Contribution of the Microenvironmental Niche to Glioblastoma Heterogeneity

Glioblastoma is the most aggressive cancer of the brain. The dismal prognosis is largely attributed to the heterogeneous nature of the tumor, which in addition to intrinsic molecular and genetic changes is also influenced by the microenvironmental niche in which the glioma cells reside. The cancer s...

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Bibliographic Details
Published in:BioMed research international Vol. 2017; no. 2017; pp. 1 - 13
Main Authors: Ho, Ivy A. W., Shim, Winston
Format: Journal Article
Language:English
Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2017
Hindawi
John Wiley & Sons, Inc
Subjects:
Animals
Brain cancer
Cancer therapies
Chemotherapy
Gene expression
Genomes
Genotype & phenotype
Glioblastoma - immunology
Glioblastoma - pathology
Glioblastoma - therapy
Glioblastoma multiforme
Humans
Hypotheses
Hypoxia
Medical prognosis
Metabolism
Neoplastic Stem Cells - immunology
Neoplastic Stem Cells - pathology
Neovascularization, Pathologic - immunology
Neovascularization, Pathologic - pathology
Neovascularization, Pathologic - therapy
Neurosciences
Physiological aspects
Radiation therapy
Review
Stem cells
Transcription factors
Tumor Microenvironment - immunology
Tumors
Vascular endothelial growth factor
ISSN:2314-6133, 2314-6141, 2314-6141
Online Access:Get full text
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Summary:Glioblastoma is the most aggressive cancer of the brain. The dismal prognosis is largely attributed to the heterogeneous nature of the tumor, which in addition to intrinsic molecular and genetic changes is also influenced by the microenvironmental niche in which the glioma cells reside. The cancer stem cells (CSCs) hypothesis suggests that all cancers arise from CSCs that possess the ability to self-renew and initiate tumor formation. CSCs reside in specialized niches where interaction with the microenvironment regulates their stem cell behavior. The reciprocal interaction between glioma stem cells (GSCs) and cells from the microenvironment, such as endothelial cells, immune cells, and other parenchymal cells, may also promote angiogenesis, invasion, proliferation, and stemness of the GSCs and be likely to have an underappreciated role in their responsiveness to therapy. This crosstalk may also promote molecular transition of GSCs. Hence the inherent plasticity of GSCs can be seen as an adaptive response, changing according to the signaling cue from the niche. Given the association of GSCs with tumor recurrence and treatment sensitivity, understanding this bidirectional crosstalk between GSCs and its niche may provide a framework to identify more effective therapeutic targets and improve treatment outcome.
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Academic Editor: Sara Piccirillo
ISSN:2314-6133
2314-6141
2314-6141
DOI:10.1155/2017/9634172