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  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
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We are analyzing https://link.springer.com/article/10.1007/s10911-010-9175-z.

Title:
Epithelial Mesenchymal Transition Traits in Human Breast Cancer Cell Lines Parallel the CD44hi/CD24lo/- Stem Cell Phenotype in Human Breast Cancer | Journal of Mammary Gland Biology and Neoplasia
Description:
We review here the recently emerging relationship between epithelial-mesenchymal transition (EMT) and breast cancer stem cells (BCSC), and provide analyses of published data on human breast cancer cell lines, supporting their utility as a model for the EMT/BCSC state. Genome-wide transcriptional profiling of these cell lines has confirmed the existence of a subgroup with mesenchymal tendencies and enhanced invasive properties (ā€˜Basal B’/Mesenchymal), distinct from subgroups with either predominantly luminal (ā€˜Luminal’) or mixed basal/luminal (ā€˜Basal A’) features (Neve et al. Cancer Cell, 2006). A literature-derived EMT gene signature has shown specific enrichment within the Basal B subgroup of cell lines, consistent with their over-expression of various EMT transcriptional drivers. Basal B cell lines are found to resemble BCSC, being CD44highCD24low. Moreover, gene products that distinguish Basal B from Basal A and Luminal cell lines (Basal B Discriminators) showed close concordance with those that define BCSC isolated from clinical material, as reported by Shipitsin et al. (Cancer Cell, 2007). CD24 mRNA levels varied across Basal B cell lines, correlating with other Basal B Discriminators. Many gene products correlating with CD24 status in Basal B cell lines were also differentially expressed in isolated BCSC. These findings confirm and extend the importance of the cellular product of the EMT with Basal B cell lines, and illustrate the value of analysing these cell lines for new leads that may improve breast cancer outcomes. Gene products specific to Basal B cell lines may serve as tools for the detection, quantification, and analysis of BCSC/EMT attributes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {šŸ“}

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 {šŸ“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 7,643,078 visitors per month in the current month.

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How Does Link.springer.com Make Money? {šŸ’ø}

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 has a revenue plan, but it's either invisible or we haven't found it.

Keywords {šŸ”}

cancer, scholar, google, pubmed, cas, breast, cell, cells, transition, res, epithelial, stem, epithelialmesenchymal, human, tumor, mammary, lines, mesenchymal, thompson, gene, carcinoma, basal, expression, emt, metastasis, protein, research, article, growth, progression, clin, molecular, biol, patients, oncogene, axl, development, bone, marrow, kinase, newgreen, signaling, snail, med, phenotype, hugo, profiling, access, receptor, factor,

Topics {āœ’ļø}

rhoa/rock-dependent pathway increasing tgf-beta signaling month download article/chapter epithelial-mesenchymal transition regulates growth-arrest-specific gene 6 human breast cancer-observations mesenchymal transition-induced regulator tumorigenic breast-cancer cells confers epithelial-mesenchymal transition large-scale transcriptional profiling literature-derived gene list ccaat/enhancer binding protein decreased e-cadherin expression epithelial-mesenchymal transition biomarkers undergo epithelial-mesenchymal transition pmc42-la cells contract de-ac03-76sf00098 genome-wide transcriptional profiling cancer stem cells epithelial-mesenchymal transition markers stem cell traits normal stem cells mammary epithelial cells cell stem cell stem cell phenotype single stem cell stem cell characteristics galliher-beckley aj breast cancer cells disseminated tumor cells human breast cancer e-cadherin cox-2 mouse mammary gland related subjects cytokeratin-positive cells circulating tumor cells breast cancer patients differentiated human breast increased cell migration human breast tumors nuclear factor kappa cervical cancer cells cancer progenitor cells atypical protein kinase privacy choices/manage cookies receptor tyrosine kinases distinct growth factors human epithelial neoplasias epithelial-mesenchymal transition epithelial mesenchymal transition

Questions {ā“}

  • Carcinoma invasion and metastasis: a role for epithelial-mesenchymal transition?
  • The origin of vimentin expression in invasive breast cancer: epithelial-mesenchymal transition, myoepithelial histogenesis or histogenesis from progenitor cells with bilinear differentiation potential?

