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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
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We began analyzing https://www.nature.com/articles/nrc1819, but it redirected us to https://www.nature.com/articles/nrc1819. The analysis below is for the second page.

Title[redir]:
Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis | Nature Reviews Cancer
Description:
Nature Reviews Cancer - Mutation or deletion of PTEN is found in many cancers — however, in others, deregulation of the PI3K–PTEN network occurs in the absence of PTEN mutation. This...

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

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 5,000,019 visitors per month in the current month.
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How Does Doi.org Make Money? {💸}

We can't figure out the monetization strategy.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Doi.org could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

pubmed, google, scholar, cas, cancer, cell, nature, pten, kinase, central, pathway, growth, mtor, mutations, pathways, gene, mice, tsc, genes, article, tumor, multiple, signalling, breast, receptor, biol, sci, suppressor, access, clin, development, dev, oncol, usa, pik, tumorigenesis, ras, tumour, science, proc, natl, acad, content, levine, human, tumours, molecular, pikpten, survival, lung,

Topics {✒️}

permissions reprints nature portfolio privacy policy breast cancer research advertising small-cell lung cancer social media author correspondence pkb/akt-dependent cell survival nature cell biol sh2 domain/phosphoprotein association radiation-induced lymphoma development phosphotyrosine-sh2 domain interactions impaired akt1–gsk3β signaling pi3k–pten signalling network nature rev tumorigenesis megan cully computer-aided molecular design age-dependent motor deficits nature med ideal/intact gefitinib trials nature genet akt-1/protein kinase bα pkb/akt phosphorylates p27 signal transduction laboratory combating pi3k-dependent tumours postnatal brain development personal data protein interaction domains raf/mek/erk pathways springerlink instant access data protection nature 428 nature 370 nature 408 nature 436 permissions nature pkb/akt-mediated phosphorylation nf1 tumor suppressor human endometrial cancer rapamycin-sensitive pathway required tacc1 promotes survival mild growth deficiency normal drosophila development article cully nutrient-sensitive interaction phase ii study small mouse phenotype protein kinase akt2

Questions {❓}

  • Does the ribosome translate cancer?
  • How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?
  • Selecting patients for epidermal growth factor receptor inhibitor treatment: a FISH story or a tale of mutations?

Schema {🗺️}

WebPage:
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         headline:Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis
         description: Mutation or deletion of PTEN is found in many cancers — however, in others, deregulation of the PI3K–PTEN network occurs in the absence of PTEN mutation. This review examines whether 'crosstalk' with other tumorigenic signalling pathways contributes to PI3K–PTEN deregulation. The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K–PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?
         datePublished:2006-02-02T00:00:00Z
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      headline:Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis
      description: Mutation or deletion of PTEN is found in many cancers — however, in others, deregulation of the PI3K–PTEN network occurs in the absence of PTEN mutation. This review examines whether 'crosstalk' with other tumorigenic signalling pathways contributes to PI3K–PTEN deregulation. The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K–PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?
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Social Networks {👍}(2)

External Links {🔗}(441)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
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Emails and Hosting {✉️}

Mail Servers:

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Name Servers:

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CDN Services {📦}

  • Crossref

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