We are analyzing https://link.springer.com/article/10.1186/bcr2876.

Title:
Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition | Breast Cancer Research
Description:
Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. In this review, we examine embryonic signaling pathways, CSCs, and factors affecting EMT.
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Keywords {🔍}

pubmed, cancer, cells, article, breast, google, scholar, cas, signaling, cell, stem, notch, emt, central, tumor, expression, metastasis, pathways, transition, growth, ecadherin, cscs, res, embryonic, metastatic, transcription, human, factors, wnt, potential, epithelial, epithelialtomesenchymal, factor, mammary, gene, tgfβ, hedgehog, therapeutic, tumors, development, receptor, crosstalk, pathway, role, targeting, microenvironment, biol, epithelialmesenchymal, target, clin,

Topics {✒️}

treatment-resistant cd44+/cd24-/low cells treatment-resistant cd44+/cd24-/lowcells cd44+cd24-/low/lin double-stranded dna breaks bone marrow-derived cells transforming growth factor-beta cd44+/cd24-/low cells stem/progenitor cells makes zinc-finger transcription factors basic helix-loop-helix mitogen-activated protein kinase cd44+/cd24- breast csc long-term oxidative stress activating nuclear factor-κb induces epithelial-mesenchymal transition meta-static tumor growth claudin-low breast tumors epithelial-mesenchymal transition induced meta-plastic breast cancers jagged1/notch signalling crucial multi-tasking components wnt/beta-catenin pathway tumor microenviron-mental level epidermal growth factor tgf-β signaling appears tgf-β signaling pathway e-cadherin promoter region fluorescence-activated cell sorting perez-moreno ma full size image numb-mediated notch inhibition repressing e-cadherin expression stem/progenitor cells nod/scid mice injected tgf-β signaling pathways reduced e-cadherin expression e-cadherin transcriptional downregulation e-cadherin gene expression cancer stem cells bone marrow micrometastases tgf-β cross-talk mesenchymal stem cells emt-inducing transcription factors mammary epithelial cells gene-expression patterns change human breast cancer breast cancer growth wnt/β-catenin signaling transforming growth factor patched-smoothened receptor complex

Schema {🗺️}

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         headline:Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition
         description:Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. In this review, we examine embryonic signaling pathways, CSCs, and factors affecting EMT.
         datePublished:2011-06-10T00:00:00Z
         dateModified:2011-06-10T00:00:00Z
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            Notch Signaling
            Cyclopamine
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            Breast CSCs
            Cancer Research
            Oncology
            Surgical Oncology
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      headline:Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition
      description:Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. In this review, we examine embryonic signaling pathways, CSCs, and factors affecting EMT.
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      dateModified:2011-06-10T00:00:00Z
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         Notch Signaling
         Cyclopamine
         Breast Cancer Stem Cell
         Breast CSCs
         Cancer Research
         Oncology
         Surgical Oncology
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      name:Ronald Q Warren
      affiliation:
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            address:
               name:PSI International, Inc., Bethesda, USA
               type:PostalAddress
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      name:S Percy Ivy
      affiliation:
            name:Cancer Therapy Evaluation Program, Investigational Drug Branch, EPN 7131
            address:
               name:National Cancer Institute, Division of Cancer Treatment and Diagnosis, Cancer Therapy Evaluation Program, Investigational Drug Branch, EPN 7131, Rockville, USA
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      name:PSI International, Inc., Bethesda, USA
      name:National Cancer Institute, Division of Cancer Treatment and Diagnosis, Cancer Therapy Evaluation Program, Investigational Drug Branch, EPN 7131, Rockville, USA

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