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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. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. CDN Services

We are analyzing https://link.springer.com/article/10.1186/s12906-016-1088-y.

Title:
All-trans retinoic acids induce differentiation and sensitize a radioresistant breast cancer cells to chemotherapy | BMC Complementary Medicine and Therapies
Description:
Background Radiotherapy is of critical importance in the treatment of breast cancer. However, not all patients derive therapeutic benefit and some breast cancers are resistant to the treatment, and are thus evidenced with prospective distant metastatic spread and local recurrence. In this study, we investigated the potential therapeutic effects of all-trans retinoic acid (ATRA) on radiation-resistant breast cancer cells and the associated invasiveness. Methods The MCF7/C6 cells with gained radiation resistance after a long term treatment with fractionated ionizing radiation were derived from human breast cancer MCF7 cell line, and are enriched with cells expressing putative breast cancer stem cell biomarker CD44+/CD24-/low/ALDH+. The enhanced invasiveness and the acquired resistances to chemotherapeutic treatments of MCF7/C6 cells were measured, and potential effects of all-trans retinoic acid (ATRA) on the induction of differentiation, invasion and migration, and on the sensitivities to chemotherapies in MCF7/C6 cells were investigated. Results MCF7/C6 cells are with enrichment of cancer stem-cell like cells with positive staining of CD44+/CD24-/low, OCT3/4 and NANOG. MCF7/C6 cells showed an increased tumoregensis potential and enhanced aggressiveness of invasion and migration. Treatment with ATRA induces the differentiation in MCF7/C6 cells, resulting in reduced invasiveness and migration, and increased sensitivity to Epirubincin treatment. Conclusion Our study suggests a potential clinic impact for ATRA as a chemotherapeutic agent for treatment of therapy-resistant breast cancer especially for the metastatic lesions. The study also provides a rationale for ATRA as a sensitizer of Epirubincin, a first-line treatment option for breast cancer patients.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • 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 7,603,724 visitors per month in the current month.

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

We can't see how the site brings in money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

cells, cancer, mcfc, breast, pubmed, atra, cell, article, google, scholar, cas, treatment, radiation, stem, mcf, central, tumor, differentiation, survival, fig, analysis, migration, bcscs, data, patients, radioresistant, potential, therapeutic, invasiveness, control, study, assay, flow, res, metastatic, treated, showed, expression, showing, invasion, results, dna, metastasis, medium, clonogenic, resistance, enhanced, enrichment, reduced, clinical,

Topics {✒️}

jian jian li 5 μg circular pdsred-express2-n1 serum-free pbs/matrigel mixture cd44+/cd24-/low/aldh+ standard-anti-breast cancer chemotherapy fitc-conjugated anti-cd44 antibodies nuclear factor kappab cd44-overexpressed mcf7/c6 cells stem-cell surface markers radiation-resistant mcf7/c6 cells pe-conjugated anti-cd24 tp53-inactive human keratinocytes cd44+/cd24-/low-positive early-stage breast cancer therapy-resistant breast cancer article download pdf radiation-resistant breast cancer atra-treated mcf7/c6 cells epirubincin-treated mcf7/c6 cells mcf7/c6 cell population full size image therapy-resistant breast cancers female nod/scid mice vivo end-joining assay mrm-based targeted proteomics radioresistant mcf7/c6 population mcf7/c6 cells comparing lymph node-negative women linearized ej5-gfp plasmid radioresistant mcf7/c6 cells bd perm/washtm buffer radiation-induced adaptive responses pe-conjugated anti-sox2 cd44+/cd24-/low atra-induced cell cycle mcf7/c6 fir cells mcf7/c6 cells showed cancer stem-cell dna damage repair breast cancer research acute promyelocytic leukemia long-term fractionated doses sensitized mcf7/c6 cells mcf7/c6 cells exposed invasive breast cancer embryonic signaling pathways major life-threatening tumors mcf + fir cellular model mapk-dependent manner mcf7/c6 cells compared

