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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s10495-017-1375-1.

Title:
Overcoming chemotherapy drug resistance by targeting inhibitors of apoptosis proteins (IAPs) | Apoptosis
Description:
Inhibitors of apoptosis (IAPs) are a family of proteins that play a significant role in the control of programmed cell death (PCD). PCD is essential to maintain healthy cell turnover within tissue but also to fight disease or infection. Uninhibited, IAPs can suppress apoptosis and promote cell cycle progression. Therefore, it is unsurprising that cancer cells demonstrate significantly elevated expression levels of IAPs, resulting in improved cell survival, enhanced tumor growth and subsequent metastasis. Therapies to target IAPs in cancer has garnered substantial scientific interest and as resistance to anti-cancer agents becomes more prevalent, targeting IAPs has become an increasingly attractive strategy to re-sensitize cancer cells to chemotherapies, antibody based-therapies and TRAIL therapy. Antagonism strategies to modulate the actions of XIAP, cIAP1/2 and survivin are the central focus of current research and this review highlights advances within this field with particular emphasis upon the development and specificity of second mitochondria-derived activator of caspase (SMAC) mimetics (synthetic analogs of endogenously expressed inhibitors of IAPs SMAC/DIABLO). While we highlight the potential of SMAC mimetics as effective single agent or combinatory therapies to treat cancer we also discuss the likely clinical implications of resistance to SMAC mimetic therapy, occasionally observed in cancer cell lines.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

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 5,000,016 visitors per month in the current month.

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

We find it hard to spot revenue streams.

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. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

pubmed, google, scholar, article, cancer, cas, apoptosis, cell, cells, smac, death, resistance, xiap, central, expression, iaps, proteins, trail, ciap, protein, inhibitor, iap, mimetic, apoptotic, caspase, mimetics, intrinsic, pathway, mitochondrial, survivin, inhibitors, bcl, targeting, treatment, domain, tumor, therapy, activation, bir, signaling, pathways, receptor, chemotherapy, carcinoma, human, biol, bax, wang, clinical, activity,

Topics {✒️}

formic acid–phenylalanine–aline–alanine isoleucine–phenylalanine–valine–alanine iv tnf-related apoptosis-inducing ligand alanine–valine–phenylalanine–isoleucine bad trail/apo-2l-mediated apoptosis dietrich büsselberg alanine–valine–phenylalanine–isoleucine isoleucine–phenylalanine–valine–alanine multi-domain pro-apoptotic proteins clinical profile bax-/bax-deficient hct-116 cells mda-mb-231-txsa cells elizabeth varghese article download pdf mda-mb-txsa tumors x-linked lymphoproliferative syndrome kainic acid-induced injury bir-ubiquitin conjugating enzyme aggressive myc-driven lymphoma retro-inverse smac peptide polyarginine-conjugated smac peptide potent small-molecule antagonist anti-tumor antibiotic bleomycin endogenous smac/diablo exerts death-inducing signaling complex tnf-alpha dependent apoptosis constitutive nf-kb signaling tnfalpha-mediated cell death tnf-α-mediated apoptosis aberrant nf-kb activity increased cell-surface expression small-cell lung cancer cancer treatment profiles alternative nf-kappab pathways tnf-alpha-independent mechanism anti-apoptotic bcl-2 proteins bcl-2 anti-apoptotic proteins retro-inverse smac peptides retro-inverso smac peptides avpi n-terminal sequence h-bond charge affinity enhanced trail-induced apoptosis patient-derived xenograft models induce tnf-α production nf-kappab-dependent manner cancer pro-apoptotic factors apoptosis-inducing caspase-cascade anti-apoptotic bcl-2 members smac-mimetic-induced apoptosis trail-mediated dr5-disc formation

