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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 |
Appears in Collections: | Elements Staff Publications |
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