Schema {🗺️}

WebPage:
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         headline:All-trans retinoic acids induce differentiation and sensitize a radioresistant breast cancer cells to chemotherapy
         description:Radiotherapy is of critical importance in the treatment of breast cancer. However, not all patients derive therapeutic benefit and some breast cancers are resistant to the treatment, and are thus evidenced with prospective distant metastatic spread and local recurrence. In this study, we investigated the potential therapeutic effects of all-trans retinoic acid (ATRA) on radiation-resistant breast cancer cells and the associated invasiveness. The MCF7/C6 cells with gained radiation resistance after a long term treatment with fractionated ionizing radiation were derived from human breast cancer MCF7 cell line, and are enriched with cells expressing putative breast cancer stem cell biomarker CD44+/CD24-/low/ALDH+. The enhanced invasiveness and the acquired resistances to chemotherapeutic treatments of MCF7/C6 cells were measured, and potential effects of all-trans retinoic acid (ATRA) on the induction of differentiation, invasion and migration, and on the sensitivities to chemotherapies in MCF7/C6 cells were investigated. MCF7/C6 cells are with enrichment of cancer stem-cell like cells with positive staining of CD44+/CD24-/low, OCT3/4 and NANOG. MCF7/C6 cells showed an increased tumoregensis potential and enhanced aggressiveness of invasion and migration. Treatment with ATRA induces the differentiation in MCF7/C6 cells, resulting in reduced invasiveness and migration, and increased sensitivity to Epirubincin treatment. Our study suggests a potential clinic impact for ATRA as a chemotherapeutic agent for treatment of therapy-resistant breast cancer especially for the metastatic lesions. The study also provides a rationale for ATRA as a sensitizer of Epirubincin, a first-line treatment option for breast cancer patients.
         datePublished:2016-03-31T00:00:00Z
         dateModified:2016-03-31T00:00:00Z
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         keywords:
            Breast cancer
            Radiation resistance
            Cancer stem cell
            ATRA
            Complementary & Alternative Medicine
            Internal Medicine
            Chiropractic Medicine
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                        type:PostalAddress
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                        name:Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China
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ScholarlyArticle:
      headline:All-trans retinoic acids induce differentiation and sensitize a radioresistant breast cancer cells to chemotherapy
      description:Radiotherapy is of critical importance in the treatment of breast cancer. However, not all patients derive therapeutic benefit and some breast cancers are resistant to the treatment, and are thus evidenced with prospective distant metastatic spread and local recurrence. In this study, we investigated the potential therapeutic effects of all-trans retinoic acid (ATRA) on radiation-resistant breast cancer cells and the associated invasiveness. The MCF7/C6 cells with gained radiation resistance after a long term treatment with fractionated ionizing radiation were derived from human breast cancer MCF7 cell line, and are enriched with cells expressing putative breast cancer stem cell biomarker CD44+/CD24-/low/ALDH+. The enhanced invasiveness and the acquired resistances to chemotherapeutic treatments of MCF7/C6 cells were measured, and potential effects of all-trans retinoic acid (ATRA) on the induction of differentiation, invasion and migration, and on the sensitivities to chemotherapies in MCF7/C6 cells were investigated. MCF7/C6 cells are with enrichment of cancer stem-cell like cells with positive staining of CD44+/CD24-/low, OCT3/4 and NANOG. MCF7/C6 cells showed an increased tumoregensis potential and enhanced aggressiveness of invasion and migration. Treatment with ATRA induces the differentiation in MCF7/C6 cells, resulting in reduced invasiveness and migration, and increased sensitivity to Epirubincin treatment. Our study suggests a potential clinic impact for ATRA as a chemotherapeutic agent for treatment of therapy-resistant breast cancer especially for the metastatic lesions. The study also provides a rationale for ATRA as a sensitizer of Epirubincin, a first-line treatment option for breast cancer patients.
      datePublished:2016-03-31T00:00:00Z
      dateModified:2016-03-31T00:00:00Z
      pageStart:1
      pageEnd:11
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12906-016-1088-y
      keywords:
         Breast cancer
         Radiation resistance
         Cancer stem cell
         ATRA
         Complementary & Alternative Medicine
         Internal Medicine
         Chiropractic Medicine
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            name:Yunwen Yan
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                  name:Institute of Clinical Pharmacology, Anhui Medical University
                  address:
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                     type:PostalAddress
                  type:Organization
                  name:Laboratory of Molecular Biology, Anhui Medical University
                  address:
                     name:Department of Biochemistry, Laboratory of Molecular Biology, Anhui Medical University, Hefei, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Zhen Li
            affiliation:
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                  address:
                     name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Xiang Xu
            affiliation:
                  name:University of California
                  address:
                     name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
                     type:PostalAddress
                  type:Organization
                  name:School of Life Sciences, Anhui University
                  address:
                     name:School of Life Sciences, Anhui University, Hefei, China
                     type:PostalAddress
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            name:Clark Chen
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                  address:
                     name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
                     type:PostalAddress
                  type:Organization
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            name:Wei Wei
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                  address:
                     name:Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ming Fan
            affiliation:
                  name:University of California
                  address:
                     name:Department of Radiation Oncology, University of California, Davis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Xufeng Chen
            affiliation:
                  name:University of California
                  address:
                     name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jian Jian Li
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                  address:
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                     type:PostalAddress
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            name:Yuan Wang
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                  name:Laboratory of Molecular Biology, Anhui Medical University
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                     type:PostalAddress
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      address:
         name:Department of Radiation Oncology, University of California, Davis, USA
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         name:Department of Radiation Oncology, University of California, Davis, USA
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      name:Xiang Xu
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      name:Clark Chen
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            address:
               name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
               type:PostalAddress
            type:Organization
      name:Wei Wei
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            name:Institute of Clinical Pharmacology, Anhui Medical University
            address:
               name:Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China
               type:PostalAddress
            type:Organization
      name:Ming Fan
      affiliation:
            name:University of California
            address:
               name:Department of Radiation Oncology, University of California, Davis, USA
               type:PostalAddress
            type:Organization
      name:Xufeng Chen
      affiliation:
            name:University of California
            address:
               name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
               type:PostalAddress
            type:Organization
      name:Jian Jian Li
      affiliation:
            name:University of California
            address:
               name:Department of Radiation Oncology, University of California, Davis, USA
               type:PostalAddress
            type:Organization
      name:Yuan Wang
      affiliation:
            name:Laboratory of Molecular Biology, Anhui Medical University
            address:
               name:Department of Biochemistry, Laboratory of Molecular Biology, Anhui Medical University, Hefei, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Jiaoti Huang
      affiliation:
            name:University of California
            address:
               name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China
      name:Department of Biochemistry, Laboratory of Molecular Biology, Anhui Medical University, Hefei, China
      name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
      name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
      name:School of Life Sciences, Anhui University, Hefei, China
      name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
      name:Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China
      name:Department of Radiation Oncology, University of California, Davis, USA
      name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA
      name:Department of Radiation Oncology, University of California, Davis, USA
      name:Department of Biochemistry, Laboratory of Molecular Biology, Anhui Medical University, Hefei, China
      name:Department of Pathology and Laboratory Medicine, University of California, Los Angeles, USA

External Links {🔗}(232)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

5.14s.