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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
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We are analyzing https://link.springer.com/article/10.1186/1471-2407-6-75.

Title:
CD40L induces multidrug resistance to apoptosis in breast carcinoma and lymphoma cells through caspase independent and dependent pathways | BMC Cancer
Description:
Background CD40L was found to reduce doxorubicin-induced apoptosis in non Hodgkin
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Telecommunications
  • Education

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 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💾}

We're unsure how the site profits.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

cell, cells, apoptosis, lines, cdl, carcinoma, breast, caspase, pubmed, google, scholar, cas, article, cancer, induced, nhl, lymphoma, cytotoxic, activity, drugs, agents, effect, ceramide, resistance, activation, dox, france, tested, cddp, ÎŒgml, human, tumor, hours, figure, modulation, inhibitors, coculture, ceramides, vin, eto, tax, table, parp, independent, pathways, expression, line, shown, blood, res,

Topics {✒}

laurent alberti & jean-yves blay jean-yves blay control c2-dihydroceramide n-acetyldihydrosphingosine open access article article voorzanger-rousselot le perray-en-yvelines n-hexanoyl-c6 ceramide human b-cell neoplasms tumor necrosis factor-alpha n-acetyl-c2 ceramide relapsed b-cell lymphoma trail death-receptor pathway drug-treated breast carcinoma alpha4beta1 integrin-mediated resistance rhÎne-poulenc-rorer pharma cd40 inhibits fas article download pdf saint-quentin en yvelines anti-cd40 antibody sgn-14 human b-lymphoma cells cytochrome c-dependent apoptosis dna damage-induced apoptosis repress drug-induced apoptosis anti-mu-induced apoptosis pre-publication history cd40/stromal cell system cytotoxic agent direct anti-proliferative effect apo-1/fas pathway preventing cd40-traf2 dissociation dna strand breaks induces fas expression yama/cpp32/apopain/caspase-3 anti-cancer drugs tested paclitaxel-induced apoptosis depends full access drug-induced cytostatic effect cisplatin-induced apoptosis proceeds 24-wells microtiter plates significant [3h]tdr incorporation de la savoie cell death differ mcf-7 cell line reduce doxorubicin-induced apoptosis carcinoma cell lines full length form tumor-infiltrating cytotoxic lymphocytes killing cancer cells fas-mediated apoptosis privacy choices/manage cookies

Questions {❓}

  • Radin NS: Killing cancer cells by poly-drug elevation of ceramide levels: a hypothesis whose time has come?

