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We are analyzing https://link.springer.com/article/10.1007/s10059-010-0122-z.

Title:
The neural stem cell fate determinant TLX promotes tumorigenesis and genesis of cells resembling glioma stem cells | Molecules and Cells
Description:
A growing body of evidence indicates that deregulation of stem cell fate determinants is a hallmark of many types of malignancies. The neural stem cell fate determinant TLX plays a pivotal role in neurogenesis in the adult brain by maintaining neural stem cells. Here, we report a tumorigenic role of TLX in brain tumor initiation and progression. Increased TLX expression was observed in a number of glioma cells and glioma stem cells, and correlated with poor survival of patients with gliomas. Ectopic expression of TLX in the U87MG glioma cell line and Ink4a/Arf-deficient mouse astrocytes (Ink4a/Arf-/- astrocytes) induced cell proliferation with a concomitant increase in cyclin D expression, and accelerated foci formation in soft agar and tumor formation in in vivo transplantation assays. Furthermore, overexpression of TLX in Ink4a/Arf-/- astrocytes inhibited cell migration and invasion and promoted neurosphere formation and Nestin expression, which are hallmark characteristics of glioma stem cells, under stem cell culture conditions. Our results indicate that TLX is involved in glioma stem cell genesis and represents a potential therapeutic target for this type of malignancy.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Education
  • Telecommunications

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 can't tell how the site generates income.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {πŸ”}

article, cell, stem, google, scholar, cas, pubmed, cells, cancer, neural, tlx, glioma, kim, park, brain, nature, nat, fate, receptor, tumor, expression, access, nuclear, privacy, cookies, content, research, genesis, jeon, human, biol, korea, information, publish, search, progression, mouse, astrocytes, cyclin, formation, rev, shi, data, log, journal, determinant, tumorigenesis, published, soeda, nam,

Topics {βœ’οΈ}

month download article/chapter ink4a/arf-deficient mouse astrocytes epithelial stem-cell compartments orphan nuclear receptor neural stem cell neural stem cells nuclear receptor tlx ink4a/arf-independent manner regulates cell numbers p53-deficient mouse astrocytes glial cells glioma stem cells cells hyo-jung park embryonic stem cell stem cell traits cancer stem cells wnt signalling pathways induced cell proliferation ink4a/arf-/- astrocytes sung-hak kim brain cancer stem related subjects full article pdf pten control neural privacy choices/manage cookies glioblastoma formation declines brain tumor initiation stem cells cells article increased tlx expression core regulatory circuit cyclin d1 mouse patched mutants jun-kyum kim glioma cells malignant tumour progression lineage-survival oncogenes conditions privacy policy european economic area potential therapeutic target double-edged sword mice lacking tcf-4 samsung medical center myung-jin park radiation molecular cancer hye-min jeon article molecules accelerated foci formation promoted neurosphere formation check access

