Document Detail


The epithelial-mesenchymal transition (EMT) phenomenon.
MedLine Citation:
PMID:  20943648     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The epithelial-mesenchymal transition (EMT) describes a rapid and often reversible modulation of phenotype by epithelial cells. EMT was originally defined in the context of developmental stages, including heart morphogenesis, mesoderm and neural crest formation. Epithelial cells loosen cell-cell adhesion structures throughout EMT. They modulate their polarity, cytoskeleton organization and typically express vimentin filaments and downregulate cytokeratins. They become isolated, mobile and resistant to anoikis. The EMT at least superficially resembles the evolution from normal to transformed cell phenotype during carcinoma progression. The relevance of the concept of EMT in this context was indicated by in vitro models using transformed epithelial cells. Transduction pathways typical of embryogenic EMT in vivo were also found to be activated during cancer progression. More recently, it has been found that such pathways indicate an increased plasticity linked to cellular stemness and ability to generate tumors. However, in the absence of direct evidence, a number of oncologists and pathologists remain skeptical about applying the EMT concept to human tumor progression. Typically in the cancer field, EMT concept appears to be fully relevant in some situations, but the concept has to be adjusted in other situations to reflect tumor cell renewal and plasticity during carcinoma progression and metastasis.
Authors:
P Savagner
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Annals of oncology : official journal of the European Society for Medical Oncology / ESMO     Volume:  21 Suppl 7     ISSN:  1569-8041     ISO Abbreviation:  Ann. Oncol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-14     Completed Date:  2011-10-17     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  9007735     Medline TA:  Ann Oncol     Country:  England    
Other Details:
Languages:  eng     Pagination:  vii89-92     Citation Subset:  IM    
Affiliation:
IRCM U896 INSERM, CRLC Val d'Aurelle-Paul Lamarque, Montpellier, France. psavagner@valdorel.fnclcc.fr
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Dedifferentiation / physiology
Epithelial-Mesenchymal Transition / physiology*
Female
Humans
Mammary Neoplasms, Experimental / pathology
Mice
Neoplasms / etiology*,  pathology
Comments/Corrections

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