Document Detail

Tumor initiation via loss of cell contact inhibition versus Ras mutation: do all roads lead to EMT?
MedLine Citation:
PMID:  20160473     Owner:  NLM     Status:  MEDLINE    
Many tumors have been found to contain a subset of cells referred to as cancer stem cells. As opposed to the remainder of the tumor, these cells are undifferentiated-they do not express markers of differentiation and they can re-express stem cell specification genes. The cells can divide asymmetrically to yield differentiated cells as well as cells comprising the original heterogeneous population of the tumor while maintaining their number. Because cancer stem cells display some properties of stem cells, it has been presumed that the presence of such cells in tumors reflects a stem cell origin for cancer. However, recent studies suggest that cancer can originate with outgrowth of differentiated somatic cells, and that cells with properties of cancer stem cells can be generated as tumors progress. Appearance of such cells may be linked to reprogramming of differentiated somatic cells to a stem cell-like phenotype by overexpression of transcription factors involved in epithelial-mesenchymal transition (EMT). We discuss recent studies from our group and other laboratories linking cell outgrowth in tumors to inhibition of the RB1 pathway, loss of cell contact inhibition and generation of undifferentiated cancer stem-like cells from somatic cells. And, we compare this pathway to that arising with introduction of mutant Ras in cells.
Yongqing Liu; Douglas C Dean
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2010-03-13
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  9     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-04-16     Completed Date:  2010-06-29     Revised Date:  2010-08-25    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  897-900     Citation Subset:  IM    
Molecular Targets Program, James Graham Brown Cancer Center and Department of Ophthalmology, University of Louisville Health Sciences Center, Louisville, KY, USA.
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MeSH Terms
ATP-Binding Cassette Transporters / metabolism
Cell Differentiation
Disease Progression
Epithelial Cells / cytology*
Homeodomain Proteins / metabolism
Neoplasm Proteins / metabolism
Neoplasms / etiology*,  genetics,  metabolism
Neoplastic Stem Cells / metabolism
Retinoblastoma Protein / genetics,  metabolism
Transcription Factors / metabolism
ras Proteins / genetics*,  metabolism
Grant Support
Reg. No./Substance:
0/ABCG2 protein, human; 0/ATP-Binding Cassette Transporters; 0/Homeodomain Proteins; 0/Neoplasm Proteins; 0/Retinoblastoma Protein; 0/Transcription Factors; 0/ZEB1 protein, human; EC Proteins

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