We are analyzing https://link.springer.com/article/10.1007/s10555-007-9054-2.

Title:
Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues | Cancer and Metastasis Reviews
Description:
The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their Gs-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1α (HIF-1α) Hence, HIF-1α activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Science
Health & Fitness

Content Management System {📝}

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 {📈}

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 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 Link.springer.com Make Money? {💸}

We can't tell how the site generates income.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

google, scholar, cas, pubmed, article, cancer, adenosine, journal, cells, immunology, cell, sitkovsky, tumor, research, factor, immunotherapy, hypoxia, lukashev, ohta, reviews, hypoxiainducible, role, human, immune, nature, protection, mechanisms, review, receptors, molecular, tissue, antitumor, inflammation, tumors, receptor, clinical, content, extracellular, development, tumour, regulation, apasov, annual, pharmacology, caldwell, biological, kinase, alpha, lymphocytes, privacy,

Topics {✒️}

hypoxia-dependent anti-inflammatory pathways tumor-induced l-selectinhigh suppressor tumor hypoxia-exposed anti-tumor month download article/chapter g-protein-coupled adenosine receptors hypoxia-inducible factor 1α hypoxia-inducible factor-1 alpha hypoxia-inducible factor 1alpha hypoxia-inducible factor 1a camp-dependent protein kinase activation-inducible short isoform targeting tumor-related immunosuppression cd39/vascular atp diphosphohydrolase phosphatidylinositol 3-kinase-mediated pathways high-resolution measurements reveal adenosine receptor-mediated mechanisms ecto-atp diphosphohydrolase/cd39 regulatory t-cell-inactivation tumor-protecting immunosuppressive effects hypoxia-inducible factor 1 shape tumour immunogenicity gs-protein-coupled tissue-protecting mechanism mediated hypoxia-driven mechanisms cell-based cancer immunotherapy van der burg hypoxia-inducible factors myeloid cell-mediated inflammation ecto-nucleotidases-molecular structures physiological tissue-protecting mechanism local-tissue oxygen tension t-cell recognition full article pdf endogenous adenosine produced cytotoxic t-lymphocytes receptor-mediated mechanisms significant compensatory increases key regulatory factor tumour growth camp-elevating a2a adenosine a2a receptors cancerous tissues published malignant melanoma ascites privacy choices/manage cookies hif-1α activity local tissue hypoxia metastasis reviews aims tumor microenvironments due inflammatory tissue damage drug discovery today

Questions {❓}

The ‘danger’ sensors that STOP the immune response: The A2 adenosine receptors?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues
         description:The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their Gs-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1α (HIF-1α) Hence, HIF-1α activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.
         datePublished:2007-04-03T00:00:00Z
         dateModified:2007-04-03T00:00:00Z
         pageStart:273
         pageEnd:279
         sameAs:https://doi.org/10.1007/s10555-007-9054-2
         keywords:
            Adenosine
            Cancer
            Hypoxia
            Immunotherapy
            T cells
            Cancer Research
            Oncology
            Biomedicine
            general
         image:
         isPartOf:
            name:Cancer and Metastasis Reviews
            issn:
               1573-7233
               0167-7659
            volumeNumber:26
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Kluwer Academic Publishers-Plenum Publishers
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:D. Lukashev
               affiliation:
                     name:Northeastern University
                     address:
                        name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:A. Ohta
               affiliation:
                     name:Northeastern University
                     address:
                        name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:M. Sitkovsky
               affiliation:
                     name:Northeastern University
                     address:
                        name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
                        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:Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues
      description:The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their Gs-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1α (HIF-1α) Hence, HIF-1α activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.
      datePublished:2007-04-03T00:00:00Z
      dateModified:2007-04-03T00:00:00Z
      pageStart:273
      pageEnd:279
      sameAs:https://doi.org/10.1007/s10555-007-9054-2
      keywords:
         Adenosine
         Cancer
         Hypoxia
         Immunotherapy
         T cells
         Cancer Research
         Oncology
         Biomedicine
         general
      image:
      isPartOf:
         name:Cancer and Metastasis Reviews
         issn:
            1573-7233
            0167-7659
         volumeNumber:26
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Kluwer Academic Publishers-Plenum Publishers
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:D. Lukashev
            affiliation:
                  name:Northeastern University
                  address:
                     name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:A. Ohta
            affiliation:
                  name:Northeastern University
                  address:
                     name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:M. Sitkovsky
            affiliation:
                  name:Northeastern University
                  address:
                     name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Cancer and Metastasis Reviews
      issn:
         1573-7233
         0167-7659
      volumeNumber:26
Organization:
      name:Kluwer Academic Publishers-Plenum Publishers
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Northeastern University
      address:
         name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
         type:PostalAddress
      name:Northeastern University
      address:
         name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
         type:PostalAddress
      name:Northeastern University
      address:
         name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:D. Lukashev
      affiliation:
            name:Northeastern University
            address:
               name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
               type:PostalAddress
            type:Organization
      name:A. Ohta
      affiliation:
            name:Northeastern University
            address:
               name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
               type:PostalAddress
            type:Organization
      name:M. Sitkovsky
      affiliation:
            name:Northeastern University
            address:
               name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
      name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
      name:New England Inflammation and Tissue Protection Institute, Northeastern University, Boston, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(248)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.31s.

LINK . SPRINGER . COM {}