Notch signaling in glioblastoma: a developmental drug target?

BMC Medicine

Review

Maria Maddalena Lino¹  Adrian Merlo¹  Jean-Louis Boulay² 

[1] Laboratory of Molecular Neuro-Oncology, Department of Biomedicine, University Hospital Basel, Basel, Switzerland;Laboratory of Molecular Neuro-Oncology, Department of Biomedicine, University Hospital Basel, Basel, Switzerland;Laboratory of Brain Tumor Biology, Department of Biomedicine, University Hospital Basel, Basel, Switzerland;

关键词: Glial Fibrillary Acidic Protein;    Cancer Stem Cell;    Medulloblastoma;    Neural Stem Cell;    Notch Signaling;   

DOI  :  10.1186/1741-7015-8-72

 received in 2010-07-12, accepted in 2010-11-15,  发布年份 2010

来源: Springer

【 摘 要 】

Malignant gliomas are among the most devastating tumors for which conventional therapies have not significantly improved patient outcome. Despite advances in imaging, surgery, chemotherapy and radiotherapy, survival is still less than 2 years from diagnosis and more targeted therapies are urgently needed. Notch signaling is central to the normal and neoplastic development of the central nervous system, playing important roles in proliferation, differentiation, apoptosis and cancer stem cell regulation. Notch is also involved in the regulation response to hypoxia and angiogenesis, which are typical tumor and more specifically glioblastoma multiforme (GBM) features. Targeting Notch signaling is therefore a promising strategy for developing future therapies for the treatment of GBM. In this review we give an overview of the mechanisms of Notch signaling, its networking pathways in gliomas, and discuss its potential for designing novel therapeutic approaches.

【 授权许可】

Unknown   
© Lino et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.