We are analyzing https://link.springer.com/article/10.1007/s00280-012-2043-3.

Title:
Overcoming acquired resistance to anticancer therapy: focus on the PI3K/AKT/mTOR pathway | Cancer Chemotherapy and Pharmacology
Description:
Background Most targeted anticancer therapies, as well as cytotoxic and radiation therapies, are encumbered by the development of secondary resistance by cancer cells. Resistance is a complex phenomenon involving multiple mechanisms, including activation of signaling pathways such as phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR). Novel strategies to overcome resistance by targeting these signaling pathways are being evaluated. Methods PubMed and key cancer congress abstracts were searched until July 2012 for preclinical and clinical data relating to the PI3K/AKT/mTOR pathway and anticancer treatment resistance, and use of PI3K/AKT/mTOR inhibitors in resistant cancer cell lines and patient populations. Results Activation of the PI3K/AKT/mTOR pathway is frequently implicated in resistance to anticancer therapies, including biologics, tyrosine kinase inhibitors, radiation, and cytotoxics. As such, inhibitors of the PI3K/AKT/mTOR pathway are being rapidly evaluated in preclinical models and in clinical studies to determine whether they can restore therapeutic sensitivity when given in combination. In breast cancer, non-small-cell lung cancer, and glioblastoma, we find compelling preclinical evidence to show that inhibitors of PI3K or mTOR can restore sensitivity in resistant cells. Although clinical evidence is less mature, a recent Phase III study with the mTORC1 inhibitor everolimus in patients with advanced breast cancer resistant to aromatase inhibition and several Phase I/II studies with PI3K inhibitors demonstrate proof-of-concept, warranting future clinical evaluation. Conclusion Current preclinical and clinical evidence suggest that inhibitors of the PI3K/AKT/mTOR pathway could have utility in combination with other anticancer therapies to circumvent resistance by cancer cells. Multiple clinical studies are ongoing.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Health & Fitness
Education
Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

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

Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We can't tell how the site generates income.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

cancer, google, scholar, article, pubmed, cas, breast, resistance, res, pathway, clin, cells, kinase, therapy, cell, pikaktmtor, inhibitors, lung, pik, trastuzumab, patients, oncol, inhibition, receptor, acquired, signaling, glioblastoma, egfr, research, phosphatidylinositol, targeting, inhibitor, wang, growth, activation, clinical, baselga, human, pten, estrogen, kim, anticancer, mtor, treatment, combination, expression, sci, mol, gefitinib, iii,

Topics {✒️}

ligand-independent her2/her3/pi3k complex dual pan-pi3-kinase/mtor inhibitor pi3k/mtor inhibitors nvp-bez235 month download article/chapter pi3k/akt/mtor axis inhibitors phosphatidylinositol 3-kinase/akt/mammalian target pi3k/akt/mtor pathway pi3k/akt/mtor pathway pi3k/akt kinase pathway phosphatidylinositol-3-kinase pathway predict 2/neu-positive breast cancer small-cell lung cancer pten/pi3k/akt pathway pi3k/akt/mtor inhibitors overcomes hgf-mediated resistance egfr-mutant lung cancer rad3-related-dependent manner pi3k/akt signaling pathways targeted anticancer therapies estrogen receptor-positive temozolomide-induced mitotic catastrophe her2-targeted agents phosphoinositide 3-kinase pathway mek/erk signaling pathways pi3-kinase inhibitor pi3k/akt pathway 2-positive breast cancer full article pdf targeted therapy article cancer chemotherapy lower estrogen-receptor drug-induced apoptosis phosphoinositide 3-kinase inhibition restore therapeutic sensitivity her2-directed therapy anti-her2 therapy erbb receptor network metastatic breast cancer breast cancer resistant neoadjuvant endocrine therapy kinase-inactive her3 pi3k inhibitor gdc-0941 estrogen-independent proliferation drug resistance mediated lung cancer cells growth factor activity advanced breast cancer privacy choices/manage cookies tyrosine kinase inhibitors breast cancer cells

