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Applications of Emerging Molecular Technologies in Glioblastoma Multiforme

Overview
Specialties Neurology
Pharmacology
Date 2008 Oct 22
PMID 18928343
Citations 10
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Abstract

Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults. Median survival from the time of diagnosis is less than a year, with less than 5% of patients surviving 5 years. These tumors are thought to arise through two different pathways. Primary GBMs represent de novo tumors, while secondary GBMs represent the malignant progression of lower-grade astrocytomas. Moreover, despite improvements in deciphering the complex biology of these tumors, the overall prognosis has not changed in the past three decades. The hope for improving the outlook for these glial-based malignancies is centered on the successful clinical application of current high-throughput technologies. For example, the complete sequencing of the human genome has brought both genomics and proteomics to the forefront of cancer research as a powerful approach to systematically identify large volumes of data that can be utilized to study the molecular and cellular basis of oncology. The organization of these data into a comprehensive view of tumor growth and progression translates into a unique opportunity to diagnose and treat cancer patients. In this review, we summarize current genomic and proteomic alterations associated with GBM and how these modalities may ultimately impact treatment and survival.

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References
1.
Meletis K, Wirta V, Hede S, Nister M, Lundeberg J, Frisen J . p53 suppresses the self-renewal of adult neural stem cells. Development. 2005; 133(2):363-9. DOI: 10.1242/dev.02208. View

2.
Hsu C, Juan H, Huang H . Characterization of microRNA-regulated protein-protein interaction network. Proteomics. 2008; 8(10):1975-9. DOI: 10.1002/pmic.200701004. View

3.
Ohgaki H, Kleihues P . Genetic pathways to primary and secondary glioblastoma. Am J Pathol. 2007; 170(5):1445-53. PMC: 1854940. DOI: 10.2353/ajpath.2007.070011. View

4.
Ciafre S, Galardi S, Mangiola A, Ferracin M, Liu C, Sabatino G . Extensive modulation of a set of microRNAs in primary glioblastoma. Biochem Biophys Res Commun. 2005; 334(4):1351-8. DOI: 10.1016/j.bbrc.2005.07.030. View

5.
Weiler J, Hunziker J, Hall J . Anti-miRNA oligonucleotides (AMOs): ammunition to target miRNAs implicated in human disease?. Gene Ther. 2005; 13(6):496-502. DOI: 10.1038/sj.gt.3302654. View