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

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

NATURE . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Nature.com Make Money
  6. How Much Does Nature.com Make
  7. Keywords
  8. Topics
  9. Questions
  10. Schema
  11. Social Networks
  12. External Links
  13. Analytics And Tracking
  14. Libraries
  15. Hosting Providers
  16. CDN Services

We are analyzing https://www.nature.com/articles/nrc.2017.28.

Title:
Exploring the TRAILs less travelled: TRAIL in cancer biology and therapy | Nature Reviews Cancer
Description:
Clinical trials testing activators of tumour necrosis factor-related apoptosis-inducing ligand receptor (TRAIL-R) signalling in cancer have not met expectations. This Review discusses new insights that might explain clinical failure, but also provide the basis for harnessing TRAIL-Rs for cancer therapy. The discovery that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis of cancer cells without causing toxicity in mice has led to the in-depth study of pro-apoptotic TRAIL receptor (TRAIL-R) signalling and the development of biotherapeutic drug candidates that activate TRAIL-Rs. The outcome of clinical trials with these TRAIL-R agonists has, however, been disappointing so far. Recent evidence indicates that many cancers, in addition to being TRAIL resistant, use the endogenous TRAIL–TRAIL-R system to their own advantage. However, novel insight on two fronts — how resistance of cancer cells to TRAIL-based pro-apoptotic therapies might be overcome, and how the pro-tumorigenic effects of endogenous TRAIL might be countered — gives reasonable hope that the TRAIL system can be harnessed to treat cancer. In this Review we assess the status quo of our understanding of the biology of the TRAIL–TRAIL-R system — as well as the gaps therein — and discuss the opportunities and challenges in effectively targeting this pathway.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is nature.com built with?

Custom-built

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

Traffic Estimate {📈}

What is the average monthly size of nature.com audience?

🚀🌠 Tremendous Traffic: 10M - 20M visitors per month


Based on our best estimate, this website will receive around 16,942,715 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Nature.com Make Money? {💸}


Display Ads {🎯}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

Ads are managed by yourbow.com. Particular relationships are as follows:

Direct Advertisers (10)
google.com, pmc.com, doceree.com, yourbow.com, audienciad.com, onlinemediasolutions.com, advibe.media, aps.amazon.com, getmediamx.com, onomagic.com

Reseller Advertisers (38)
conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.com

How Much Does Nature.com Make? {💰}


Display Ads {🎯}

$213,500 per month
Our analysis indicates Nature.com generates between $142,361 and $391,492 monthly online from display ads.

Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, trail, cell, death, apoptosis, central, receptor, cells, tumor, ligand, necrosis, trailr, nature, biol, apoptosisinducing, caspase, factorrelated, human, chem, receptors, study, med, complex, activation, nat, mol, mice, immunol, tumour, factor, trailinduced, res, clin, tnf, induction, therapeutic, access, patients, antibody, activity, differ, lung, walczak, expression, references,

Topics {✒️}

tnf-alpha-related apoptosis-inducing ligand permissions reprints releases tumour-necrosis factor-alpha nature portfolio journals tnf-related apoptosis-inducing ligand trail-r2/killer/dr5 mrna isoforms privacy policy nature portfolio european research council advertising open-label study il6/stat3-dependent trail expression cancer research uk c-jun n-terminal kinase apoptosis-inducing ligand belonging trail/apo2l gene-deficient mice trail-mediated dr5-disc formation trail-based pro-apoptotic therapies social media tumor necrosis factor tumour necrosis factor rankl/opg/trail plasma levels agonistic trail-r2-specific antibody cycloheximide-sensitive factor occurs death-inducing signalling complex membrane-targeted death ligand modern research death receptor–ligand systems endotoxin-induced serum factor trail/dr5-dependent suppression induced trail-induced programmed necrosis cell-surface death ligand cyclooxygenase-dependent tumor growth myeloid-derived suppressor cells membrane-bound fas ligand tumor-cell-derived interleukin-4 trail-r2-targeting nanobody tas266 death receptor-induced apoptosis retinoic acid-induced apoptosis scientific adviser ifn-gamma-dependent suppression antonella montinaro & henning walczak modulates fasl-induced cytotoxicity tumor-supportive immune microenvironment proapoptotic ligand apo2l/trail trail-induced apoptosis mediated university college london author correspondence trail-r2- mediated apoptosis trail-r-mediated apoptosis

