Document Detail

Glioma cell death: cell-cell interactions and signalling networks.
MedLine Citation:
PMID:  20443079     Owner:  NLM     Status:  MEDLINE    
The prognosis for patients with malignant gliomas is poor, but improvements may emerge from a better understanding of the pathophysiology of glioma signalling. Recent therapeutic developments have implicated lipid signalling in glioma cell death. Stress signalling in glioma cell death involves mitochondria and endoplasmic reticulum. Lipid mediators also signal via extrinsic pathways in glioma cell proliferation, migration and interaction with endothelial and microglial cells. Glioma cell death and tumour regression have been reported using polyunsaturated fatty acids in animal models, human ex vivo explants, glioma cell preparations and in clinical case reports involving intratumoral infusion. Cell death signalling was associated with generation of reactive oxygen intermediates and mitochondrial and other signalling pathways. In this review, evidence for mitochondrial responses to stress signals, including polyunsaturated fatty acids, peroxidizing agents and calcium is presented. Additionally, evidence for interaction of glioma cells with primary brain endothelial cells is described, modulating human glioma peroxidative signalling. Glioma responses to potential therapeutic agents should be analysed in systems reflecting tumour connectivity and CNS structural and functional integrity. Future insights may also be derived from studies of signalling in glioma-derived tumour stem cells.
H Anne Leaver; Maria Theresa Rizzo; Ian R Whittle
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2010-05-05
Journal Detail:
Title:  Molecular neurobiology     Volume:  42     ISSN:  1559-1182     ISO Abbreviation:  Mol. Neurobiol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-06-30     Completed Date:  2010-09-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8900963     Medline TA:  Mol Neurobiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  89-96     Citation Subset:  IM    
Department of Clinical Neurosciences, University of Edinburgh, Edinburgh, UK.
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MeSH Terms
Brain Neoplasms / metabolism,  pathology*
Cell Communication*
Cell Death
Fatty Acids, Unsaturated / metabolism
Glioma / metabolism,  pathology*
Signal Transduction*
Reg. No./Substance:
0/Fatty Acids, Unsaturated

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

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