We are analyzing https://link.springer.com/article/10.1186/bcr2789.

Title:
Epithelial-mesenchymal transition and cancer stem cells: a dangerously dynamic duo in breast cancer progression | Breast Cancer Research
Description:
Aberrant activation of a latent embryonic program - known as the epithelial-mesenchymal transition (EMT) - can endow cancer cells with the migratory and invasive capabilities associated with metastatic competence. The induction of EMT entails the loss of epithelial characteristics and the de novo acquisition of a mesenchymal phenotype. In breast cancer, the EMT state has been associated with cancer stem cell properties including expression of the stem cell-associated CD44+/CD24-/low antigenic profile, self-renewal capabilities and resistance to conventional therapies. Intriguingly, EMT features are also associated with stem cells isolated from the normal mouse mammary gland and human breast reduction tissues as well as the highly aggressive metaplastic and claudin-low breast tumor subtypes. This has implications for the origin of these breast tumors as it remains unclear whether they derive from cells that have undergone EMT or whether they represent an expansion of a pre-existing stem cell population that expresses EMT-associated markers to begin with. In the present review, we consider the current evidence connecting EMT and stem cell attributes and discuss the ramifications of these newly recognized links for our understanding of the emergence of distinct breast cancer subtypes and breast cancer progression.
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Keywords {🔍}

cells, cancer, breast, pubmed, emt, cell, stem, article, scholar, google, mammary, cas, expression, central, epithelial, tumor, tumors, gland, transition, normal, phenotype, cscs, molecular, gene, mesenchymal, human, luminal, basallike, claudinlow, res, epithelialmesenchymal, markers, progression, features, cdcdlow, mouse, genes, resistance, invasive, properties, subtypes, lines, differentiation, subtype, metastatic, progenitors, development, basal, zeb, twist,

Topics {✒️}

e-cadherin releases β-catenin cd44+/cd24-/low antigenic profile cd44+/cd24-/low expression profiles twist1-induced epithelial-mesenchymal transition radiation-resistant tumor-initiating cells cd44+/cd24-/low cells cd44+/cd24-/low cells [61] cd44+cd24-/low cells exhibit epithelial-mesenchymal transition cd44-/cd24+ cells isolated tumorigenic breast-cancer cells cd44+/cd24-/low phenotype anti-diabetic drug metformin develop csc-targeted therapeutics platelet-derived growth factor full-blown mesenchymal state stem cell-related markers α-smooth muscle actin epithelial-mesenchymal transition markers promote cap-independent translation high-throughput chemical screen anchorage-independent growth properties repressing stemness-inhibiting micrornas mesenchymal/claudin-low features [14] genome-wide transcript analysis cancer-initiating cell features loosen cell-cell contacts claudin-low tumors share claudin-low breast tumors influencing emt-dependent manifestation claudin-low intrinsic subtype emt-related transcription factors human mda-mb-231 cells breast cancer relates override oncogene-induced senescence mda-mb-468 cells exposed mammary branching morphogenesis mammary gland cells emt-type spindle tumors comprise slow-cycling tumors normal mammary gland increased tumor-free survival induces mammary tumors functional mammary gland increased migration mammary gland epithelium mouse mammary gland genome-wide transcriptional profiling combined emt/csc properties cd44+/cd24-/low

Schema {🗺️}

WebPage:
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         headline:Epithelial-mesenchymal transition and cancer stem cells: a dangerously dynamic duo in breast cancer progression
         description:Aberrant activation of a latent embryonic program - known as the epithelial-mesenchymal transition (EMT) - can endow cancer cells with the migratory and invasive capabilities associated with metastatic competence. The induction of EMT entails the loss of epithelial characteristics and the de novo acquisition of a mesenchymal phenotype. In breast cancer, the EMT state has been associated with cancer stem cell properties including expression of the stem cell-associated CD44+/CD24-/low antigenic profile, self-renewal capabilities and resistance to conventional therapies. Intriguingly, EMT features are also associated with stem cells isolated from the normal mouse mammary gland and human breast reduction tissues as well as the highly aggressive metaplastic and claudin-low breast tumor subtypes. This has implications for the origin of these breast tumors as it remains unclear whether they derive from cells that have undergone EMT or whether they represent an expansion of a pre-existing stem cell population that expresses EMT-associated markers to begin with. In the present review, we consider the current evidence connecting EMT and stem cell attributes and discuss the ramifications of these newly recognized links for our understanding of the emergence of distinct breast cancer subtypes and breast cancer progression.
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      headline:Epithelial-mesenchymal transition and cancer stem cells: a dangerously dynamic duo in breast cancer progression
      description:Aberrant activation of a latent embryonic program - known as the epithelial-mesenchymal transition (EMT) - can endow cancer cells with the migratory and invasive capabilities associated with metastatic competence. The induction of EMT entails the loss of epithelial characteristics and the de novo acquisition of a mesenchymal phenotype. In breast cancer, the EMT state has been associated with cancer stem cell properties including expression of the stem cell-associated CD44+/CD24-/low antigenic profile, self-renewal capabilities and resistance to conventional therapies. Intriguingly, EMT features are also associated with stem cells isolated from the normal mouse mammary gland and human breast reduction tissues as well as the highly aggressive metaplastic and claudin-low breast tumor subtypes. This has implications for the origin of these breast tumors as it remains unclear whether they derive from cells that have undergone EMT or whether they represent an expansion of a pre-existing stem cell population that expresses EMT-associated markers to begin with. In the present review, we consider the current evidence connecting EMT and stem cell attributes and discuss the ramifications of these newly recognized links for our understanding of the emergence of distinct breast cancer subtypes and breast cancer progression.
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         Mammary Gland
         Cancer Stem Cell
         Salinomycin
         Breast CSCs
         Mammosphere Formation
         Cancer Research
         Oncology
         Surgical Oncology
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            address:
               name:The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, USA
               type:PostalAddress
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            address:
               name:Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA
               type:PostalAddress
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      affiliation:
            name:The University of Texas MD Anderson Cancer Center
            address:
               name:Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
      name:Wenjun Guo
      affiliation:
            name:Whitehead Institute for Biomedical Research, 9 Cambridge Center
            address:
               name:Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, USA
               type:PostalAddress
            type:Organization
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      affiliation:
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      name:Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA
      name:Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA
      name:Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, USA
      name:Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA

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