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We are analyzing https://link.springer.com/article/10.1186/1471-2407-11-529.

Title:
Human cancer cells express Slug-based epithelial-mesenchymal transition gene expression signature obtained in vivo | BMC Cancer
Description:
Background The biological mechanisms underlying cancer cell motility and invasiveness remain unclear, although it has been hypothesized that they involve some type of epithelial-mesenchymal transition (EMT). Methods We used xenograft models of human cancer cells in immunocompromised mice, profiling the harvested tumors separately with species-specific probes and computationally analyzing the results. Results Here we show that human cancer cells express in vivo a precise multi-cancer invasion-associated gene expression signature that prominently includes many EMT markers, among them the transcription factor Slug, fibronectin, and α-SMA. We found that human, but not mouse, cells express the signature and Slug is the only upregulated EMT-inducing transcription factor. The signature is also present in samples from many publicly available cancer gene expression datasets, suggesting that it is produced by the cancer cells themselves in multiple cancer types, including nonepithelial cancers such as neuroblastoma. Furthermore, we found that the presence of the signature in human xenografted cells was associated with a downregulation of adipocyte markers in the mouse tissue adjacent to the invasive tumor, suggesting that the signature is triggered by contextual microenvironmental interactions when the cancer cells encounter adipocytes, as previously reported. Conclusions The known, precise and consistent gene composition of this cancer mesenchymal transition signature, particularly when combined with simultaneous analysis of the adjacent microenvironment, provides unique opportunities for shedding light on the underlying mechanisms of cancer invasiveness as well as identifying potential diagnostic markers and targets for metastasis-inhibiting therapeutics.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

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 8,150,568 visitors per month in the current month.

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

We can't tell how the site generates income.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

cancer, cells, signature, genes, human, expression, emt, transition, cola, article, mouse, file, mesenchymal, pubmed, data, gene, additional, set, heat, google, scholar, tumor, figure, map, samples, markers, cas, cell, expressed, stem, found, presence, authors, analysis, tumors, transcription, slug, usa, central, epithelialmesenchymal, results, neuroblastoma, consistent, inhba, open, pdf, xenograft, upregulated, adipocyte, adipocytes,

Topics {✒️}

cancer cell-adipocyte interaction/crosstalk pre-publication history emt-inducing transcription factors article download pdf precise multi-cancer invasion epithelial-mesenchymal transition mesenchymal-epithelial transition cancer-type-specific stage suggests emt-specific gene expression transcription factor slug weiyi cheng & jianzhong huang slug-based emt slug-based signature originally obtained full size image epithelial-mesenchymal transitions underlying biological mechanism bmc med genomics mesenchymal transition process emt-related transition invasiveness remain unclear real-time pcr mesenchymal transition signature core epithelial related subjects investigate gene expression gene expression omnibus privacy choices/manage cookies gene expression analysis gene expression signature full access bmc cancer 11 mesenchymal stem cell inhba-transfected ngp cells breast cancer invasion emt core signature ovarian cancer development epithelio-mesenchymal transformation human cancer cells tumour progression underlying biological mechanisms full size table cancer stem cells cells express nat rev cancer motrescu er emt generates cells metastasis-inhibiting therapeutics biomed central article anastassiou

