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  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
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  7. Topics
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  15. CDN Services

We began analyzing https://breast-cancer-research.biomedcentral.com/articles/10.1186/bcr920, but it redirected us to https://breast-cancer-research.biomedcentral.com/articles/10.1186/bcr920. The analysis below is for the second page.

Title[redir]:
Role of Notch signaling in cell-fate determination of human mammary stem/progenitor cells | Breast Cancer Research | Full Text
Description:
Introduction Notch signaling has been implicated in the regulation of cell-fate decisions such as self-renewal of adult stem cells and differentiation of progenitor cells along a particular lineage. Moreover, depending on the cellular and developmental context, the Notch pathway acts as a regulator of cell survival and cell proliferation. Abnormal expression of Notch receptors has been found in different types of epithelial metaplastic lesions and neoplastic lesions, suggesting that Notch may act as a proto-oncogene. The vertebrate Notch1 and Notch4 homologs are involved in normal development of the mammary gland, and mutated forms of these genes are associated with development of mouse mammary tumors. Methods In order to determine the role of Notch signaling in mammary cell-fate determination, we have utilized a newly described in vitro system in which mammary stem/progenitor cells can be cultured in suspension as nonadherent

Matching Content Categories {📚}

  • Science
  • Education
  • Social Networks

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🚄 Respectable Traffic: 10k - 20k visitors per month


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How Does Doi.org Make Money? {💸}

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Keywords {🔍}

cells, notch, mammary, signaling, stem, cell, pubmed, article, dsl, google, scholar, cas, progenitor, mammospheres, effect, selfrenewal, fig, peptide, antibody, treatment, mammosphere, myoepithelial, epithelial, development, culture, differentiation, human, number, formation, activation, cancer, proliferation, expression, normal, suspension, usa, breast, role, lineage, shown, cultures, collagen, gland, vitro, primary, previously, secondary, branching, increase, matrigel,

Topics {✒️}

z-leu-leu-nle-cho springer nature recombinant ligand–receptor complexes real-time rt-pcr showed author information authors tissue sections hes-1-driven luciferase expression mammary cell-fate determination anti-epithelial-specific antigen fire-polished pasteur pipette biases cell-fate decisions mammary stem/progenitor cells asymmetric cell-fate decisions human ras-transformed cells authors scientific editing dsl-induced luciferase expression authors’ original file anti-human fc antibody mouse mammary tumors mammosphere-initiating cells reflects mammosphere-derived cells passaged nomarski contrast-phase image human mammary gland materials mammosphere-derived cells cultivated hepatocyte growth factor tertiary mammosphere-derived cells affect lineage-specific commitment epithelial-specific antigen privacy choices/manage cookies pgl3-promoter vector adult mammary gland mammosphere-derived cells treated cell-fate decisions mammary epithelial cells cell-fate determination bmc developing mammary gland epithelial cell fate mammary progenitor cells ductal epithelial cells mammary stem cell neural stem cell luciferase expression induced normal mammary development mammary stem cells notch4 knockout mouse neural stem cells human breast cancer alveolar epithelial cells

Questions {❓}

  • Brennan K, Brown AMC: Is there a role for Notch signalling in human breast cancer?

