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We are analyzing https://link.springer.com/article/10.1186/gb-2008-9-5-r83.

Title:
Gene expression profiling of human prostate cancer stem cells reveals a pro-inflammatory phenotype and the importance of extracellular matrix interactions | Genome Biology
Description:
Background The tumor-initiating capacity of many cancers is considered to reside in a small subpopulation of cells (cancer stem cells). We have previously shown that rare prostate epithelial cells with a CD133+/α2β1 hi phenotype have the properties of prostate cancer stem cells. We have compared gene expression in these cells relative to their normal and differentiated (CD133-/α2β1 low) counterparts, resulting in an informative cancer stem cell gene-expression signature. Results Cell cultures were generated from specimens of human prostate cancers (n = 12) and non-malignant control tissues (n = 7). Affymetrix gene-expression arrays were used to analyze total cell RNA from sorted cell populations, and expression changes were selectively validated by quantitative RT-PCR, flow cytometry and immunocytochemistry. Differential expression of multiple genes associated with inflammation, cellular adhesion, and metastasis was observed. Functional studies, using an inhibitor of nuclear factor κB (NF-κB), revealed preferential targeting of the cancer stem cell and progenitor population for apoptosis whilst sparing normal stem cells. NF-κB is a major factor controlling the ability of tumor cells to resist apoptosis and provides an attractive target for new chemopreventative and chemotherapeutic approaches. Conclusion We describe an expression signature of 581 genes whose levels are significantly different in prostate cancer stem cells. Functional annotation of this signature identified the JAK-STAT pathway and focal adhesion signaling as key processes in the biology of cancer stem cells.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
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Content Management System {📝}

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Custom-built

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Traffic Estimate {📈}

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

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Topics {✒️}

/support/technical/manual/expression_manual human colon-cancer-initiating cells benign prostatic hyperplasia article number r83 article download pdf affymetrix hg-u133plus2 genechip cytokine-cytokine receptor interaction nf-κb p65 subunit extracellular matrix-receptor interaction full size image extracellular matrix-receptor signaling extracellular matrix-receptor system ice-cold methanol/acetone ikk/nf-κb signaling qiagen rneasy micro-columns qiagen rneasy mini-columns 5-trisphosphate kinase/akt axis transcription factor nf-κb gene expression profiling cd34+cd38- surface antigens alpha-methylacyl-coa racemase cancer-specific cd133 population micro-dissected prostate tumors annexin-v-/dapi- cells anti-photobleaching medium vectashield similar tumor-initiating cells growth factor-modulated proteolysis blocking nf-κb signaling benign rt-pcr results secreted metallo-protease pappalysin yorkshire cancer research bone marrow-derived cells affymetrix gene-expression arrays cancer stem cell stem-cell biology hormone-refractory tumors form stem cell isolations nf-κb inhibitor studies real-time pcr probes received hormone therapy stem cell population cd133-/α2β1 low cells human prostate cancer article birnie dual-color imaging wnt/beta-catenin signaling sesquiterpene lactone parthenolide fusion product tmpss2 cancer stem cells authors’ original file