Questions {❓}

  • How best to target IAPs to overcome drug resistance?
  • How to tackle acquired resistance to IAP antagonism?
  • Van Roosmalen IA, Quax WJ, Kruyt FA (2014) Two death-inducing human TRAIL receptors to target in cancer: similar or distinct regulation and function?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Overcoming chemotherapy drug resistance by targeting inhibitors of apoptosis proteins (IAPs)
         description:Inhibitors of apoptosis (IAPs) are a family of proteins that play a significant role in the control of programmed cell death (PCD). PCD is essential to maintain healthy cell turnover within tissue but also to fight disease or infection. Uninhibited, IAPs can suppress apoptosis and promote cell cycle progression. Therefore, it is unsurprising that cancer cells demonstrate significantly elevated expression levels of IAPs, resulting in improved cell survival, enhanced tumor growth and subsequent metastasis. Therapies to target IAPs in cancer has garnered substantial scientific interest and as resistance to anti-cancer agents becomes more prevalent, targeting IAPs has become an increasingly attractive strategy to re-sensitize cancer cells to chemotherapies, antibody based-therapies and TRAIL therapy. Antagonism strategies to modulate the actions of XIAP, cIAP1/2 and survivin are the central focus of current research and this review highlights advances within this field with particular emphasis upon the development and specificity of second mitochondria-derived activator of caspase (SMAC) mimetics (synthetic analogs of endogenously expressed inhibitors of IAPs SMAC/DIABLO). While we highlight the potential of SMAC mimetics as effective single agent or combinatory therapies to treat cancer we also discuss the likely clinical implications of resistance to SMAC mimetic therapy, occasionally observed in cancer cell lines.
         datePublished:2017-04-19T00:00:00Z
         dateModified:2017-04-19T00:00:00Z
         pageStart:898
         pageEnd:919
         license:http://creativecommons.org/licenses/by/4.0/
         sameAs:https://doi.org/10.1007/s10495-017-1375-1
         keywords:
            Chemotherapy resistance
            Inhibitors of apoptosis proteins
            Combination therapy
            Intrinsic apoptotic pathway
            Extrinsic apoptotic pathway
            Cancer Research
            Cell Biology
            Oncology
            Biochemistry
            general
            Virology
         image:
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         isPartOf:
            name:Apoptosis
            issn:
               1573-675X
               1360-8185
            volumeNumber:22
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Rama Rathore
               affiliation:
                     name:University of Michigan-Ann Arbor
                     address:
                        name:College of Literature, Sciences and the Arts, University of Michigan-Ann Arbor, Ann Arbor, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jennifer E. McCallum
               affiliation:
                     name:Weill Cornell Medicine-Qatar
                     address:
                        name:Weill Cornell Medicine-Qatar, Doha, Qatar
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Elizabeth Varghese
               affiliation:
                     name:Weill Cornell Medicine-Qatar
                     address:
                        name:Weill Cornell Medicine-Qatar, Doha, Qatar
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ana-Maria Florea
               affiliation:
                     name:Heinrich Heine University Düsseldorf
                     address:
                        name:Institute of Neuropathology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Dietrich Büsselberg
               url:http://orcid.org/0000-0001-5196-3366
               affiliation:
                     name:Weill Cornell Medicine-Qatar
                     address:
                        name:Weill Cornell Medicine-Qatar, Doha, Qatar
                        type:PostalAddress
                     type:Organization
               email:[email protected]
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      context:https://schema.org
ScholarlyArticle:
      headline:Overcoming chemotherapy drug resistance by targeting inhibitors of apoptosis proteins (IAPs)
      description:Inhibitors of apoptosis (IAPs) are a family of proteins that play a significant role in the control of programmed cell death (PCD). PCD is essential to maintain healthy cell turnover within tissue but also to fight disease or infection. Uninhibited, IAPs can suppress apoptosis and promote cell cycle progression. Therefore, it is unsurprising that cancer cells demonstrate significantly elevated expression levels of IAPs, resulting in improved cell survival, enhanced tumor growth and subsequent metastasis. Therapies to target IAPs in cancer has garnered substantial scientific interest and as resistance to anti-cancer agents becomes more prevalent, targeting IAPs has become an increasingly attractive strategy to re-sensitize cancer cells to chemotherapies, antibody based-therapies and TRAIL therapy. Antagonism strategies to modulate the actions of XIAP, cIAP1/2 and survivin are the central focus of current research and this review highlights advances within this field with particular emphasis upon the development and specificity of second mitochondria-derived activator of caspase (SMAC) mimetics (synthetic analogs of endogenously expressed inhibitors of IAPs SMAC/DIABLO). While we highlight the potential of SMAC mimetics as effective single agent or combinatory therapies to treat cancer we also discuss the likely clinical implications of resistance to SMAC mimetic therapy, occasionally observed in cancer cell lines.
