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    
Abstract/OtherAbstract:
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.
Authors:
Yongqing Liu; Douglas C Dean
Related Documents :
19800383 - Glutathione s-transferase expression and isoenzyme composition during cell differentiat...
2483683 - Cell lines with developmental potential restricted to mesodermal lineages isolated from...
22035653 - Human beta-defensin-3 (hbd-3) upregulated by lps via epidermal growth factor receptor (...
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    
Affiliation:
Molecular Targets Program, James Graham Brown Cancer Center and Department of Ophthalmology, University of Louisville Health Sciences Center, Louisville, KY, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
ATP-Binding Cassette Transporters / metabolism
Cell Differentiation
Disease Progression
Epithelial Cells / cytology*
Homeodomain Proteins / metabolism
Humans
Mutation
Neoplasm Proteins / metabolism
Neoplasms / etiology*,  genetics,  metabolism
Neoplastic Stem Cells / metabolism
Retinoblastoma Protein / genetics,  metabolism
Transcription Factors / metabolism
ras Proteins / genetics*,  metabolism
Grant Support
ID/Acronym/Agency:
EY015636/EY/NEI NIH HHS; EY018603/EY/NEI NIH HHS; EY019113/EY/NEI NIH HHS; RR018733/RR/NCRR NIH HHS
Chemical
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 3.6.5.2/ras Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Regulation of myogenic stem cell behavior by vessel cells: The "m??nage ?? trois" of satellite cells...
Next Document:  Characterization of structural variability sheds light on the specificity determinants of the intera...