Schema {šŸ—ŗļø}

WebPage:
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         headline:Epithelial Mesenchymal Transition Traits in Human Breast Cancer Cell Lines Parallel the CD44hi/CD24lo/- Stem Cell Phenotype in Human Breast Cancer
         description:We review here the recently emerging relationship between epithelial-mesenchymal transition (EMT) and breast cancer stem cells (BCSC), and provide analyses of published data on human breast cancer cell lines, supporting their utility as a model for the EMT/BCSC state. Genome-wide transcriptional profiling of these cell lines has confirmed the existence of a subgroup with mesenchymal tendencies and enhanced invasive properties (ā€˜Basal B’/Mesenchymal), distinct from subgroups with either predominantly luminal (ā€˜Luminal’) or mixed basal/luminal (ā€˜Basal A’) features (Neve et al. Cancer Cell, 2006). A literature-derived EMT gene signature has shown specific enrichment within the Basal B subgroup of cell lines, consistent with their over-expression of various EMT transcriptional drivers. Basal B cell lines are found to resemble BCSC, being CD44highCD24low. Moreover, gene products that distinguish Basal B from Basal A and Luminal cell lines (Basal B Discriminators) showed close concordance with those that define BCSC isolated from clinical material, as reported by Shipitsin et al. (Cancer Cell, 2007). CD24 mRNA levels varied across Basal B cell lines, correlating with other Basal B Discriminators. Many gene products correlating with CD24 status in Basal B cell lines were also differentially expressed in isolated BCSC. These findings confirm and extend the importance of the cellular product of the EMT with Basal B cell lines, and illustrate the value of analysing these cell lines for new leads that may improve breast cancer outcomes. Gene products specific to Basal B cell lines may serve as tools for the detection, quantification, and analysis of BCSC/EMT attributes.
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      headline:Epithelial Mesenchymal Transition Traits in Human Breast Cancer Cell Lines Parallel the CD44hi/CD24lo/- Stem Cell Phenotype in Human Breast Cancer
      description:We review here the recently emerging relationship between epithelial-mesenchymal transition (EMT) and breast cancer stem cells (BCSC), and provide analyses of published data on human breast cancer cell lines, supporting their utility as a model for the EMT/BCSC state. Genome-wide transcriptional profiling of these cell lines has confirmed the existence of a subgroup with mesenchymal tendencies and enhanced invasive properties (ā€˜Basal B’/Mesenchymal), distinct from subgroups with either predominantly luminal (ā€˜Luminal’) or mixed basal/luminal (ā€˜Basal A’) features (Neve et al. Cancer Cell, 2006). A literature-derived EMT gene signature has shown specific enrichment within the Basal B subgroup of cell lines, consistent with their over-expression of various EMT transcriptional drivers. Basal B cell lines are found to resemble BCSC, being CD44highCD24low. Moreover, gene products that distinguish Basal B from Basal A and Luminal cell lines (Basal B Discriminators) showed close concordance with those that define BCSC isolated from clinical material, as reported by Shipitsin et al. (Cancer Cell, 2007). CD24 mRNA levels varied across Basal B cell lines, correlating with other Basal B Discriminators. Many gene products correlating with CD24 status in Basal B cell lines were also differentially expressed in isolated BCSC. These findings confirm and extend the importance of the cellular product of the EMT with Basal B cell lines, and illustrate the value of analysing these cell lines for new leads that may improve breast cancer outcomes. Gene products specific to Basal B cell lines may serve as tools for the detection, quantification, and analysis of BCSC/EMT attributes.
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         Breast cancer
         Breast cancer stem cell
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      affiliation:
            name:Lawrence Berkeley National Laboratory
            address:
               name:Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, USA
               type:PostalAddress
            type:Organization
            name:Boston University School of Medicine
            address:
               name:Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, USA
               type:PostalAddress
            type:Organization
      name:Erik W. Thompson
      affiliation:
            name:St. Vincent’s Institute
            address:
               name:Invasion and Metastasis Unit, St. Vincent’s Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
            name:St. Vincent’s Hospital, University of Melbourne
            address:
               name:Department of Surgery, St. Vincent’s Hospital, University of Melbourne, Fitzroy, Australia
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Invasion and Metastasis Unit, St. Vincent’s Institute, Melbourne, Australia
      name:Invasion and Metastasis Unit, St. Vincent’s Institute, Melbourne, Australia
      name:Department of Surgery, St. Vincent’s Hospital, University of Melbourne, Fitzroy, Australia
      name:Faculty of Medicine, Brawijaya University, East Java, Indonesia
      name:Invasion and Metastasis Unit, St. Vincent’s Institute, Melbourne, Australia
      name:Department of Surgery, St. Vincent’s Hospital, University of Melbourne, Fitzroy, Australia
      name:Invasion and Metastasis Unit, St. Vincent’s Institute, Melbourne, Australia
      name:Department of Surgery, St. Vincent’s Hospital, University of Melbourne, Fitzroy, Australia
      name:Department of Molecular Pathology, Unit 951, The University of Texas M. D. Anderson Cancer Center, Houston, USA
      name:Whitehead Institute for Biomedical Research, 9 Cambridge Center, and Department of Biology, Massachusetts Institute of Technology, Cambridge, USA
      name:Molecular Biology Department, Genentech Inc, South San Francisco, USA
      name:Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, USA
      name:Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, USA
      name:Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, USA
      name:Invasion and Metastasis Unit, St. Vincent’s Institute, Melbourne, Australia
      name:Department of Surgery, St. Vincent’s Hospital, University of Melbourne, Fitzroy, Australia
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