      datePublished:2017-04-19T00:00:00Z
      dateModified:2017-04-19T00:00:00Z
      pageStart:898
      pageEnd:919
      license:http://creativecommons.org/licenses/by/4.0/
      sameAs:https://doi.org/10.1007/s10495-017-1375-1
      keywords:
         Chemotherapy resistance
         Inhibitors of apoptosis proteins
         Combination therapy
         Intrinsic apoptotic pathway
         Extrinsic apoptotic pathway
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
         general
         Virology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-017-1375-1/MediaObjects/10495_2017_1375_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10495-017-1375-1/MediaObjects/10495_2017_1375_Fig2_HTML.gif
      isPartOf:
         name:Apoptosis
         issn:
            1573-675X
            1360-8185
         volumeNumber:22
         type:
            Periodical
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      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Rama Rathore
            affiliation:
                  name:University of Michigan-Ann Arbor
                  address:
                     name:College of Literature, Sciences and the Arts, University of Michigan-Ann Arbor, Ann Arbor, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jennifer E. McCallum
            affiliation:
                  name:Weill Cornell Medicine-Qatar
                  address:
                     name:Weill Cornell Medicine-Qatar, Doha, Qatar
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Elizabeth Varghese
            affiliation:
                  name:Weill Cornell Medicine-Qatar
                  address:
                     name:Weill Cornell Medicine-Qatar, Doha, Qatar
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ana-Maria Florea
            affiliation:
                  name:Heinrich Heine University Düsseldorf
                  address:
                     name:Institute of Neuropathology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Dietrich Büsselberg
            url:http://orcid.org/0000-0001-5196-3366
            affiliation:
                  name:Weill Cornell Medicine-Qatar
                  address:
                     name:Weill Cornell Medicine-Qatar, Doha, Qatar
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
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      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
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      name:University of Michigan-Ann Arbor
      address:
         name:College of Literature, Sciences and the Arts, University of Michigan-Ann Arbor, Ann Arbor, USA
         type:PostalAddress
      name:Weill Cornell Medicine-Qatar
      address:
         name:Weill Cornell Medicine-Qatar, Doha, Qatar
         type:PostalAddress
      name:Weill Cornell Medicine-Qatar
      address:
         name:Weill Cornell Medicine-Qatar, Doha, Qatar
         type:PostalAddress
      name:Heinrich Heine University Düsseldorf
      address:
         name:Institute of Neuropathology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
         type:PostalAddress
      name:Weill Cornell Medicine-Qatar
      address:
         name:Weill Cornell Medicine-Qatar, Doha, Qatar
         type:PostalAddress
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      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Rama Rathore
      affiliation:
            name:University of Michigan-Ann Arbor
            address:
               name:College of Literature, Sciences and the Arts, University of Michigan-Ann Arbor, Ann Arbor, USA
               type:PostalAddress
            type:Organization
      name:Jennifer E. McCallum
      affiliation:
            name:Weill Cornell Medicine-Qatar
            address:
               name:Weill Cornell Medicine-Qatar, Doha, Qatar
               type:PostalAddress
            type:Organization
      name:Elizabeth Varghese
      affiliation:
            name:Weill Cornell Medicine-Qatar
            address:
               name:Weill Cornell Medicine-Qatar, Doha, Qatar
               type:PostalAddress
            type:Organization
      name:Ana-Maria Florea
      affiliation:
            name:Heinrich Heine University Düsseldorf
            address:
               name:Institute of Neuropathology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
               type:PostalAddress
            type:Organization
      name:Dietrich Büsselberg
      url:http://orcid.org/0000-0001-5196-3366
      affiliation:
            name:Weill Cornell Medicine-Qatar
            address:
               name:Weill Cornell Medicine-Qatar, Doha, Qatar
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:College of Literature, Sciences and the Arts, University of Michigan-Ann Arbor, Ann Arbor, USA
      name:Weill Cornell Medicine-Qatar, Doha, Qatar
      name:Weill Cornell Medicine-Qatar, Doha, Qatar
      name:Institute of Neuropathology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
      name:Weill Cornell Medicine-Qatar, Doha, Qatar

External Links {🔗}(788)

Analytics and Tracking {📊}

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Libraries {📚}

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CDN Services {📦}

  • Crossref

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