Schema {🗺️}

WebPage:
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         headline:Role of Notch signaling in cell-fate determination of human mammary stem/progenitor cells
         description:Notch signaling has been implicated in the regulation of cell-fate decisions such as self-renewal of adult stem cells and differentiation of progenitor cells along a particular lineage. Moreover, depending on the cellular and developmental context, the Notch pathway acts as a regulator of cell survival and cell proliferation. Abnormal expression of Notch receptors has been found in different types of epithelial metaplastic lesions and neoplastic lesions, suggesting that Notch may act as a proto-oncogene. The vertebrate Notch1 and Notch4 homologs are involved in normal development of the mammary gland, and mutated forms of these genes are associated with development of mouse mammary tumors. In order to determine the role of Notch signaling in mammary cell-fate determination, we have utilized a newly described in vitro system in which mammary stem/progenitor cells can be cultured in suspension as nonadherent 'mammospheres'. Notch signaling was activated using exogenous ligands, or was inhibited using previously characterized Notch signaling antagonists. Utilizing this system, we demonstrate that Notch signaling can act on mammary stem cells to promote self-renewal and on early progenitor cells to promote their proliferation, as demonstrated by a 10-fold increase in secondary mammosphere formation upon addition of a Notch-activating DSL peptide. In addition to acting on stem cells, Notch signaling is also able to act on multipotent progenitor cells, facilitating myoepithelial lineage-specific commitment and proliferation. Stimulation of this pathway also promotes branching morphogenesis in three-dimensional Matrigel cultures. These effects are completely inhibited by a Notch4 blocking antibody or a gamma secretase inhibitor that blocks Notch processing. In contrast to the effects of Notch signaling on mammary stem/progenitor cells, modulation of this pathway has no discernable effect on fully committed, differentiated, mammary epithelial cells. These studies suggest that Notch signaling plays a critical role in normal human mammary development by acting on both stem cells and progenitor cells, affecting self-renewal and lineage-specific differentiation. Based on these findings we propose that abnormal Notch signaling may contribute to mammary carcinogenesis by deregulating the self-renewal of normal mammary stem cells.
         datePublished:2004-08-16T00:00:00Z
         dateModified:2004-08-16T00:00:00Z
         pageStart:1
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            Oncology
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      headline:Role of Notch signaling in cell-fate determination of human mammary stem/progenitor cells
      description:Notch signaling has been implicated in the regulation of cell-fate decisions such as self-renewal of adult stem cells and differentiation of progenitor cells along a particular lineage. Moreover, depending on the cellular and developmental context, the Notch pathway acts as a regulator of cell survival and cell proliferation. Abnormal expression of Notch receptors has been found in different types of epithelial metaplastic lesions and neoplastic lesions, suggesting that Notch may act as a proto-oncogene. The vertebrate Notch1 and Notch4 homologs are involved in normal development of the mammary gland, and mutated forms of these genes are associated with development of mouse mammary tumors. In order to determine the role of Notch signaling in mammary cell-fate determination, we have utilized a newly described in vitro system in which mammary stem/progenitor cells can be cultured in suspension as nonadherent 'mammospheres'. Notch signaling was activated using exogenous ligands, or was inhibited using previously characterized Notch signaling antagonists. Utilizing this system, we demonstrate that Notch signaling can act on mammary stem cells to promote self-renewal and on early progenitor cells to promote their proliferation, as demonstrated by a 10-fold increase in secondary mammosphere formation upon addition of a Notch-activating DSL peptide. In addition to acting on stem cells, Notch signaling is also able to act on multipotent progenitor cells, facilitating myoepithelial lineage-specific commitment and proliferation. Stimulation of this pathway also promotes branching morphogenesis in three-dimensional Matrigel cultures. These effects are completely inhibited by a Notch4 blocking antibody or a gamma secretase inhibitor that blocks Notch processing. In contrast to the effects of Notch signaling on mammary stem/progenitor cells, modulation of this pathway has no discernable effect on fully committed, differentiated, mammary epithelial cells. These studies suggest that Notch signaling plays a critical role in normal human mammary development by acting on both stem cells and progenitor cells, affecting self-renewal and lineage-specific differentiation. Based on these findings we propose that abnormal Notch signaling may contribute to mammary carcinogenesis by deregulating the self-renewal of normal mammary stem cells.
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      pageEnd:11
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         mammary stem cells
         Notch
         Cancer Research
         Oncology
         Surgical Oncology
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      name:Wissam M Abdallah
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      name:Comprehensive Cancer Center, Department of Internal Medicine, University of Michigan, Ann Arbor, USA
      name:Comprehensive Cancer Center, Department of Internal Medicine, University of Michigan, Ann Arbor, USA
      name:Comprehensive Cancer Center, Department of Internal Medicine, University of Michigan, Ann Arbor, USA
      name:Comprehensive Cancer Center, Department of Internal Medicine, University of Michigan, Ann Arbor, USA
      name:Comprehensive Cancer Center, Department of Internal Medicine, University of Michigan, Ann Arbor, USA

Social Networks {👍}(2)

External Links {🔗}(296)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

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Emails and Hosting {✉️}

Mail Servers:

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CDN Services {📦}

  • Crossref

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