Literature DB >> 21792896

Phenotypic plasticity and epithelial-mesenchymal transitions in cancer and normal stem cells?

Christina Scheel1, Robert A Weinberg.   

Abstract

Cancer stem cells (CSCs) are similar to normal stem cells in their ability to self-renew and to generate large populations of more differentiated descendants. In contrast to the hierarchical organization that is presumed to be the prevalent mode of normal tissue homeostasis, phenotypic plasticity allows cancer cells to dynamically enter into and exit from stem-cell states. The epithelial-mesenchymal transition (EMT) has been closely associated with the acquisition of both invasive and stem-cell properties in cancer cells. Thereby, EMT programs emerge as important regulators of phenotypic plasticity in cancer cells including their entrance into stem-cell states. Much is still to be learned about the regulation of EMTs through epigenetic mechanisms in cancer cells and the contributions that EMT programs make to normal tissue homeostasis.
Copyright © 2011 UICC.

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Year:  2011        PMID: 21792896      PMCID: PMC3357895          DOI: 10.1002/ijc.26311

Source DB:  PubMed          Journal:  Int J Cancer        ISSN: 0020-7136            Impact factor:   7.396


  43 in total

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Review 5.  Epithelial-mesenchymal transitions in development and disease.

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  99 in total

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Review 2.  Aiming to immune elimination of ovarian cancer stem cells.

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Review 6.  Regulation of epithelial-mesenchymal and mesenchymal-epithelial transitions by microRNAs.

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7.  Downregulation of Lnc-Spry1 mediates TGF-β-induced epithelial-mesenchymal transition by transcriptional and posttranscriptional regulatory mechanisms.

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Review 9.  Circulating tumor cells: from bench to bedside.

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10.  Tumor microenvironment regulates epithelial-mesenchymal transitions in metastasis.

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