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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Vydáno v:BioMed research international Ročník 2017; číslo 2017; s. 1 - 13
Hlavní autoři: Ho, Ivy A. W., Shim, Winston
Médium: Journal Article
Jazyk:angličtina
Vydáno: Cairo, Egypt Hindawi Publishing Corporation 01.01.2017
Hindawi
John Wiley & Sons, Inc
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ISSN:2314-6133, 2314-6141, 2314-6141
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Shrnutí: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