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Etiology and Pathogenesis > Stem Cells


Lancet Oncololy, Volume 5, Issue 8, 1 August 2004, Pages 511-514. Available online 29 July 2004.


Abstract

Development of gliomas: potential role of asymmetrical cell division of neural stem cells

François Bergera, Emmanuel Gayb, Laurent Pelletierc, Philippe Tropeld and Didier Wione

aNeurooncologist, group leader, and professor, University of Grenoble, Members of the Preclinical Neuroscience Laboratory, INSERM Unit 318, Grenoble, France; bNeurosurgeon and professor University of Grenoble, Members of the Preclinical Neuroscience Laboratory, INSERM Unit 318, Grenoble, France; cAssistant professor, University of Grenoble, Members of the Preclinical Neuroscience Laboratory, INSERM Unit 318, Grenoble, France; dPostdoctoral researcher, French association against Myopathies, Members of the Preclinical Neuroscience Laboratory, INSERM Unit 318, Grenoble, France; eResearch scientist at INSERM, Members of the Preclinical Neuroscience Laboratory, INSERM Unit 318, Grenoble, France. Correspondence: Dr Didier Wion, INSERM U318, CHU Michallon, 38043 Grenoble, France. Tel: +33 4 7676 5653. Fax: +33 4 7676 5619.

Asymmetrical cell division is a mechanism that gives rise to two daughter cells with different proliferative and differentiative fates. 
It occurs mainly during development and in adult stem cells. 
Accumulating evidence suggests that tumour cells arise from the transformation of normal stem cells. 
Here, we propose that the asymmetrical mitosis potential of stem cells is associated with the generation of migrating tumour progenitors. 
Application of this speculative model to glioma proposes that the sites where tumour-initiating stem cells reside are indolent and distinct from the tumour mass, and implies that the tumour mass is continuously replenished with new migrating tumour cells from these clinically silent regions. 
This hypothesis offers explanations for our inability to cure glioblastoma and points to asymmetrical division as a new potential therapeutic target.

Copyright © 2004 Elsevier Ltd. All rights reserved.
Abstract


 

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