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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
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We are analyzing https://link.springer.com/article/10.1186/1475-2867-6-24.

Title:
Lymphokine-activated killer cell susceptibility and adhesion molecule expression of multidrug resistant breast carcinoma | Cancer Cell International
Description:
Reports showing susceptibility of multidrug resistant (MDR) cancer cells to immune effectors, together with P-glycoprotein (P-gp) expression in immune effector subsets, including immature natural killer (NK) cells, and some activated T cells, suggest P-gp or some changes associated with it, have implications in immune-mediated mechanisms. A series of experiments were done to determine the nature of alterations associated with susceptibility to immune effector cells of MDR tumor cells. A cell line isolated from the malignant pleural effusion of a breast cancer patient was transfected with human and murine MDR1 genes, and four variants with different levels of MDR were obtained. Lymphokine-activated killer (LAK) activity was measured by a 51Chromium release, and conjugate formation assays. MDR1 transfectant P-gp+ breast carcinoma lines had increased LAK susceptibility compared to their parent line. Some part of the increased LAK susceptibility of drug-resistant cell lines was at the binding/recognition level as shown by conjugate formation assays. This suggests that differences may exist between paired cell lines with respect to the expression of cell adhesion molecules (CAMs). Monoclonal antibodies (mAbs) to CAMs and flow cytometry were used to quantitate these antigens. The CAMs studied were those previously found to be upregulated by stimulating NK cells with (interleukin-2) IL-2; ICAM-1 (CD54), LFA-3 (CD58), N-CAM (CD56), and the Ξ² chain of LFA-1 (CD18). Although no differences in these CAMs were found between the breast carcinoma line and its MDR1-transfected variants, the target susceptibility results given above suggest that IL-2 treatment could be effective in combination with current protocols using chemotherapeutics, monoclonal antibodies (mAbs) and stem cell transplantation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Telecommunications
  • Education

Content Management System {πŸ“}

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 {πŸ“ˆ}

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? {πŸ’Έ}

We don't see any clear sign of profit-making.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {πŸ”}

cell, cells, lak, breast, cancer, pgp, mdr, human, lines, carcinoma, google, scholar, line, cas, expression, pubmed, article, susceptibility, increased, mdamb, tumor, mpahs, target, data, adhesion, binding, resistant, percent, release, mab, cml, killer, transfected, mdrtransfected, drug, test, mpam, min, multidrug, results, observed, determined, number, paired, lysis, sensitive, mpahsdox, surface, fluorescence, murine,

Topics {βœ’οΈ}

open access article wilcoxon signed-ranks matched-pairs node-negative breast carcinomas drug-resistant tumour cells full size image lymphokine-activated killer cells increased lymphokine-activated killer p-glycoprotein-mediated multidrug resistance her2-positive breast cancer drug-resistant cell lines mdr1-transfected cell lines lymphocyte-tumor cell conjugates full access targets-crossed species barriers article download pdf breast carcinoma line primary breast cancers variant h69/ar compared percent cell-mediated lysis lak cell-mediated cytotoxicity energy-dependent efflux pump breast carcinomas [11 colon-carcinoma cells resistant glutathione-s-transferase pi argon-ion laser running lymphokine-activated killer lak cell-mediated lysis blue-dead tumor cell goat-antimouse ig conjugated drug-sensitive parents suggest anti-p-gp mab mrk16 previously nk-resistant targets primary breast carcinoma human breast cancer mouse mdr1-transfected variants lobular breast carcinoma cell line variants goat anti-mouse ig peripheral blood lymphocytes derived tumour target cells human colon carcinoma colon-carcinoma lines paired cell lines cell line isolated mdr-transfected variants mpam-26 blue-dead tumor cells chronic myelogenous leukemia c-erbb-2 proto-oncogene mdr cell lines

