androgen therapy multiple mammary tumors pymt-positive primary tumors anti-androgen therapies breast cancer subtypes human breast cancer primary mammary tumors gene signature similar steroid hormone receptors anti-androgens affect national cancer institute transgenic mouse models mouse monoclonal antibody mmtv-pymt lung metastases related subjects human cell lines breast cancer progression immunocompetent mouse models metastatic breast cancer metastatic breast cancer breast cancer cells tissue culture core breast cancer patients multiple molecular subtypes metastatic breast carcinoma human prostate cancer privacy choices/manage cookies

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:MMTV-PyMT and Derived Met-1 Mouse Mammary Tumor Cells as Models for Studying the Role of the Androgen Receptor in Triple-Negative Breast Cancer Progression
         description:Triple-negative breast cancer (TNBC) has a faster rate of metastasis compared to other breast cancer subtypes, and no effective targeted therapies are currently FDA-approved. Recent data indicate that the androgen receptor (AR) promotes tumor survival and may serve as a potential therapeutic target in TNBC. Studies of AR in disease progression and the systemic effects of anti-androgens have been hindered by the lack of an AR-positive (AR+) immunocompetent preclinical model. In this study, we identified the transgenic MMTV-PyMT (mouse mammary tumor virus-polyoma middle tumor-antigen) mouse mammary gland carcinoma model of breast cancer and Met-1 cells derived from this model as tools to study the role of AR in breast cancer progression. AR protein expression was examined in late-stage primary tumors and lung metastases from MMTV-PyMT mice as well as in Met-1 cells by immunohistochemistry (IHC). Sensitivity of Met-1 cells to the AR agonist dihydrotestosterone (DHT) and anti-androgen therapy was examined using cell viability, migration/invasion, and anchorage-independent growth assays. Late-stage primary tumors and lung metastases from MMTV-PyMT mice and Met-1 cells expressed abundant nuclear AR protein, while negative for estrogen and progesterone receptors. Met-1 sensitivity to DHT and AR antagonists demonstrated a reliance on AR for survival, and AR antagonists inhibited invasion and anchorage-independent growth. These data suggest that the MMTV-PyMT model and Met-1 cells may serve as valuable tools for mechanistic studies of the role of AR in disease progression and how anti-androgens affect the tumor microenvironment.
         datePublished:2017-02-13T00:00:00Z
         dateModified:2017-02-13T00:00:00Z
         pageStart:69
         pageEnd:77
         sameAs:https://doi.org/10.1007/s12672-017-0285-6
         keywords:
            Breast Cancer
            Androgen Receptor
            Enzalutamide
            Androgen Receptor Expression
            TNBC Cell
            Oncology
            Cancer Research
            Surgical Oncology
            Molecular Medicine
            Radiotherapy
            Internal Medicine
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig4_HTML.gif
         isPartOf:
            name:Hormones and Cancer
            issn:
               1868-8500
               1868-8497
            volumeNumber:8
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Jessica L. Christenson
               affiliation:
                     name:University of Colorado
                     address:
                        name:Department of Pathology, University of Colorado, Aurora, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Kiel T. Butterfield
               affiliation:
                     name:University of Colorado
                     address:
                        name:Department of Pathology, University of Colorado, Aurora, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Nicole S. Spoelstra
               affiliation:
                     name:University of Colorado
                     address:
                        name:Department of Pathology, University of Colorado, Aurora, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:John D. Norris
               affiliation:
                     name:Duke University
                     address:
                        name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jatinder S. Josan
               affiliation:
                     name:Virginia Tech University
                     address:
                        name:Department of Chemistry, Virginia Tech University, Blacksburg, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Julie A. Pollock
               affiliation:
                     name:University of Richmond
                     address:
                        name:Department of Chemistry, University of Richmond, Richmond, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Donald P. McDonnell
               affiliation:
                     name:Duke University
                     address:
                        name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Benita S. Katzenellenbogen
               affiliation:
                     name:University of Illinois
                     address:
                        name:Department of Molecular and Integrative Physiology, University of Illinois, Urbana, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:John A. Katzenellenbogen
