PMID- 20457135 OWN - NLM STAT- MEDLINE DCOM- 20100719 LR - 20220310 IS - 1873-2968 (Electronic) IS - 0006-2952 (Print) IS - 0006-2952 (Linking) VI - 80 IP - 5 DP - 2010 Sep 1 TI - Potential therapeutic implications of cancer stem cells in glioblastoma. PG - 654-65 LID - 10.1016/j.bcp.2010.04.035 [doi] AB - Glioblastoma is the most common and lethal type of primary brain tumor. Despite recent therapeutic advances in other cancers, the treatment of glioblastomas remains ineffective and essentially palliative. The treatment failure is a result of a number of causes, but we and others have demonstrated that a highly tumorigenic subpopulation of cancer cells called glioblastoma stem cells (GSCs) display relative resistance to radiation and chemotherapy. GSCs also contribute to tumor growth through the stimulation of angiogenesis, which has been shown to be a useful therapeutic target in the treatment of recurrent or progressive malignant gliomas. Cancer stem cells also have been hypothesized as a contributor to systemic metastases. While glioblastomas rarely metastasize beyond the central nervous system, glioblastomas invade into brain structures to prevent surgical cure and GSCs have an extremely invasive phenotype. Collectively, these studies and others suggest that GSCs may be important therapeutic targets not only to achieve cure but even reduce tumor relapse and improve overall survival. Many recent studies suggest that GSCs share core regulatory pathways with normal embryonic and somatic stem cells, but display important distinctions that provide clues into useful treatment targets. The cancer stem cell hypothesis may also modify our approaches in tumor imaging and biomarker development, but clinical validation waits. In this review, we summarize the current understanding of GSC biology with a focus on potential anti-GSC therapies. CI - Copyright 2010 Elsevier Inc. All rights reserved. FAU - Cheng, Lin AU - Cheng L AD - Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA. FAU - Bao, Shideng AU - Bao S FAU - Rich, Jeremy N AU - Rich JN LA - eng GR - NS054276/NS/NINDS NIH HHS/United States GR - NS070315/NS/NINDS NIH HHS/United States GR - R01 CA129958-03/CA/NCI NIH HHS/United States GR - R01 CA129958-04/CA/NCI NIH HHS/United States GR - R01 CA116659-05/CA/NCI NIH HHS/United States GR - R01 NS070315-02/NS/NINDS NIH HHS/United States GR - CA112958/CA/NCI NIH HHS/United States GR - CA116659/CA/NCI NIH HHS/United States GR - R01 NS054276-05/NS/NINDS NIH HHS/United States GR - R01 CA129958/CA/NCI NIH HHS/United States GR - R01 NS070315/NS/NINDS NIH HHS/United States GR - R01 CA116659/CA/NCI NIH HHS/United States GR - R01 CA116659-06/CA/NCI NIH HHS/United States GR - R01 NS070315-01/NS/NINDS NIH HHS/United States GR - K02 NS047409/NS/NINDS NIH HHS/United States GR - NS047409/NS/NINDS NIH HHS/United States GR - R01 NS054276/NS/NINDS NIH HHS/United States GR - R01 NS054276-04/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20100510 PL - England TA - Biochem Pharmacol JT - Biochemical pharmacology JID - 0101032 RN - 0 (MicroRNAs) RN - 0 (Transcription Factors) SB - IM MH - Brain Neoplasms/metabolism/pathology/*therapy MH - Cell Hypoxia MH - Glioblastoma/metabolism/pathology/*therapy MH - Humans MH - MicroRNAs/genetics MH - *Neoplastic Stem Cells MH - Signal Transduction MH - Transcription Factors/metabolism PMC - PMC2897968 MID - NIHMS209499 EDAT- 2010/05/12 06:00 MHDA- 2010/07/20 06:00 PMCR- 2011/09/01 CRDT- 2010/05/12 06:00 PHST- 2010/03/05 00:00 [received] PHST- 2010/04/27 00:00 [revised] PHST- 2010/04/29 00:00 [accepted] PHST- 2010/05/12 06:00 [entrez] PHST- 2010/05/12 06:00 [pubmed] PHST- 2010/07/20 06:00 [medline] PHST- 2011/09/01 00:00 [pmc-release] AID - S0006-2952(10)00336-9 [pii] AID - 10.1016/j.bcp.2010.04.035 [doi] PST - ppublish SO - Biochem Pharmacol. 2010 Sep 1;80(5):654-65. doi: 10.1016/j.bcp.2010.04.035. Epub 2010 May 10.