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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
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  15. CDN Services

We began analyzing https://www.nature.com/articles/nrc.2017.28, but it redirected us to https://www.nature.com/articles/nrc.2017.28. The analysis below is for the second page.

Title[redir]:
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.

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

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?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,420 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We're unsure how the site profits.

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 has a secret sauce for making money, but we can't detect it yet.

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, references, patients, antibody, activity, differ, lung, walczak, expression,

Topics {✒️}

tnf-alpha-related apoptosis-inducing ligand releases tumour-necrosis factor-alpha nature portfolio journals tnf-related apoptosis-inducing ligand trail-r2/killer/dr5 mrna isoforms permissions reprints 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 author correspondence tumor-supportive immune microenvironment proapoptotic ligand apo2l/trail trail-induced apoptosis mediated university college london 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 {🗺️}

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         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.
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      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.
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Analytics and Tracking {📊}

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Libraries {📚}

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Emails and Hosting {✉️}

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CDN Services {📦}

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