               affiliation:
                     name:University of Illinois
                     address:
                        name:Department of Chemistry, University of Illinois, Urbana, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jennifer K. Richer
               affiliation:
                     name:University of Colorado
                     address:
                        name:Department of Pathology, University of Colorado, Aurora, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:MMTV-PyMT and Derived Met-1 Mouse Mammary Tumor Cells as Models for Studying the Role of the Androgen Receptor in Triple-Negative Breast Cancer Progression
      description:Triple-negative breast cancer (TNBC) has a faster rate of metastasis compared to other breast cancer subtypes, and no effective targeted therapies are currently FDA-approved. Recent data indicate that the androgen receptor (AR) promotes tumor survival and may serve as a potential therapeutic target in TNBC. Studies of AR in disease progression and the systemic effects of anti-androgens have been hindered by the lack of an AR-positive (AR+) immunocompetent preclinical model. In this study, we identified the transgenic MMTV-PyMT (mouse mammary tumor virus-polyoma middle tumor-antigen) mouse mammary gland carcinoma model of breast cancer and Met-1 cells derived from this model as tools to study the role of AR in breast cancer progression. AR protein expression was examined in late-stage primary tumors and lung metastases from MMTV-PyMT mice as well as in Met-1 cells by immunohistochemistry (IHC). Sensitivity of Met-1 cells to the AR agonist dihydrotestosterone (DHT) and anti-androgen therapy was examined using cell viability, migration/invasion, and anchorage-independent growth assays. Late-stage primary tumors and lung metastases from MMTV-PyMT mice and Met-1 cells expressed abundant nuclear AR protein, while negative for estrogen and progesterone receptors. Met-1 sensitivity to DHT and AR antagonists demonstrated a reliance on AR for survival, and AR antagonists inhibited invasion and anchorage-independent growth. These data suggest that the MMTV-PyMT model and Met-1 cells may serve as valuable tools for mechanistic studies of the role of AR in disease progression and how anti-androgens affect the tumor microenvironment.
      datePublished:2017-02-13T00:00:00Z
      dateModified:2017-02-13T00:00:00Z
      pageStart:69
      pageEnd:77
      sameAs:https://doi.org/10.1007/s12672-017-0285-6
      keywords:
         Breast Cancer
         Androgen Receptor
         Enzalutamide
         Androgen Receptor Expression
         TNBC Cell
         Oncology
         Cancer Research
         Surgical Oncology
         Molecular Medicine
         Radiotherapy
         Internal Medicine
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-017-0285-6/MediaObjects/12672_2017_285_Fig4_HTML.gif
      isPartOf:
         name:Hormones and Cancer
         issn:
            1868-8500
            1868-8497
         volumeNumber:8
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Jessica L. Christenson
            affiliation:
                  name:University of Colorado
                  address:
                     name:Department of Pathology, University of Colorado, Aurora, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Kiel T. Butterfield
            affiliation:
                  name:University of Colorado
                  address:
                     name:Department of Pathology, University of Colorado, Aurora, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Nicole S. Spoelstra
            affiliation:
                  name:University of Colorado
                  address:
                     name:Department of Pathology, University of Colorado, Aurora, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:John D. Norris
            affiliation:
                  name:Duke University
                  address:
                     name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jatinder S. Josan
            affiliation:
                  name:Virginia Tech University
                  address:
                     name:Department of Chemistry, Virginia Tech University, Blacksburg, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Julie A. Pollock
            affiliation:
                  name:University of Richmond
                  address:
                     name:Department of Chemistry, University of Richmond, Richmond, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Donald P. McDonnell
            affiliation:
                  name:Duke University
                  address:
                     name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Benita S. Katzenellenbogen
            affiliation:
                  name:University of Illinois
                  address:
                     name:Department of Molecular and Integrative Physiology, University of Illinois, Urbana, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:John A. Katzenellenbogen
            affiliation:
                  name:University of Illinois
                  address:
                     name:Department of Chemistry, University of Illinois, Urbana, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jennifer K. Richer
