Here's how LINK.SPRINGER.COM makes money* and how much!

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

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
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s13277-016-5098-7.

Title:
Role of interleukin-6 in cancer progression and therapeutic resistance | Tumor Biology
Description:
In the last several decades, the number of people dying from cancer-related deaths has not reduced significantly despite phenomenal advances in the technologies related to diagnosis and therapeutic modalities. The principal cause behind limitations in the curability of this disease is the reducing sensitivity of the cancer cells towards conventional anticancer therapeutic modalities, particularly in advance stages of the disease. Amongst several reasons, certain secretory factors released by the tumour cells into the microenvironment have been found to confer resistance towards chemo- and radiotherapy, besides promoting growth. Interleukin-6 (IL-6), one of the major cytokines in the tumour microenvironment, is an important factor which is found at high concentrations and known to be deregulated in cancer. Its overexpression has been reported in almost all types of tumours. The strong association between inflammation and cancer is reflected by the high IL-6 levels in the tumour microenvironment, where it promotes tumorigenesis by regulating all hallmarks of cancer and multiple signalling pathways, including apoptosis, survival, proliferation, angiogenesis, invasiveness and metastasis, and, most importantly, the metabolism. Moreover, IL-6 protects the cancer cells from therapy-induced DNA damage, oxidative stress and apoptosis by facilitating the repair and induction of countersignalling (antioxidant and anti-apoptotic/pro-survival) pathways. Therefore, blocking IL-6 or inhibiting its associated signalling independently or in combination with conventional anticancer therapies could be a potential therapeutic strategy for the treatment of cancers with IL-6-dominated signalling.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

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're unsure how the site profits.

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. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

pubmed, google, scholar, article, cas, cancer, central, interleukin, cell, cells, stat, res, human, signaling, biol, breast, chen, receptor, clin, tumor, role, factor, pathway, expression, mol, cytokine, patients, activation, growth, inflammation, zhang, resistance, med, carcinoma, oncogene, myeloma, response, therapeutic, multiple, apoptosis, sci, oncol, immunol, dna, int, prostate, ovarian, signal, transcription, cytokines,

Topics {✒️}

gi/pi3k-akt/nf-kappab pathway low-molecular-weight compound discovered ikk–nf-kappab pathway anant narayan bhatt il-6–jak1–stat3–oct-4 pathway month download article/chapter glycolysis confers radio-resistance tumour necrosis factor inhibited tumour–stroma interaction hyperoxia-induced mitochondrial damage kcnn4 channel-dependent manner radiation-induced hematopoietic depression colonic f4/80+cd11bhighgr1low macrophages anti-interleukin-6 monoclonal antibody anti-interleukin-6 receptor antibody therapy-induced dna damage anti-vegf therapy mediated p38-dependent pathway occurs il-6 induces nf-kappa anti-apoptotic gene mcl-1 interleukin6-expressing lung cancer ovarian cancer-activating factor multiple au-rich elements colitis-induced colorectal cancer protein kinase c-{alpha} bcl-2-induced bak interactions inhibit il-6-induced activation myd88-dependent il-6 production anti-apoptotic/pro-survival tumor microenvironment biology dna damage-mediated induction anti-interleukin-6 antibody siltuximab il-6/il-6 receptor system il-6/stat3 signaling pathway nuclear factor-kappab full article pdf tumor suppressor genes gp130-mediated stat-3 dna damage induces vegf-dependent angiogenesis acute myeloid leukemia article kumari interleukin-6-mediated mcl-1 upregulation autocrine il-6/stat3 signaling squamous cell carcinoma de la fuente antibody-based therapies cooperative nf-kb nf-kb collaboration human glioblastoma cells