Questions {❓}

  • Bortezomib and TRAIL: a perfect match for apoptotic elimination of tumour cells?
  • Is TRAIL the holy grail of cancer therapy?
  • Metastasis suppressor function of tumor necrosis factor-related apoptosis-inducing ligand-R in mice: implications for TRAIL-based therapy in humans?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Exploring the TRAILs less travelled: TRAIL in cancer biology and therapy
         description: Clinical trials testing activators of tumour necrosis factor-related apoptosis-inducing ligand receptor (TRAIL-R) signalling in cancer have not met expectations. This Review discusses new insights that might explain clinical failure, but also provide the basis for harnessing TRAIL-Rs for cancer therapy. The discovery that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis of cancer cells without causing toxicity in mice has led to the in-depth study of pro-apoptotic TRAIL receptor (TRAIL-R) signalling and the development of biotherapeutic drug candidates that activate TRAIL-Rs. The outcome of clinical trials with these TRAIL-R agonists has, however, been disappointing so far. Recent evidence indicates that many cancers, in addition to being TRAIL resistant, use the endogenous TRAIL–TRAIL-R system to their own advantage. However, novel insight on two fronts — how resistance of cancer cells to TRAIL-based pro-apoptotic therapies might be overcome, and how the pro-tumorigenic effects of endogenous TRAIL might be countered — gives reasonable hope that the TRAIL system can be harnessed to treat cancer. In this Review we assess the status quo of our understanding of the biology of the TRAIL–TRAIL-R system — as well as the gaps therein — and discuss the opportunities and challenges in effectively targeting this pathway.
         datePublished:2017-05-24T00:00:00Z
         dateModified:2017-05-24T00:00:00Z
         pageStart:352
         pageEnd:366
         sameAs:https://doi.org/10.1038/nrc.2017.28
         keywords:
            Apoptosis
            Cancer therapeutic resistance
            Targeted therapies
            Tumour biomarkers
            Tumour immunology
            Biomedicine
            general
            Cancer Research
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig3_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig4_HTML.jpg
         isPartOf:
            name:Nature Reviews Cancer
            issn:
               1474-1768
               1474-175X
            volumeNumber:17
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Nature Publishing Group UK
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Silvia von Karstedt
               affiliation:
                     name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
                     address:
                        name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
                        type:PostalAddress
                     type:Organization
                     name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
                     address:
                        name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.,
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Antonella Montinaro
               affiliation:
                     name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
                     address:
                        name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Henning Walczak
               affiliation:
                     name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
                     address:
                        name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College 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:Exploring the TRAILs less travelled: TRAIL in cancer biology and therapy
      description: Clinical trials testing activators of tumour necrosis factor-related apoptosis-inducing ligand receptor (TRAIL-R) signalling in cancer have not met expectations. This Review discusses new insights that might explain clinical failure, but also provide the basis for harnessing TRAIL-Rs for cancer therapy. The discovery that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis of cancer cells without causing toxicity in mice has led to the in-depth study of pro-apoptotic TRAIL receptor (TRAIL-R) signalling and the development of biotherapeutic drug candidates that activate TRAIL-Rs. The outcome of clinical trials with these TRAIL-R agonists has, however, been disappointing so far. Recent evidence indicates that many cancers, in addition to being TRAIL resistant, use the endogenous TRAIL–TRAIL-R system to their own advantage. However, novel insight on two fronts — how resistance of cancer cells to TRAIL-based pro-apoptotic therapies might be overcome, and how the pro-tumorigenic effects of endogenous TRAIL might be countered — gives reasonable hope that the TRAIL system can be harnessed to treat cancer. In this Review we assess the status quo of our understanding of the biology of the TRAIL–TRAIL-R system — as well as the gaps therein — and discuss the opportunities and challenges in effectively targeting this pathway.
      datePublished:2017-05-24T00:00:00Z
      dateModified:2017-05-24T00:00:00Z
      pageStart:352
      pageEnd:366
      sameAs:https://doi.org/10.1038/nrc.2017.28
      keywords:
         Apoptosis
         Cancer therapeutic resistance
         Targeted therapies
         Tumour biomarkers
         Tumour immunology
         Biomedicine
         general
         Cancer Research
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig3_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrc.2017.28/MediaObjects/41568_2017_Article_BFnrc201728_Fig4_HTML.jpg
      isPartOf:
         name:Nature Reviews Cancer
         issn:
            1474-1768
            1474-175X
         volumeNumber:17
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Nature Publishing Group UK
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Silvia von Karstedt
            affiliation:
                  name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
                  address:
                     name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
                     type:PostalAddress
                  type:Organization
                  name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
                  address:
                     name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.,
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Antonella Montinaro
            affiliation:
                  name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
                  address:
                     name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Henning Walczak
            affiliation:
                  name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
                  address:
                     name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Nature Reviews Cancer
      issn:
         1474-1768
         1474-175X
      volumeNumber:17
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
      address:
         name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
         type:PostalAddress
      name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
      address:
         name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.,
         type:PostalAddress
      name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
      address:
         name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
         type:PostalAddress
      name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
      address:
         name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Silvia von Karstedt
      affiliation:
            name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
            address:
               name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
               type:PostalAddress
            type:Organization
            name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
            address:
               name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.,
               type:PostalAddress
            type:Organization
      name:Antonella Montinaro
      affiliation:
            name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
            address:
               name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
               type:PostalAddress
            type:Organization
      name:Henning Walczak
      affiliation:
            name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London
            address:
               name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
      name:Present address: The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.,
      name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
      name:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, UK
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(638)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Backbone.js
  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mxa-002c5801.gslb.pphosted.com
  • mxb-002c5801.gslb.pphosted.com

Name Servers:

  • pdns1.ultradns.net
  • pdns2.ultradns.net
  • pdns3.ultradns.org
  • pdns4.ultradns.org
  • pdns5.ultradns.info
  • pdns6.ultradns.co.uk

CDN Services {📦}

  • Crossref

5.8s.