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. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://link.springer.com/article/10.1007/s10875-012-9847-0, but it redirected us to https://link.springer.com/article/10.1007/s10875-012-9847-0. The analysis below is for the second page.

Title[redir]:
Cancer-Related Inflammation | Journal of Clinical Immunology
Description:
Solid tumors consist of neoplastic cells, non-malignant stromal cells, and migratory hematopoietic cells. Complex interactions between the cell types in this microenvironment regulate tumor growth, progression, metastasis, and angiogenesis. The cells and mediators of inflammation form a major part of the epithelial tumor microenvironment. In some cancers, inflammatory conditions precede development of malignancy; in others, oncogenic change drives a tumor-promoting inflammatory milieu. Whatever its origin, this “smoldering” inflammation aids proliferation and survival of malignant cells, stimulates angiogenesis and metastasis, subverts adaptive immunity, and alters response to hormones and chemotherapy. Cytokines are major mediators of communication between cells in the inflammatory tumor microenvironment. It is known that neoplastic cells often over-express proinflammatory mediators including proteases, eicosanoids, cytokines, and chemokines. Several cytokines such as macrophage migratory inhibitory factor (MIF), TNF-α, IL-6, IL-17, IL-12, IL-23, IL-10, and TGF-β have been linked with both experimental and human cancers and can either promote or inhibit tumor development. MIF is a major cytokine in many cancers and there is evidence that the cytokine is produced by both malignant cells and infiltrating leukocytes. In this article we will discuss the role of cancer-associated inflammation and the particular role of MIF in malignant disease.

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

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 {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,479,999 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {💸}

We don’t know how the website earns money.

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

Keywords {🔍}

google, scholar, article, pubmed, cas, cancer, factor, tumor, cells, cell, macrophage, inhibitory, migration, inflammation, necrosis, balkwill, growth, cytokine, ovarian, receptor, res, inflammatory, mif, human, med, immunol, clin, metastasis, hagemann, cytokines, nature, chemokine, promotes, interleukin, wilson, development, role, rev, pancreatic, nat, mice, expression, progression, epithelial, malignant, tumour, exp, macrophages, wang, metz,

Topics {✒️}

month download article/chapter tumor necrosis factor-alpha tumour necrosis factor autocrine tumor-promoting network colony-stimulating factor-1 pathway tumor growth-promoting response tnf-alpha receptor subtypes tnf-alpha involve tnfr1 tumor-promoting inflammatory milieu cytokine-driven compensatory proliferation bone marrow-derived cells smac-mimetic-induced apoptosis tumor-induced immune dysfunction tumor necrosis factor tumor necrosis factor oncogenic ras-induced secretion il-6-stat3 signaling pathway cell-free substances formed lymphoid cell-antigen interaction adenoma-linked barrier defects myd88-dependent il-6 production nf-kappab-dependent pathway reduced tumor growth /ebp beta-deficient mice chemokine receptor expression full article pdf promote tumor growth clinical immunology aims cell-derived il-6 epithelial tumor cells th2 cytokine interleukin-13 epithelial tumor microenvironment inflammatory tumor microenvironment blocking tnf-alpha tnf-alpha inhibitor asbestos-induced oncogenesis cytokine expression profile p53-dependent effects privacy choices/manage cookies article candido promotes chemical hepatocarcinogenesis tumor-promoting actions cxc chemokine receptors inhibit tumor development ovarian cancer therapy thorsten hagemann solid ovarian tumours il-10-activated macrophages independent prognostic factor glucocorticoid-induced modulator

