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ISSN: 2157-7013

Journal of Cell Science & Therapy
Open Access

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Review Article

Targeting Glioma Stem Cells for Therapy: Perspectives and Challenges

Shaofang Wu, Norihiko Saito, W.K. Alfred Yung and Dimpy Koul*

Brain Tumor Center, Departments of Neuro-Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA

*Corresponding Author:
Dimpy Koul
Department of Neuro-Oncology, Unit 1001
The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd
Houston, TX 77030, USA
Tel: 713-834-16202
Fax: 713-794-4999
E-mail: [email protected]

Received Date: November 4, 2014; Accepted Date: June 15, 2015; Published Date: June 18, 2015

Citation: Wu S, Saito N, Yung A, Koul D (2015) Targeting Glioma Stem Cells for Therapy: Perspectives and Challenges. J Cell Sci Ther 6:207. doi: 10.4172/2157-7013.1000207

Copyright: © 2015 Shaofang Wu, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Glioblastoma multiforme (GBM, WHO grade IV) is the most aggressive and lethal subtype of primary brain tumor with a median overall survival of 15 months from the time of diagnosis. Recent studies indicate that some neoplastic cells within human high-grade glioma have the capacity for self-renewal and multi-lineage differentiation, properties associated with normal neural stem cells. These stem-like tumor cells known as GBM stem cells (GSCs) are responsible for tumor progression and recurrence. Therefore, GSCs are attractive targets for novel glioma therapies. Mounting studied have evidenced that some molecular signaling pathways (including EGFR, PI3K, PDGFR, TGF and Notch.), which are critically important for GSCs self-renew and proliferation, are activated by genetically mutation or amplification in GSCs. Targeting these molecules might be promising novel treatment strategies to eliminate GSCs, however, crosstalk and compensation between different signaling pathways as well as intratumoral heterogeneity make it more complicate and a big challenge.


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