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NATURE . COM {}

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We are analyzing https://www.nature.com/articles/nrc1819.

Title:
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...
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

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?

🌆 Monumental Traffic: 20M - 50M visitors per month


Based on our best estimate, this website will receive around 42,554,915 visitors per month in the current month.

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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 {🎯}

$536,300 per month
According to our algorithms, Nature.com's monthly online income from display advertising ranges from $357,503 to $983,134.

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 {🗺️}

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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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