Questions {❓}

  • Could this increased LAK susceptibility of P-gp+ cells be due to a change in adhesion molecules?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Lymphokine-activated killer cell susceptibility and adhesion molecule expression of multidrug resistant breast carcinoma
         description:Reports showing susceptibility of multidrug resistant (MDR) cancer cells to immune effectors, together with P-glycoprotein (P-gp) expression in immune effector subsets, including immature natural killer (NK) cells, and some activated T cells, suggest P-gp or some changes associated with it, have implications in immune-mediated mechanisms. A series of experiments were done to determine the nature of alterations associated with susceptibility to immune effector cells of MDR tumor cells. A cell line isolated from the malignant pleural effusion of a breast cancer patient was transfected with human and murine MDR1 genes, and four variants with different levels of MDR were obtained. Lymphokine-activated killer (LAK) activity was measured by a 51Chromium release, and conjugate formation assays. MDR1 transfectant P-gp+ breast carcinoma lines had increased LAK susceptibility compared to their parent line. Some part of the increased LAK susceptibility of drug-resistant cell lines was at the binding/recognition level as shown by conjugate formation assays. This suggests that differences may exist between paired cell lines with respect to the expression of cell adhesion molecules (CAMs). Monoclonal antibodies (mAbs) to CAMs and flow cytometry were used to quantitate these antigens. The CAMs studied were those previously found to be upregulated by stimulating NK cells with (interleukin-2) IL-2; ICAM-1 (CD54), LFA-3 (CD58), N-CAM (CD56), and the Ξ² chain of LFA-1 (CD18). Although no differences in these CAMs were found between the breast carcinoma line and its MDR1-transfected variants, the target susceptibility results given above suggest that IL-2 treatment could be effective in combination with current protocols using chemotherapeutics, monoclonal antibodies (mAbs) and stem cell transplantation.
         datePublished:2006-11-03T00:00:00Z
         dateModified:2006-11-03T00:00:00Z
         pageStart:1
         pageEnd:13
         license:https://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1475-2867-6-24
         keywords:
            Breast Carcinoma Cell Line
            51Cr Release
            Ovarian Carcinoma Cell Line
            Paired Cell Line
            Percent Positive Cell
            Cancer Research
            Cell Biology
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            issn:
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            volumeNumber:6
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            name:BioMed Central
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      headline:Lymphokine-activated killer cell susceptibility and adhesion molecule expression of multidrug resistant breast carcinoma
      description:Reports showing susceptibility of multidrug resistant (MDR) cancer cells to immune effectors, together with P-glycoprotein (P-gp) expression in immune effector subsets, including immature natural killer (NK) cells, and some activated T cells, suggest P-gp or some changes associated with it, have implications in immune-mediated mechanisms. A series of experiments were done to determine the nature of alterations associated with susceptibility to immune effector cells of MDR tumor cells. A cell line isolated from the malignant pleural effusion of a breast cancer patient was transfected with human and murine MDR1 genes, and four variants with different levels of MDR were obtained. Lymphokine-activated killer (LAK) activity was measured by a 51Chromium release, and conjugate formation assays. MDR1 transfectant P-gp+ breast carcinoma lines had increased LAK susceptibility compared to their parent line. Some part of the increased LAK susceptibility of drug-resistant cell lines was at the binding/recognition level as shown by conjugate formation assays. This suggests that differences may exist between paired cell lines with respect to the expression of cell adhesion molecules (CAMs). Monoclonal antibodies (mAbs) to CAMs and flow cytometry were used to quantitate these antigens. The CAMs studied were those previously found to be upregulated by stimulating NK cells with (interleukin-2) IL-2; ICAM-1 (CD54), LFA-3 (CD58), N-CAM (CD56), and the Ξ² chain of LFA-1 (CD18). Although no differences in these CAMs were found between the breast carcinoma line and its MDR1-transfected variants, the target susceptibility results given above suggest that IL-2 treatment could be effective in combination with current protocols using chemotherapeutics, monoclonal antibodies (mAbs) and stem cell transplantation.
      datePublished:2006-11-03T00:00:00Z
      dateModified:2006-11-03T00:00:00Z
      pageStart:1
      pageEnd:13
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1475-2867-6-24
      keywords:
         Breast Carcinoma Cell Line
         51Cr Release
         Ovarian Carcinoma Cell Line
         Paired Cell Line
         Percent Positive Cell
         Cancer Research
         Cell Biology
      image:
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            1475-2867
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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:Burhan Savas
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                  name:Akdeniz University
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                     type:PostalAddress
                  type:Organization
                  name:Queen's University
                  address:
                     name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
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         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
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      name:Akdeniz University
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         name:Dept. of Oncology, Akdeniz University, Antalya, Turkiye
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      name:Queen's University
      address:
         name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
         type:PostalAddress
      name:Queen's University
      address:
         name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
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         name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
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      name:Burhan Savas
      affiliation:
            name:Akdeniz University
            address:
               name:Dept. of Oncology, Akdeniz University, Antalya, Turkiye
               type:PostalAddress
            type:Organization
            name:Queen's University
            address:
               name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Pauline E Kerr
      affiliation:
            name:Queen's University
            address:
               name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
               type:PostalAddress
            type:Organization
      name:Hugh F Pross
      affiliation:
            name:Queen's University
            address:
               name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Dept. of Oncology, Akdeniz University, Antalya, Turkiye
      name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
      name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada
      name:Dept. of Microbiology and Immunology, Queen's University, Kingston, Canada

External Links {πŸ”—}(133)

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