Schema {đŸ—ș}

WebPage:
      mainEntity:
         headline:CD40L induces multidrug resistance to apoptosis in breast carcinoma and lymphoma cells through caspase independent and dependent pathways
         description:CD40L was found to reduce doxorubicin-induced apoptosis in non Hodgkin's lymphoma cell lines through caspase-3 dependent mechanism. Whether this represents a general mechanism for other tumor types is unknown. The resistance induced by CD40L against apoptosis induced by a panel of cytotoxic chemotherapeutic drugs in non Hodgkin's lymphoma and breast carcinoma cell lines was investigated. Doxorubicin, cisplatyl, etoposide, vinblastin and paclitaxel increased apoptosis in a dose-dependent manner in breast carcinoma as well as in non Hodgkin's lymphoma cell lines. Co-culture with irradiated L cells expressing CD40L significantly reduced the percentage of apoptotic cells in breast carcinoma and non Hodgkin's lymphoma cell lines treated with these drugs. In breast carcinoma cell lines, these 5 drugs induced an inconsistent increase of caspase-3/7 activity, while in non Hodgkin's lymphoma cell lines all 5 drugs increased caspase-3/7 activity up to 28-fold above baseline. Co-culture with CD40L L cells reduced (-39% to -89%) the activation of caspase-3/7 induced by these agents in all 5 non Hodgkin's lymphoma cell lines, but in none of the 2 breast carcinoma cell lines. Co culture with CD40L L cells also blocked the apoptosis induced by exogenous ceramides in breast carcinoma and non Hodgkin's lymphoma cell lines through a caspase-3-like, 8-like and 9-like dependent pathways. These results indicate that CD40L expressed on adjacent non tumoral cells induces multidrug resistance to cytotoxic agents and ceramides in both breast carcinoma and non Hodgkin's lymphoma cell lines, albeit through a caspase independent and dependent pathway respectively.
         datePublished:2006-03-18T00:00:00Z
         dateModified:2006-03-18T00:00:00Z
         pageStart:1
         pageEnd:12
         license:https://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1471-2407-6-75
         keywords:
            Ceramide
            CDDP
            Cytotoxic Agent
            PARP Cleavage
            Lymphoma Cell Line
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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         isPartOf:
            name:BMC Cancer
            issn:
               1471-2407
            volumeNumber:6
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
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               type:ImageObject
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         author:
               name:Nathalie Voorzanger-Rousselot
               affiliation:
                     name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
                     address:
                        name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Laurent Alberti
               affiliation:
                     name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
                     address:
                        name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jean-Yves Blay
               affiliation:
                     name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
                     address:
                        name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
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ScholarlyArticle:
      headline:CD40L induces multidrug resistance to apoptosis in breast carcinoma and lymphoma cells through caspase independent and dependent pathways
      description:CD40L was found to reduce doxorubicin-induced apoptosis in non Hodgkin's lymphoma cell lines through caspase-3 dependent mechanism. Whether this represents a general mechanism for other tumor types is unknown. The resistance induced by CD40L against apoptosis induced by a panel of cytotoxic chemotherapeutic drugs in non Hodgkin's lymphoma and breast carcinoma cell lines was investigated. Doxorubicin, cisplatyl, etoposide, vinblastin and paclitaxel increased apoptosis in a dose-dependent manner in breast carcinoma as well as in non Hodgkin's lymphoma cell lines. Co-culture with irradiated L cells expressing CD40L significantly reduced the percentage of apoptotic cells in breast carcinoma and non Hodgkin's lymphoma cell lines treated with these drugs. In breast carcinoma cell lines, these 5 drugs induced an inconsistent increase of caspase-3/7 activity, while in non Hodgkin's lymphoma cell lines all 5 drugs increased caspase-3/7 activity up to 28-fold above baseline. Co-culture with CD40L L cells reduced (-39% to -89%) the activation of caspase-3/7 induced by these agents in all 5 non Hodgkin's lymphoma cell lines, but in none of the 2 breast carcinoma cell lines. Co culture with CD40L L cells also blocked the apoptosis induced by exogenous ceramides in breast carcinoma and non Hodgkin's lymphoma cell lines through a caspase-3-like, 8-like and 9-like dependent pathways. These results indicate that CD40L expressed on adjacent non tumoral cells induces multidrug resistance to cytotoxic agents and ceramides in both breast carcinoma and non Hodgkin's lymphoma cell lines, albeit through a caspase independent and dependent pathway respectively.
      datePublished:2006-03-18T00:00:00Z
      dateModified:2006-03-18T00:00:00Z
      pageStart:1
      pageEnd:12
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1471-2407-6-75
      keywords:
         Ceramide
         CDDP
         Cytotoxic Agent
         PARP Cleavage
         Lymphoma Cell Line
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-6-75/MediaObjects/12885_2005_Article_427_Fig1_HTML.jpg
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-6-75/MediaObjects/12885_2005_Article_427_Fig3_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-6-75/MediaObjects/12885_2005_Article_427_Fig4_HTML.jpg
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            1471-2407
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         name:BioMed Central
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            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
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      author:
            name:Nathalie Voorzanger-Rousselot
            affiliation:
                  name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
                  address:
                     name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Laurent Alberti
            affiliation:
                  name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
                  address:
                     name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jean-Yves Blay
            affiliation:
                  name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
                  address:
                     name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
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         name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
         type:PostalAddress
      name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
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      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Nathalie Voorzanger-Rousselot
      affiliation:
            name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
            address:
               name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
               type:PostalAddress
            type:Organization
      name:Laurent Alberti
      affiliation:
            name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
            address:
               name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
               type:PostalAddress
            type:Organization
      name:Jean-Yves Blay
      affiliation:
            name:UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard
            address:
               name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
      name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France
      name:Equipe Cytokines et Cancer, UnitĂ© INSERM U590, Centre LĂ©on BĂ©rard, LYON cedex 08, France

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