Questions {❓}

  • Autocrine IL-6 signaling: a key event in tumorigenesis?
  • Interleukin‐6 myokine signaling in skeletal muscle: a double‐edged sword?
  • Oxidative stress, inflammation, and cancer: how are they linked?
  • Targeting STAT3 in cancer: how successful are we?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Role of interleukin-6 in cancer progression and therapeutic resistance
         description:In the last several decades, the number of people dying from cancer-related deaths has not reduced significantly despite phenomenal advances in the technologies related to diagnosis and therapeutic modalities. The principal cause behind limitations in the curability of this disease is the reducing sensitivity of the cancer cells towards conventional anticancer therapeutic modalities, particularly in advance stages of the disease. Amongst several reasons, certain secretory factors released by the tumour cells into the microenvironment have been found to confer resistance towards chemo- and radiotherapy, besides promoting growth. Interleukin-6 (IL-6), one of the major cytokines in the tumour microenvironment, is an important factor which is found at high concentrations and known to be deregulated in cancer. Its overexpression has been reported in almost all types of tumours. The strong association between inflammation and cancer is reflected by the high IL-6 levels in the tumour microenvironment, where it promotes tumorigenesis by regulating all hallmarks of cancer and multiple signalling pathways, including apoptosis, survival, proliferation, angiogenesis, invasiveness and metastasis, and, most importantly, the metabolism. Moreover, IL-6 protects the cancer cells from therapy-induced DNA damage, oxidative stress and apoptosis by facilitating the repair and induction of countersignalling (antioxidant and anti-apoptotic/pro-survival) pathways. Therefore, blocking IL-6 or inhibiting its associated signalling independently or in combination with conventional anticancer therapies could be a potential therapeutic strategy for the treatment of cancers with IL-6-dominated signalling.
         datePublished:2016-06-03T00:00:00Z
         dateModified:2016-06-03T00:00:00Z
         pageStart:11553
         pageEnd:11572
         sameAs:https://doi.org/10.1007/s13277-016-5098-7
         keywords:
            IL-6
            Cancer
            Therapeutic resistance
            STAT-3
            Chemotherapy
            Radio-resistance
            Cancer Research
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig5_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig6_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig7_HTML.gif
         isPartOf:
            name:Tumor Biology
            issn:
               1423-0380
               1010-4283
            volumeNumber:37
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Netherlands
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Neeraj Kumari
               affiliation:
                     name:Institute of Nuclear Medicine and Allied Sciences
                     address:
                        name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
                        type:PostalAddress
                     type:Organization
                     name:Delhi Technological University
                     address:
                        name:Department of Biotechnology, Delhi Technological University, Delhi, India
                        type:PostalAddress
                     type:Organization
               type:Person
               name:B. S. Dwarakanath
               affiliation:
                     name:Sri Ramachandra University
                     address:
                        name:Central Research Facility, Sri Ramachandra University, Chennai, India
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Asmita Das
               affiliation:
                     name:Delhi Technological University
                     address:
                        name:Department of Biotechnology, Delhi Technological University, Delhi, India
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Anant Narayan Bhatt
               affiliation:
                     name:Institute of Nuclear Medicine and Allied Sciences
                     address:
                        name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
                        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:Role of interleukin-6 in cancer progression and therapeutic resistance
      description:In the last several decades, the number of people dying from cancer-related deaths has not reduced significantly despite phenomenal advances in the technologies related to diagnosis and therapeutic modalities. The principal cause behind limitations in the curability of this disease is the reducing sensitivity of the cancer cells towards conventional anticancer therapeutic modalities, particularly in advance stages of the disease. Amongst several reasons, certain secretory factors released by the tumour cells into the microenvironment have been found to confer resistance towards chemo- and radiotherapy, besides promoting growth. Interleukin-6 (IL-6), one of the major cytokines in the tumour microenvironment, is an important factor which is found at high concentrations and known to be deregulated in cancer. Its overexpression has been reported in almost all types of tumours. The strong association between inflammation and cancer is reflected by the high IL-6 levels in the tumour microenvironment, where it promotes tumorigenesis by regulating all hallmarks of cancer and multiple signalling pathways, including apoptosis, survival, proliferation, angiogenesis, invasiveness and metastasis, and, most importantly, the metabolism. Moreover, IL-6 protects the cancer cells from therapy-induced DNA damage, oxidative stress and apoptosis by facilitating the repair and induction of countersignalling (antioxidant and anti-apoptotic/pro-survival) pathways. Therefore, blocking IL-6 or inhibiting its associated signalling independently or in combination with conventional anticancer therapies could be a potential therapeutic strategy for the treatment of cancers with IL-6-dominated signalling.