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Overcoming acquired resistance to anticancer therapy: focus on the PI3K/AKT/mTOR pathway
         description:Most targeted anticancer therapies, as well as cytotoxic and radiation therapies, are encumbered by the development of secondary resistance by cancer cells. Resistance is a complex phenomenon involving multiple mechanisms, including activation of signaling pathways such as phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR). Novel strategies to overcome resistance by targeting these signaling pathways are being evaluated. PubMed and key cancer congress abstracts were searched until July 2012 for preclinical and clinical data relating to the PI3K/AKT/mTOR pathway and anticancer treatment resistance, and use of PI3K/AKT/mTOR inhibitors in resistant cancer cell lines and patient populations. Activation of the PI3K/AKT/mTOR pathway is frequently implicated in resistance to anticancer therapies, including biologics, tyrosine kinase inhibitors, radiation, and cytotoxics. As such, inhibitors of the PI3K/AKT/mTOR pathway are being rapidly evaluated in preclinical models and in clinical studies to determine whether they can restore therapeutic sensitivity when given in combination. In breast cancer, non-small-cell lung cancer, and glioblastoma, we find compelling preclinical evidence to show that inhibitors of PI3K or mTOR can restore sensitivity in resistant cells. Although clinical evidence is less mature, a recent Phase III study with the mTORC1 inhibitor everolimus in patients with advanced breast cancer resistant to aromatase inhibition and several Phase I/II studies with PI3K inhibitors demonstrate proof-of-concept, warranting future clinical evaluation. Current preclinical and clinical evidence suggest that inhibitors of the PI3K/AKT/mTOR pathway could have utility in combination with other anticancer therapies to circumvent resistance by cancer cells. Multiple clinical studies are ongoing.
         datePublished:2013-02-03T00:00:00Z
         dateModified:2013-02-03T00:00:00Z
         pageStart:829
         pageEnd:842
         sameAs:https://doi.org/10.1007/s00280-012-2043-3
         keywords:
            PI3K/AKT/mTOR pathway
            Resistance
            Sensitivity
            Breast cancer
            Lung cancer
            Glioblastoma
            Oncology
            Pharmacology/Toxicology
            Cancer Research
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00280-012-2043-3/MediaObjects/280_2012_2043_Fig1_HTML.gif
         isPartOf:
            name:Cancer Chemotherapy and Pharmacology
            issn:
               1432-0843
               0344-5704
            volumeNumber:71
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer-Verlag
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Howard A. Burris
               affiliation:
                     name:Sarah Cannon Research Institute
                     address:
                        name:Sarah Cannon Research Institute, Nashville, USA
                        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:Overcoming acquired resistance to anticancer therapy: focus on the PI3K/AKT/mTOR pathway
      description:Most targeted anticancer therapies, as well as cytotoxic and radiation therapies, are encumbered by the development of secondary resistance by cancer cells. Resistance is a complex phenomenon involving multiple mechanisms, including activation of signaling pathways such as phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR). Novel strategies to overcome resistance by targeting these signaling pathways are being evaluated. PubMed and key cancer congress abstracts were searched until July 2012 for preclinical and clinical data relating to the PI3K/AKT/mTOR pathway and anticancer treatment resistance, and use of PI3K/AKT/mTOR inhibitors in resistant cancer cell lines and patient populations. Activation of the PI3K/AKT/mTOR pathway is frequently implicated in resistance to anticancer therapies, including biologics, tyrosine kinase inhibitors, radiation, and cytotoxics. As such, inhibitors of the PI3K/AKT/mTOR pathway are being rapidly evaluated in preclinical models and in clinical studies to determine whether they can restore therapeutic sensitivity when given in combination. In breast cancer, non-small-cell lung cancer, and glioblastoma, we find compelling preclinical evidence to show that inhibitors of PI3K or mTOR can restore sensitivity in resistant cells. Although clinical evidence is less mature, a recent Phase III study with the mTORC1 inhibitor everolimus in patients with advanced breast cancer resistant to aromatase inhibition and several Phase I/II studies with PI3K inhibitors demonstrate proof-of-concept, warranting future clinical evaluation. Current preclinical and clinical evidence suggest that inhibitors of the PI3K/AKT/mTOR pathway could have utility in combination with other anticancer therapies to circumvent resistance by cancer cells. Multiple clinical studies are ongoing.
      datePublished:2013-02-03T00:00:00Z
      dateModified:2013-02-03T00:00:00Z
      pageStart:829
      pageEnd:842
      sameAs:https://doi.org/10.1007/s00280-012-2043-3
      keywords:
         PI3K/AKT/mTOR pathway
         Resistance
         Sensitivity
         Breast cancer
         Lung cancer
         Glioblastoma
         Oncology
         Pharmacology/Toxicology
         Cancer Research
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00280-012-2043-3/MediaObjects/280_2012_2043_Fig1_HTML.gif
      isPartOf:
         name:Cancer Chemotherapy and Pharmacology
         issn:
            1432-0843
            0344-5704
         volumeNumber:71
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Howard A. Burris
            affiliation:
                  name:Sarah Cannon Research Institute
                  address:
                     name:Sarah Cannon Research Institute, Nashville, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Cancer Chemotherapy and Pharmacology
      issn:
         1432-0843
         0344-5704
      volumeNumber:71
Organization:
      name:Springer-Verlag
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Sarah Cannon Research Institute
      address:
         name:Sarah Cannon Research Institute, Nashville, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Howard A. Burris
      affiliation:
            name:Sarah Cannon Research Institute
            address:
               name:Sarah Cannon Research Institute, Nashville, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Sarah Cannon Research Institute, Nashville, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(310)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

4.52s.

LINK . SPRINGER . COM {}