Please use this identifier to cite or link to this item: https://doi.org/10.1155/2017/9634172
Title: Contribution of the microenvironmental niche to glioblastoma heterogeneity
Authors: Ho, I.A.W 
Shim, W.S.N 
Keywords: antineoplastic agent
bevacizumab
osteopontin
temozolomide
transcription factor
adaptive immunity
cancer chemotherapy
cancer patient
cancer radiotherapy
cell heterogeneity
cell hypoxia
cell lineage
glioblastoma
glioma stem cell
human
in vitro study
in vivo study
inflammation
microglia
myeloid-derived suppressor cell
nerve cell plasticity
nonhuman
perivascular space
Review
signal transduction
stem cell niche
stem cell self-renewal
treatment outcome
tumor associated leukocyte
tumor microenvironment
tumor recurrence
tumor xenograft
animal
cancer stem cell
glioblastoma
immunology
neovascularization (pathology)
pathology
tumor microenvironment
Animals
Glioblastoma
Humans
Neoplastic Stem Cells
Neovascularization, Pathologic
Tumor Microenvironment
Issue Date: 2017
Publisher: Hindawi
Citation: Ho, I.A.W, Shim, W.S.N (2017). Contribution of the microenvironmental niche to glioblastoma heterogeneity. BioMed Research International 2017 : 9634172. ScholarBank@NUS Repository. https://doi.org/10.1155/2017/9634172
Rights: Attribution 4.0 International
Abstract: 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. © 2017 Ivy A. W. Ho and Winston S. N. Shim.
Source Title: BioMed Research International
URI: https://scholarbank.nus.edu.sg/handle/10635/183564
ISSN: 2314-6133
DOI: 10.1155/2017/9634172
Rights: Attribution 4.0 International
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