Questions {❓}

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Schema {🗺️}

WebPage:
      mainEntity:
         headline:Human cancer cells express Slug-based epithelial-mesenchymal transition gene expression signature obtained in vivo
         description:The biological mechanisms underlying cancer cell motility and invasiveness remain unclear, although it has been hypothesized that they involve some type of epithelial-mesenchymal transition (EMT). We used xenograft models of human cancer cells in immunocompromised mice, profiling the harvested tumors separately with species-specific probes and computationally analyzing the results. Here we show that human cancer cells express in vivo a precise multi-cancer invasion-associated gene expression signature that prominently includes many EMT markers, among them the transcription factor Slug, fibronectin, and α-SMA. We found that human, but not mouse, cells express the signature and Slug is the only upregulated EMT-inducing transcription factor. The signature is also present in samples from many publicly available cancer gene expression datasets, suggesting that it is produced by the cancer cells themselves in multiple cancer types, including nonepithelial cancers such as neuroblastoma. Furthermore, we found that the presence of the signature in human xenografted cells was associated with a downregulation of adipocyte markers in the mouse tissue adjacent to the invasive tumor, suggesting that the signature is triggered by contextual microenvironmental interactions when the cancer cells encounter adipocytes, as previously reported. The known, precise and consistent gene composition of this cancer mesenchymal transition signature, particularly when combined with simultaneous analysis of the adjacent microenvironment, provides unique opportunities for shedding light on the underlying mechanisms of cancer invasiveness as well as identifying potential diagnostic markers and targets for metastasis-inhibiting therapeutics.
         datePublished:2011-12-30T00:00:00Z
         dateModified:2011-12-30T00:00:00Z
         pageStart:1
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         license:http://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1471-2407-11-529
         keywords:
            Epithelial-mesenchymal transition
            Cancer stem cells
            Cancer invasiveness
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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ScholarlyArticle:
      headline:Human cancer cells express Slug-based epithelial-mesenchymal transition gene expression signature obtained in vivo
      description:The biological mechanisms underlying cancer cell motility and invasiveness remain unclear, although it has been hypothesized that they involve some type of epithelial-mesenchymal transition (EMT). We used xenograft models of human cancer cells in immunocompromised mice, profiling the harvested tumors separately with species-specific probes and computationally analyzing the results. Here we show that human cancer cells express in vivo a precise multi-cancer invasion-associated gene expression signature that prominently includes many EMT markers, among them the transcription factor Slug, fibronectin, and α-SMA. We found that human, but not mouse, cells express the signature and Slug is the only upregulated EMT-inducing transcription factor. The signature is also present in samples from many publicly available cancer gene expression datasets, suggesting that it is produced by the cancer cells themselves in multiple cancer types, including nonepithelial cancers such as neuroblastoma. Furthermore, we found that the presence of the signature in human xenografted cells was associated with a downregulation of adipocyte markers in the mouse tissue adjacent to the invasive tumor, suggesting that the signature is triggered by contextual microenvironmental interactions when the cancer cells encounter adipocytes, as previously reported. The known, precise and consistent gene composition of this cancer mesenchymal transition signature, particularly when combined with simultaneous analysis of the adjacent microenvironment, provides unique opportunities for shedding light on the underlying mechanisms of cancer invasiveness as well as identifying potential diagnostic markers and targets for metastasis-inhibiting therapeutics.
      datePublished:2011-12-30T00:00:00Z
      dateModified:2011-12-30T00:00:00Z
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      license:http://creativecommons.org/licenses/by/2.0
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         Epithelial-mesenchymal transition
         Cancer stem cells
         Cancer invasiveness
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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                  address:
                     name:Department of Electrical Engineering, Columbia University, New York, USA
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                  address:
                     name:Department of Pathology and Cell Biology, Columbia University, New York, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Darrell J Yamashiro
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                  address:
                     name:Institute for Cancer Genetics, Columbia University, New York, USA
                     type:PostalAddress
                  type:Organization
                  name:Columbia University
                  address:
                     name:Department of Pathology and Cell Biology, Columbia University, New York, USA
                     type:PostalAddress
                  type:Organization
                  name:Columbia University
                  address:
                     name:Department of Pediatrics, Columbia University, New York, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jessica J Kandel
            affiliation:
                  name:Columbia University
                  address:
                     name:Institute for Cancer Genetics, Columbia University, New York, USA
                     type:PostalAddress
                  type:Organization
                  name:Columbia University
                  address:
                     name:Department of Surgery, Columbia University, New York, USA
                     type:PostalAddress
                  type:Organization
                  name:Columbia University
                  address:
                     name:Department of Pediatrics, Columbia University, New York, USA
                     type:PostalAddress
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         name:Department of Pathology and Cell Biology, Columbia University, New York, USA
         type:PostalAddress
      name:Columbia University
      address:
         name:Institute for Cancer Genetics, Columbia University, New York, USA
         type:PostalAddress
      name:Columbia University
      address:
         name:Department of Pathology and Cell Biology, Columbia University, New York, USA
         type:PostalAddress
      name:Columbia University
      address:
         name:Department of Pediatrics, Columbia University, New York, USA
         type:PostalAddress
      name:Columbia University
      address:
         name:Institute for Cancer Genetics, Columbia University, New York, USA
         type:PostalAddress
      name:Columbia University
      address:
         name:Department of Surgery, Columbia University, New York, USA
         type:PostalAddress
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      affiliation:
            name:Columbia University
            address:
               name:Center for Computational Biology and Bioinformatics, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
            name:Columbia University
            address:
               name:Department of Electrical Engineering, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
      name:Jianzhong Huang
      affiliation:
            name:Columbia University
            address:
               name:Department of Electrical Engineering, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
      name:Peter D Canoll
      affiliation:
            name:Columbia University
            address:
               name:Department of Pathology and Cell Biology, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
      name:Darrell J Yamashiro
      affiliation:
            name:Columbia University
            address:
               name:Institute for Cancer Genetics, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
            name:Columbia University
            address:
               name:Department of Pathology and Cell Biology, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
            name:Columbia University
            address:
               name:Department of Pediatrics, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
      name:Jessica J Kandel
      affiliation:
            name:Columbia University
            address:
               name:Institute for Cancer Genetics, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
            name:Columbia University
            address:
               name:Department of Surgery, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
            name:Columbia University
            address:
               name:Department of Pediatrics, Columbia University, New York, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Center for Computational Biology and Bioinformatics, Columbia University, New York, USA
      name:Department of Electrical Engineering, Columbia University, New York, USA
      name:Department of Electrical Engineering, Columbia University, New York, USA
      name:Center for Computational Biology and Bioinformatics, Columbia University, New York, USA
      name:Department of Electrical Engineering, Columbia University, New York, USA
      name:Department of Electrical Engineering, Columbia University, New York, USA
      name:Department of Pathology and Cell Biology, Columbia University, New York, USA
      name:Institute for Cancer Genetics, Columbia University, New York, USA
      name:Department of Pathology and Cell Biology, Columbia University, New York, USA
      name:Department of Pediatrics, Columbia University, New York, USA
      name:Institute for Cancer Genetics, Columbia University, New York, USA
      name:Department of Surgery, Columbia University, New York, USA
      name:Department of Pediatrics, Columbia University, New York, USA

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