Schema {🗺️}

WebPage:
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         headline:Gene expression profiling of human prostate cancer stem cells reveals a pro-inflammatory phenotype and the importance of extracellular matrix interactions
         description:The tumor-initiating capacity of many cancers is considered to reside in a small subpopulation of cells (cancer stem cells). We have previously shown that rare prostate epithelial cells with a CD133+/α2β1 hi phenotype have the properties of prostate cancer stem cells. We have compared gene expression in these cells relative to their normal and differentiated (CD133-/α2β1 low) counterparts, resulting in an informative cancer stem cell gene-expression signature. Cell cultures were generated from specimens of human prostate cancers (n = 12) and non-malignant control tissues (n = 7). Affymetrix gene-expression arrays were used to analyze total cell RNA from sorted cell populations, and expression changes were selectively validated by quantitative RT-PCR, flow cytometry and immunocytochemistry. Differential expression of multiple genes associated with inflammation, cellular adhesion, and metastasis was observed. Functional studies, using an inhibitor of nuclear factor κB (NF-κB), revealed preferential targeting of the cancer stem cell and progenitor population for apoptosis whilst sparing normal stem cells. NF-κB is a major factor controlling the ability of tumor cells to resist apoptosis and provides an attractive target for new chemopreventative and chemotherapeutic approaches. We describe an expression signature of 581 genes whose levels are significantly different in prostate cancer stem cells. Functional annotation of this signature identified the JAK-STAT pathway and focal adhesion signaling as key processes in the biology of cancer stem cells.
         datePublished:2008-05-20T00:00:00Z
         dateModified:2008-05-20T00:00:00Z
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            Prostate Cancer
            Gene Ontology
            Cancer Stem Cell
            Benign Prostatic Hyperplasia
            Stem Cell Population
            Animal Genetics and Genomics
            Human Genetics
            Plant Genetics and Genomics
            Microbial Genetics and Genomics
            Bioinformatics
            Evolutionary Biology
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ScholarlyArticle:
      headline:Gene expression profiling of human prostate cancer stem cells reveals a pro-inflammatory phenotype and the importance of extracellular matrix interactions
      description:The tumor-initiating capacity of many cancers is considered to reside in a small subpopulation of cells (cancer stem cells). We have previously shown that rare prostate epithelial cells with a CD133+/α2β1 hi phenotype have the properties of prostate cancer stem cells. We have compared gene expression in these cells relative to their normal and differentiated (CD133-/α2β1 low) counterparts, resulting in an informative cancer stem cell gene-expression signature. Cell cultures were generated from specimens of human prostate cancers (n = 12) and non-malignant control tissues (n = 7). Affymetrix gene-expression arrays were used to analyze total cell RNA from sorted cell populations, and expression changes were selectively validated by quantitative RT-PCR, flow cytometry and immunocytochemistry. Differential expression of multiple genes associated with inflammation, cellular adhesion, and metastasis was observed. Functional studies, using an inhibitor of nuclear factor κB (NF-κB), revealed preferential targeting of the cancer stem cell and progenitor population for apoptosis whilst sparing normal stem cells. NF-κB is a major factor controlling the ability of tumor cells to resist apoptosis and provides an attractive target for new chemopreventative and chemotherapeutic approaches. We describe an expression signature of 581 genes whose levels are significantly different in prostate cancer stem cells. Functional annotation of this signature identified the JAK-STAT pathway and focal adhesion signaling as key processes in the biology of cancer stem cells.
      datePublished:2008-05-20T00:00:00Z
      dateModified:2008-05-20T00:00:00Z
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      pageEnd:13
      license:http://creativecommons.org/licenses/by/2.0/
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         Prostate Cancer
         Gene Ontology
         Cancer Stem Cell
         Benign Prostatic Hyperplasia
         Stem Cell Population
         Animal Genetics and Genomics
         Human Genetics
         Plant Genetics and Genomics
         Microbial Genetics and Genomics
         Bioinformatics
         Evolutionary Biology
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                  address:
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                     type:PostalAddress
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            name:Alastair Droop
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                     type:PostalAddress
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            name:Norman J Maitland
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      address:
         name:YCR Cancer Research Unit, Department of Biology, University of York, UK
         type:PostalAddress
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               type:PostalAddress
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            address:
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               type:PostalAddress
            type:Organization
      name:Catherine F Hyde
      affiliation:
            name:University of York
            address:
               name:YCR Cancer Research Unit, Department of Biology, University of York, UK
               type:PostalAddress
            type:Organization
      name:John L Lewis
      affiliation:
            name:University of York
            address:
               name:YCR Cancer Research Unit, Department of Biology, University of York, UK
               type:PostalAddress
            type:Organization
      name:Michael J Stower
      affiliation:
            name:York Hospital
            address:
               name:Department of Urology, York Hospital, UK
               type:PostalAddress
            type:Organization
      name:Norman J Maitland
      affiliation:
            name:University of York
            address:
               name:YCR Cancer Research Unit, Department of Biology, University of York, UK
               type:PostalAddress
            type:Organization
      name:Anne T Collins
      affiliation:
            name:University of York
            address:
               name:YCR Cancer Research Unit, Department of Biology, University of York, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:The Biocentre, Pro-Cure Therapeutics Ltd, Heslington, UK
      name:YCR Cancer Research Unit, Department of Biology, University of York, UK
      name:Hull York Medical School, University of York, Heslington, UK
      name:The Biocentre, Pro-Cure Therapeutics Ltd, Heslington, UK
      name:York Centre for Complex Systems Analysis, Department of Biology, University of York, UK
      name:YCR Cancer Research Unit, Department of Biology, University of York, UK
      name:YCR Cancer Research Unit, Department of Biology, University of York, UK
      name:YCR Cancer Research Unit, Department of Biology, University of York, UK
      name:YCR Cancer Research Unit, Department of Biology, University of York, UK
      name:Department of Urology, York Hospital, UK
      name:YCR Cancer Research Unit, Department of Biology, University of York, UK
      name:YCR Cancer Research Unit, Department of Biology, University of York, UK

External Links {🔗}(203)

Analytics and Tracking {📊}

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