Editorial: glioma subpopulations

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It has been more than 25 years since investigators first discussed the existence of glioma “stem” cells,7,8 but only in the last 5 years or so have scientists been able to identify such cells in tumors based on expression of specific markers or defined phenotypes and behaviors.1,3,6,9,10 This type of identification has led to the hypothesis that therapies aimed at such cells within tumors would eliminate the glioma's ability to self-renew and thus be more efficacious than current treatments that target all of the neoplasm, but

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Please include this information when citing this paper: published online November 5, 2010; DOI: 10.3171/2009.11.JNS091668.

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References

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Griguer CEOliva CRGobin EMarcorelles PBenos DJLancaster JR Jr: CD133 is a marker of bioenergetic stress in human glioma. PLoS One 3:e36552008

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Hemmati HDNakano ILazareff JAMasterman-Smith MGeschwind DHBronner-Fraser M: Cancerous stem cells can arise from pediatric brain tumors. Proc Natl Acad Sci U S A 100:15178151832003

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Kesari SSchiff DHenson JWMuzikansky AGigas DCDoherty L: Phase II study of temozolomide, thalidomide, and celecoxib for newly diagnosed glioblastoma in adults. Neuro Oncol 10:3003082008

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Bao SWu QMcLendon REHao YShi QHjelmeland AB: Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature 444:7567602006

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Joki THeese ONikas DCBello LZhang JKraeft SK: Expression of cyclooxygenase 2 (COX-2) in human glioma and in vitro inhibition by a specific COX-2 inhibitor, NS-398. Cancer Res 60:492649312000

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Kang KBZhu CYong SKGao QWong MC: Enhanced sensitivity of celecoxib in human glioblastoma cells: induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy. Mol Cancer 8:662009

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Kardosh ABlumenthal MWang WJChen TCSchönthal AH: Differential effects of selective COX-2 inhibitors on cell cycle regulation and proliferation of glioblastoma cell lines. Cancer Biol Ther 3:55622004

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