Questions {❓}

  • Epithelial cancer cell migration: a role for chemokine receptors?
  • Inflammation and cancer: back to Virchow?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Cancer-Related Inflammation
         description:Solid tumors consist of neoplastic cells, non-malignant stromal cells, and migratory hematopoietic cells. Complex interactions between the cell types in this microenvironment regulate tumor growth, progression, metastasis, and angiogenesis. The cells and mediators of inflammation form a major part of the epithelial tumor microenvironment. In some cancers, inflammatory conditions precede development of malignancy; in others, oncogenic change drives a tumor-promoting inflammatory milieu. Whatever its origin, this “smoldering” inflammation aids proliferation and survival of malignant cells, stimulates angiogenesis and metastasis, subverts adaptive immunity, and alters response to hormones and chemotherapy. Cytokines are major mediators of communication between cells in the inflammatory tumor microenvironment. It is known that neoplastic cells often over-express proinflammatory mediators including proteases, eicosanoids, cytokines, and chemokines. Several cytokines such as macrophage migratory inhibitory factor (MIF), TNF-α, IL-6, IL-17, IL-12, IL-23, IL-10, and TGF-β have been linked with both experimental and human cancers and can either promote or inhibit tumor development. MIF is a major cytokine in many cancers and there is evidence that the cytokine is produced by both malignant cells and infiltrating leukocytes. In this article we will discuss the role of cancer-associated inflammation and the particular role of MIF in malignant disease.
         datePublished:2012-12-09T00:00:00Z
         dateModified:2012-12-09T00:00:00Z
         pageStart:79
         pageEnd:84
         sameAs:https://doi.org/10.1007/s10875-012-9847-0
         keywords:
            Cytokines
            cancer
            malignant disease
            inflammation
            MIF
            tumorigenesis
            Immunology
            Infectious Diseases
            Internal Medicine
            Medical Microbiology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10875-012-9847-0/MediaObjects/10875_2012_9847_Fig1_HTML.gif
         isPartOf:
            name:Journal of Clinical Immunology
            issn:
               1573-2592
               0271-9142
            volumeNumber:33
            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:Juliana Candido
               affiliation:
                     name:Queen Mary, University of London
                     address:
                        name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Thorsten Hagemann
               affiliation:
                     name:Queen Mary, University of London
                     address:
                        name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Cancer-Related Inflammation
      description:Solid tumors consist of neoplastic cells, non-malignant stromal cells, and migratory hematopoietic cells. Complex interactions between the cell types in this microenvironment regulate tumor growth, progression, metastasis, and angiogenesis. The cells and mediators of inflammation form a major part of the epithelial tumor microenvironment. In some cancers, inflammatory conditions precede development of malignancy; in others, oncogenic change drives a tumor-promoting inflammatory milieu. Whatever its origin, this “smoldering” inflammation aids proliferation and survival of malignant cells, stimulates angiogenesis and metastasis, subverts adaptive immunity, and alters response to hormones and chemotherapy. Cytokines are major mediators of communication between cells in the inflammatory tumor microenvironment. It is known that neoplastic cells often over-express proinflammatory mediators including proteases, eicosanoids, cytokines, and chemokines. Several cytokines such as macrophage migratory inhibitory factor (MIF), TNF-α, IL-6, IL-17, IL-12, IL-23, IL-10, and TGF-β have been linked with both experimental and human cancers and can either promote or inhibit tumor development. MIF is a major cytokine in many cancers and there is evidence that the cytokine is produced by both malignant cells and infiltrating leukocytes. In this article we will discuss the role of cancer-associated inflammation and the particular role of MIF in malignant disease.
      datePublished:2012-12-09T00:00:00Z
      dateModified:2012-12-09T00:00:00Z
      pageStart:79
      pageEnd:84
      sameAs:https://doi.org/10.1007/s10875-012-9847-0
      keywords:
         Cytokines
         cancer
         malignant disease
         inflammation
         MIF
         tumorigenesis
         Immunology
         Infectious Diseases
         Internal Medicine
         Medical Microbiology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10875-012-9847-0/MediaObjects/10875_2012_9847_Fig1_HTML.gif
      isPartOf:
         name:Journal of Clinical Immunology
         issn:
            1573-2592
            0271-9142
         volumeNumber:33
         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:Juliana Candido
            affiliation:
                  name:Queen Mary, University of London
                  address:
                     name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Thorsten Hagemann
            affiliation:
                  name:Queen Mary, University of London
                  address:
                     name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Journal of Clinical Immunology
      issn:
         1573-2592
         0271-9142
      volumeNumber:33
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Queen Mary, University of London
      address:
         name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
         type:PostalAddress
      name:Queen Mary, University of London
      address:
         name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Juliana Candido
      affiliation:
            name:Queen Mary, University of London
            address:
               name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
               type:PostalAddress
            type:Organization
      name:Thorsten Hagemann
      affiliation:
            name:Queen Mary, University of London
            address:
               name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
      name:Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary, University of London, London, UK
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(326)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

Emails and Hosting {✉️}

Mail Servers:

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

Name Servers:

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

CDN Services {📦}

  • Crossref

5.24s.