Abstract
The discovery of discrete functional components in cancer systems advocates a paradigm shift in therapeutic design towards the targeted destruction of critical cellular constituents that fuel tumorigenic potential. In astrocytomas, malignant growth can be propagated and sustained by glioma stem cells (GSCs) endowed with highly efficient clonogenic and tumor initiation capacities. Given their disproportionate oncogenic contribution, GSCs are often considered the optimal targets for curative treatment because their eradication may subvert the refractory nature of GBMs. However, the close affinity of GSCs and normal neural stem cells (NSCs) is a cautionary note for off-target effects of GSC-based therapies. In fact, many parallels can be drawn between GSC and NSC functions, which ostensibly rely on a communal collection of stem cell-promoting transcription factors (TFs). Only through rigorous scrutiny of nuances in the stemness program of GSCs and NSCs may we clarify the pathogenic mechanisms of stemness factors and reveal processes exploited by cancer cells to co-opt stem cell traits. Importantly, discerning the specific requirements for GSC and NSC maintenance may be an essential requisite when assessing molecular targets for discriminatory targeting of GSCs with minimal sequelae.
Keywords: Glioblastoma, Cancer therapy, Cancer stem cells, Neural stem cells, tumors, neurogenesis, bevacizumab, oncogenes, gliomas, hypoxia
Current Pharmaceutical Design
Title: Collateral Damage Control in Cancer Therapy: Defining the Stem Identity in Gliomas
Volume: 17 Issue: 23
Author(s): David Hsieh
Affiliation:
Keywords: Glioblastoma, Cancer therapy, Cancer stem cells, Neural stem cells, tumors, neurogenesis, bevacizumab, oncogenes, gliomas, hypoxia
Abstract: The discovery of discrete functional components in cancer systems advocates a paradigm shift in therapeutic design towards the targeted destruction of critical cellular constituents that fuel tumorigenic potential. In astrocytomas, malignant growth can be propagated and sustained by glioma stem cells (GSCs) endowed with highly efficient clonogenic and tumor initiation capacities. Given their disproportionate oncogenic contribution, GSCs are often considered the optimal targets for curative treatment because their eradication may subvert the refractory nature of GBMs. However, the close affinity of GSCs and normal neural stem cells (NSCs) is a cautionary note for off-target effects of GSC-based therapies. In fact, many parallels can be drawn between GSC and NSC functions, which ostensibly rely on a communal collection of stem cell-promoting transcription factors (TFs). Only through rigorous scrutiny of nuances in the stemness program of GSCs and NSCs may we clarify the pathogenic mechanisms of stemness factors and reveal processes exploited by cancer cells to co-opt stem cell traits. Importantly, discerning the specific requirements for GSC and NSC maintenance may be an essential requisite when assessing molecular targets for discriminatory targeting of GSCs with minimal sequelae.
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Cite this article as:
Hsieh David, Collateral Damage Control in Cancer Therapy: Defining the Stem Identity in Gliomas, Current Pharmaceutical Design 2011; 17 (23) . https://dx.doi.org/10.2174/138161211797249198
DOI https://dx.doi.org/10.2174/138161211797249198 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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