      datePublished:2016-06-03T00:00:00Z
      dateModified:2016-06-03T00:00:00Z
      pageStart:11553
      pageEnd:11572
      sameAs:https://doi.org/10.1007/s13277-016-5098-7
      keywords:
         IL-6
         Cancer
         Therapeutic resistance
         STAT-3
         Chemotherapy
         Radio-resistance
         Cancer Research
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig5_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig6_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs13277-016-5098-7/MediaObjects/13277_2016_5098_Fig7_HTML.gif
      isPartOf:
         name:Tumor Biology
         issn:
            1423-0380
            1010-4283
         volumeNumber:37
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer Netherlands
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Neeraj Kumari
            affiliation:
                  name:Institute of Nuclear Medicine and Allied Sciences
                  address:
                     name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
                     type:PostalAddress
                  type:Organization
                  name:Delhi Technological University
                  address:
                     name:Department of Biotechnology, Delhi Technological University, Delhi, India
                     type:PostalAddress
                  type:Organization
            type:Person
            name:B. S. Dwarakanath
            affiliation:
                  name:Sri Ramachandra University
                  address:
                     name:Central Research Facility, Sri Ramachandra University, Chennai, India
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Asmita Das
            affiliation:
                  name:Delhi Technological University
                  address:
                     name:Department of Biotechnology, Delhi Technological University, Delhi, India
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Anant Narayan Bhatt
            affiliation:
                  name:Institute of Nuclear Medicine and Allied Sciences
                  address:
                     name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Tumor Biology
      issn:
         1423-0380
         1010-4283
      volumeNumber:37
Organization:
      name:Springer Netherlands
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Institute of Nuclear Medicine and Allied Sciences
      address:
         name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
         type:PostalAddress
      name:Delhi Technological University
      address:
         name:Department of Biotechnology, Delhi Technological University, Delhi, India
         type:PostalAddress
      name:Sri Ramachandra University
      address:
         name:Central Research Facility, Sri Ramachandra University, Chennai, India
         type:PostalAddress
      name:Delhi Technological University
      address:
         name:Department of Biotechnology, Delhi Technological University, Delhi, India
         type:PostalAddress
      name:Institute of Nuclear Medicine and Allied Sciences
      address:
         name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Neeraj Kumari
      affiliation:
            name:Institute of Nuclear Medicine and Allied Sciences
            address:
               name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
               type:PostalAddress
            type:Organization
            name:Delhi Technological University
            address:
               name:Department of Biotechnology, Delhi Technological University, Delhi, India
               type:PostalAddress
            type:Organization
      name:B. S. Dwarakanath
      affiliation:
            name:Sri Ramachandra University
            address:
               name:Central Research Facility, Sri Ramachandra University, Chennai, India
               type:PostalAddress
            type:Organization
      name:Asmita Das
      affiliation:
            name:Delhi Technological University
            address:
               name:Department of Biotechnology, Delhi Technological University, Delhi, India
               type:PostalAddress
            type:Organization
      name:Anant Narayan Bhatt
      affiliation:
            name:Institute of Nuclear Medicine and Allied Sciences
            address:
               name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
      name:Department of Biotechnology, Delhi Technological University, Delhi, India
      name:Central Research Facility, Sri Ramachandra University, Chennai, India
      name:Department of Biotechnology, Delhi Technological University, Delhi, India
      name:Division of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Delhi, India
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(689)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

5.16s.