            affiliation:
                  name:University of Colorado
                  address:
                     name:Department of Pathology, University of Colorado, Aurora, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Hormones and Cancer
      issn:
         1868-8500
         1868-8497
      volumeNumber:8
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Colorado
      address:
         name:Department of Pathology, University of Colorado, Aurora, USA
         type:PostalAddress
      name:University of Colorado
      address:
         name:Department of Pathology, University of Colorado, Aurora, USA
         type:PostalAddress
      name:University of Colorado
      address:
         name:Department of Pathology, University of Colorado, Aurora, USA
         type:PostalAddress
      name:Duke University
      address:
         name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
         type:PostalAddress
      name:Virginia Tech University
      address:
         name:Department of Chemistry, Virginia Tech University, Blacksburg, USA
         type:PostalAddress
      name:University of Richmond
      address:
         name:Department of Chemistry, University of Richmond, Richmond, USA
         type:PostalAddress
      name:Duke University
      address:
         name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
         type:PostalAddress
      name:University of Illinois
      address:
         name:Department of Molecular and Integrative Physiology, University of Illinois, Urbana, USA
         type:PostalAddress
      name:University of Illinois
      address:
         name:Department of Chemistry, University of Illinois, Urbana, USA
         type:PostalAddress
      name:University of Colorado
      address:
         name:Department of Pathology, University of Colorado, Aurora, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Jessica L. Christenson
      affiliation:
            name:University of Colorado
            address:
               name:Department of Pathology, University of Colorado, Aurora, USA
               type:PostalAddress
            type:Organization
      name:Kiel T. Butterfield
      affiliation:
            name:University of Colorado
            address:
               name:Department of Pathology, University of Colorado, Aurora, USA
               type:PostalAddress
            type:Organization
      name:Nicole S. Spoelstra
      affiliation:
            name:University of Colorado
            address:
               name:Department of Pathology, University of Colorado, Aurora, USA
               type:PostalAddress
            type:Organization
      name:John D. Norris
      affiliation:
            name:Duke University
            address:
               name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
               type:PostalAddress
            type:Organization
      name:Jatinder S. Josan
      affiliation:
            name:Virginia Tech University
            address:
               name:Department of Chemistry, Virginia Tech University, Blacksburg, USA
               type:PostalAddress
            type:Organization
      name:Julie A. Pollock
      affiliation:
            name:University of Richmond
            address:
               name:Department of Chemistry, University of Richmond, Richmond, USA
               type:PostalAddress
            type:Organization
      name:Donald P. McDonnell
      affiliation:
            name:Duke University
            address:
               name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
               type:PostalAddress
            type:Organization
      name:Benita S. Katzenellenbogen
      affiliation:
            name:University of Illinois
            address:
               name:Department of Molecular and Integrative Physiology, University of Illinois, Urbana, USA
               type:PostalAddress
            type:Organization
      name:John A. Katzenellenbogen
      affiliation:
            name:University of Illinois
            address:
               name:Department of Chemistry, University of Illinois, Urbana, USA
               type:PostalAddress
            type:Organization
      name:Jennifer K. Richer
      affiliation:
            name:University of Colorado
            address:
               name:Department of Pathology, University of Colorado, Aurora, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pathology, University of Colorado, Aurora, USA
      name:Department of Pathology, University of Colorado, Aurora, USA
      name:Department of Pathology, University of Colorado, Aurora, USA
      name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
      name:Department of Chemistry, Virginia Tech University, Blacksburg, USA
      name:Department of Chemistry, University of Richmond, Richmond, USA
      name:Department of Pharmacology and Cancer Biology, Duke University, Durham, USA
      name:Department of Molecular and Integrative Physiology, University of Illinois, Urbana, USA
      name:Department of Chemistry, University of Illinois, Urbana, USA
      name:Department of Pathology, University of Colorado, Aurora, USA

External Links {πŸ”—}(256)

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

5.28s.