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We began analyzing https://www.tandfonline.com/doi/full/10.3109/07853890.2014.912836, but it redirected us to https://www.tandfonline.com/doi/full/10.3109/07853890.2014.912836. The analysis below is for the second page.

Title[redir]:
Full article: PI3K/AKT signaling pathway and cancer: an updated review
Description:
Key messagesThe PI3K pathway is one of the most frequently activated signal transduction pathways in human cancer.Alterations of the PI3K pathway may be responsible for drug sensitivity or resistan...

Matching Content Categories {πŸ“š}

  • Dating & Relationships
  • Education
  • Science

Content Management System {πŸ“}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {πŸ“ˆ}

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πŸ™οΈ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 96,105,781 visitors per month in the current month.

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We can't tell how the site generates income.

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 has a revenue plan, but it's either invisible or we haven't found it.

Keywords {πŸ”}

open, windowgoogle, scholar, cancer, science, windowpubmed, windowweb, citation, pik, mutations, kinase, akt, cell, class, pathway, pten, pikca, activation, breast, tumor, inhibitors, signaling, cells, piks, tumors, protein, patients, role, activity, mutation, mtor, phosphoinositide, clinical, res, studies, ras, citationcitation, inhibitor, reported, cancers, genetic, human, domain, treatment, phosphatidylinositol, clin, function, phosphatase, sciences, development,

Topics {βœ’οΈ}

4]oxazepin-9-yl]-1h-pyrazol-1-yl}-2-methylpropanamide social care medicine google scholar reprints pi3k/akt/mtor signaling pathway pi3k-akt pro-survival pathway igf-1/pi3k/akt signaling pathway survival/proliferative akt-mediated pathway anti-egfr monoclonal antibodies pi3k/akt/mtor inhibitors compared s6k1/pi3k/ras-dependent pathway references kaplan dr pik3c2a endothelial-restricted knock specific inflammatory conditions google scholar garrido-laguna google scholar sartore-bianchi egfr-targeted monoclonal antibodies pro-apoptotic foxo proteins pi3k-mediated cytoskeletal remodeling dual pi3k/mtor inhibitors journals medicine annals pi3k/akt/mtor inhibitors demonstrated phosphoinositide-3-kinase-protein kinase proline-rich akt substrate glucocorticoid-induced protein kinase refractory renal-cell carcinoma amp-activated protein kinase mitogen-activated protein kinase health sciences irinotecan-based adjuvant chemotherapy vivo pro-angiogenetic function kras-driven lung adenocarcinoma ubiquitin-mediated proteosome degradation toxic anti-cancer agents obligate p85-p110 heterodimers pi3k-regulated metabolic reactions pi3k-dependent feedback loop advanced renal-cell carcinoma erbb2-mediated breast cancer p84/p87 regulatory subunits liver-specific pi3k-c2Ξ³ essential spatio-temporal regulator pi3k/akt/mtor pathway pi3k inhibitor nvp-bkm120 include pi3k/mammalian target endothelial cell-specific deficiency insulin-mediated pi3k signaling request academic permissions pi3k/akt/mtor axis pi3k/akt/mtor inhibitors rac-related guanosine triphosphatases

Questions {❓}

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Schema {πŸ—ΊοΈ}

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            name:PI3K/AKT signaling pathway and cancer: a ....
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      publisher:Taylor & Francis Group
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      articleSection:Review Article
      name:PI3K/AKT signaling pathway and cancer: an updated review
      headline:PI3K/AKT signaling pathway and cancer: an updated review
      abstract:Despite development of novel agents targeting oncogenic pathways, matching targeted therapies to the genetic status of individual tumors is proving to be a daunting task for clinicians. To improve the clinical efficacy and to reduce the toxic side effects of treatments, a deep characterization of genetic alterations in different tumors is required. The mutational profile often evidences a gain of function or hyperactivity of phosphoinositide 3-kinases (PI3Ks) in tumors. These enzymes are activated downstream tyrosine kinase receptors (RTKs) and/or G proteins coupled receptors (GPCRs) and, via AKT, are able to induce mammalian target of rapamycin (mTOR) stimulation. Here, we elucidate the impact of class I (p110α, β, γ, and δ) catalytic subunit mutations on AKT-mediated cellular processes that control crucial mechanisms in tumor development. Moreover, the interrelation of PI3K signaling with mTOR, ERK, and RAS pathways will be discussed, exploiting the potential benefits of PI3K signaling inhibitors in clinical use.
      description:Despite development of novel agents targeting oncogenic pathways, matching targeted therapies to the genetic status of individual tumors is proving to be a daunting task for clinicians. To improve the clinical efficacy and to reduce the toxic side effects of treatments, a deep characterization of genetic alterations in different tumors is required. The mutational profile often evidences a gain of function or hyperactivity of phosphoinositide 3-kinases (PI3Ks) in tumors. These enzymes are activated downstream tyrosine kinase receptors (RTKs) and/or G proteins coupled receptors (GPCRs) and, via AKT, are able to induce mammalian target of rapamycin (mTOR) stimulation. Here, we elucidate the impact of class I (p110α, β, γ, and δ) catalytic subunit mutations on AKT-mediated cellular processes that control crucial mechanisms in tumor development. Moreover, the interrelation of PI3K signaling with mTOR, ERK, and RAS pathways will be discussed, exploiting the potential benefits of PI3K signaling inhibitors in clinical use.
      author:
            type:Person
            name:Federico Gulluni
            type:Person
            name:Maria Chiara De Santis
            type:Person
            name:Emilio Hirsch
            type:Person
            name:Miriam Martini
            type:Person
            name:Laura Braccini
            type:Person
            name:Emilio Hirsch
      keywords:Cancer, mTOR, PI3K, PI3K inhibitors, Ras, signaling
      pageStart:372
      pageEnd:383
      datePublished:2014-06-05
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      name:Maria Chiara De Santis
      name:Emilio Hirsch
      name:Miriam Martini
      name:Laura Braccini
      name:Emilio Hirsch
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