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:The neural stem cell fate determinant TLX promotes tumorigenesis and genesis of cells resembling glioma stem cells
         description:A growing body of evidence indicates that deregulation of stem cell fate determinants is a hallmark of many types of malignancies. The neural stem cell fate determinant TLX plays a pivotal role in neurogenesis in the adult brain by maintaining neural stem cells. Here, we report a tumorigenic role of TLX in brain tumor initiation and progression. Increased TLX expression was observed in a number of glioma cells and glioma stem cells, and correlated with poor survival of patients with gliomas. Ectopic expression of TLX in the U87MG glioma cell line and Ink4a/Arf-deficient mouse astrocytes (Ink4a/Arf-/- astrocytes) induced cell proliferation with a concomitant increase in cyclin D expression, and accelerated foci formation in soft agar and tumor formation in in vivo transplantation assays. Furthermore, overexpression of TLX in Ink4a/Arf-/- astrocytes inhibited cell migration and invasion and promoted neurosphere formation and Nestin expression, which are hallmark characteristics of glioma stem cells, under stem cell culture conditions. Our results indicate that TLX is involved in glioma stem cell genesis and represents a potential therapeutic target for this type of malignancy.
         datePublished:2010-08-31T00:00:00Z
         dateModified:2010-08-31T00:00:00Z
         pageStart:403
         pageEnd:408
         sameAs:https://doi.org/10.1007/s10059-010-0122-z
         keywords:
            cancer stem cells
            cyclin D1
            glioma
            TLX
            Tumorigenesis
            Cell Biology
            Biochemistry
            general
            Biomedicine
            Biotechnology
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            issn:
               0219-1032
               1016-8478
            volumeNumber:30
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      headline:The neural stem cell fate determinant TLX promotes tumorigenesis and genesis of cells resembling glioma stem cells
      description:A growing body of evidence indicates that deregulation of stem cell fate determinants is a hallmark of many types of malignancies. The neural stem cell fate determinant TLX plays a pivotal role in neurogenesis in the adult brain by maintaining neural stem cells. Here, we report a tumorigenic role of TLX in brain tumor initiation and progression. Increased TLX expression was observed in a number of glioma cells and glioma stem cells, and correlated with poor survival of patients with gliomas. Ectopic expression of TLX in the U87MG glioma cell line and Ink4a/Arf-deficient mouse astrocytes (Ink4a/Arf-/- astrocytes) induced cell proliferation with a concomitant increase in cyclin D expression, and accelerated foci formation in soft agar and tumor formation in in vivo transplantation assays. Furthermore, overexpression of TLX in Ink4a/Arf-/- astrocytes inhibited cell migration and invasion and promoted neurosphere formation and Nestin expression, which are hallmark characteristics of glioma stem cells, under stem cell culture conditions. Our results indicate that TLX is involved in glioma stem cell genesis and represents a potential therapeutic target for this type of malignancy.
      datePublished:2010-08-31T00:00:00Z
      dateModified:2010-08-31T00:00:00Z
      pageStart:403
      pageEnd:408
      sameAs:https://doi.org/10.1007/s10059-010-0122-z
      keywords:
         cancer stem cells
         cyclin D1
         glioma
         TLX
         Tumorigenesis
         Cell Biology
         Biochemistry
         general
         Biomedicine
         Biotechnology
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            Periodical
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                     type:PostalAddress
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            name:Hye-Min Jeon
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                     name:Laboratory of Radiation Molecular Cancer, Korea Institute of Radiological and Medical Sciences, Seoul, Korea
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            address:
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               name:Cell Growth Regulation Laboratory, School of Life Sciences and Biotechnology, Korea University, Seoul, Korea
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               type:PostalAddress
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      name:Akio Soeda
      affiliation:
            name:University of Pittsburgh Cancer Institute
            address:
               name:Department of Medicine, Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, USA
               type:PostalAddress
            type:Organization
      name:Do-Hyun Nam
      affiliation:
            name:Sungkyunkwan University School of Medicine
            address:
               name:Department of Neurosurgery, Samsung Medical Center and Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea
               type:PostalAddress
            type:Organization
      name:Hyunggee Kim
      affiliation:
            name:Korea University
            address:
               name:Cell Growth Regulation Laboratory, School of Life Sciences and Biotechnology, Korea University, Seoul, Korea
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      name:Cell Growth Regulation Laboratory, School of Life Sciences and Biotechnology, Korea University, Seoul, Korea
      name:Cell Growth Regulation Laboratory, School of Life Sciences and Biotechnology, Korea University, Seoul, Korea
      name:Laboratory of Radiation Molecular Cancer, Korea Institute of Radiological and Medical Sciences, Seoul, Korea
      name:Department of Medicine, Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, USA
      name:Department of Neurosurgery, Samsung Medical Center and Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea
      name:Cell Growth Regulation Laboratory, School of Life Sciences and Biotechnology, Korea University, Seoul, Korea
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