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6. Meletis K, Wirta V, Hede SM, Nistér M, Lundeberg J, Frisén J: p53 suppresses the self-renewal of adult neural stem cells. Development; 2006 Jan;133(2):363-9
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  • [Title] p53 suppresses the self-renewal of adult neural stem cells.
  • There is increasing evidence that tumors are heterogeneous and that a subset of cells act as cancer stem cells.
  • Several proto-oncogenes and tumor suppressors control key aspects of stem cell function, suggesting that similar mechanisms control normal and cancer stem cell properties.
  • We show here that the prototypical tumor suppressor p53, which plays an important role in brain tumor initiation and growth, is expressed in the neural stem cell lineage in the adult brain. p53 negatively regulates proliferation and survival, and thereby self-renewal, of neural stem cells.
  • Analysis of the neural stem cell transcriptome identified the dysregulation of several cell cycle regulators in the absence of p53, most notably a pronounced downregulation of p21 expression.
  • These data implicate p53 as a suppressor of tissue and cancer stem cell self-renewal.
  • [MeSH-major] Neurons / metabolism. Stem Cells / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Apoptosis. Cell Proliferation. Cells, Cultured. Gene Expression Profiling. Genes, p53. Male. Mice. Mice, Knockout. Models, Neurological. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Oligonucleotide Array Sequence Analysis. Transcription, Genetic

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  • (PMID = 16368933.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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7. Panagiotakos G, Tabar V: Brain tumor stem cells. Curr Neurol Neurosci Rep; 2007 May;7(3):215-20
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  • [Title] Brain tumor stem cells.
  • The concept of brain tumor stem cells is gaining increased recognition in neuro-oncology.
  • Until recently, the paradigm of a tumor-initiating stem cell was confined to hematopoietic malignancies where the hierarchical lineages of stem progenitor cells are well established.
  • The demonstration of persistent stem cells and cycling progenitors in the adult brain, coupled with the expansion of the cancer stem cell concept to solid tumors, has led to the exploration of "stemness" within gliomas.
  • Emerging data are highly suggestive of the subsistence of transformed multipotential cells within a glioma, with a subfraction of cells exhibiting increased efficiency at tumor initiation.
  • However, data in support of true glioma stem cells are inconclusive to date, particularly with respect to functional characterization of these cells.
  • Ongoing work aims at the identification of unique pathways governing self-renewal of these putative stem cells and at their validation as ultimate therapeutic targets.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplastic Stem Cells / physiology

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  • (PMID = 17488587.001).
  • [ISSN] 1528-4042
  • [Journal-full-title] Current neurology and neuroscience reports
  • [ISO-abbreviation] Curr Neurol Neurosci Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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8. Palm T, Schwamborn JC: Brain tumor stem cells. Biol Chem; 2010 Jun;391(6):607-17
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  • [Title] Brain tumor stem cells.
  • Since the end of the 'no-new-neuron' theory, emerging evidence from multiple studies has supported the existence of stem cells in neurogenic areas of the adult brain.
  • Along with this discovery, neural stem cells became candidate cells being at the origin of brain tumors.
  • In fact, it has been demonstrated that molecular mechanisms controlling self-renewal and differentiation are shared between brain tumor stem cells and neural stem cells and that corruption of genes implicated in these pathways can direct tumor growth.
  • In this regard, future anticancer approaches could be inspired by uncovering such redundancies and setting up treatments leading to exhaustion of the cancer stem cell pool.
  • However, deleterious effects on (normal) neural stem cells should be minimized.
  • Such therapeutic models underline the importance to study the cellular mechanisms implicated in fate decisions of neural stem cells and the oncogenic derivation of adult brain cells.
  • In this review, we discuss the putative origins of brain tumor stem cells and their possible implications on future therapies.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology

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  • (PMID = 20370314.001).
  • [ISSN] 1437-4315
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 107
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9. Nern C, Sommerlad D, Acker T, Plate KH: Brain tumor stem cells. Recent Results Cancer Res; 2009;171:241-59
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  • [Title] Brain tumor stem cells.
  • The dogma that solid tumors are composed of tumor cells that all share the same ability to produce proliferating daughter cells has been challenged in recent years.
  • There is growing evidence that many adult tissues contain a set of tissue stem cells, which might undergo malignant transformation while retaining their stem cell characteristics.
  • Brain tumors such as medulloblastomas or glioblastomas often contain areas of divergent differentiation, which raises the intriguing question of whether these tumors could derive from neural stem cells (NSCs).This chapter reviews the current knowledge of NSCs and relates them to brain tumor pathology.
  • Current therapy protocols for malignant brain tumors are targeted toward the reduction of bulk tumor mass.
  • The concept of brain-tumor stem cells could provide new insights for future therapies, if the capacity for self-renewal of tumor cells and growth of the tumor mass would reside within a small subset of cancer cells.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Antigens, CD / analysis. Glycoproteins / analysis. Humans. Neurons / cytology. Peptides / analysis. Signal Transduction. Stem Cells / physiology

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  • (PMID = 19322548.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides
  • [Number-of-references] 117
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10. Sauvageot CM, Kesari S, Stiles CD: Molecular pathogenesis of adult brain tumors and the role of stem cells. Neurol Clin; 2007 Nov;25(4):891-924, vii
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  • [Title] Molecular pathogenesis of adult brain tumors and the role of stem cells.
  • Primary brain tumors consist of neoplasms with varied molecular defects, morphologic phenotypes, and clinical outcomes.
  • The genetic and signaling abnormalities involved in tumor initiation and progression of the most prevalent adult primary brain tumors, including gliomas, meningiomas, and medulloblastomas, are described in this article.
  • The current understanding of the cell-of-origin of these neoplasms is reviewed, which suggests that the malignant phenotype is propelled by cells with stem-like qualities.
  • [MeSH-major] Brain Neoplasms / pathology. Stem Cells / pathology. Stem Cells / physiology
  • [MeSH-minor] Adult. Genes, p53 / genetics. Humans. Intercellular Signaling Peptides and Proteins / genetics. Phenotype. RNA, Messenger / genetics. Signal Transduction

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  • (PMID = 17964020.001).
  • [ISSN] 0733-8619
  • [Journal-full-title] Neurologic clinics
  • [ISO-abbreviation] Neurol Clin
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger
  • [Number-of-references] 272
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11. Olstorn H, Moe MC, Røste GK, Bueters T, Langmoen IA: Transplantation of stem cells from the adult human brain to the adult rat brain. Neurosurgery; 2007 Jun;60(6):1089-98; discussion 1098-9
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  • [Title] Transplantation of stem cells from the adult human brain to the adult rat brain.
  • OBJECTIVE: To investigate the migration, proliferation, and differentiation of stem cells and neural progenitor cells (NPCs) from the adult human brain after transplantation into adult rodent brains.
  • METHODS: Adult human NPCs were obtained from temporal lobe specimens removed because of medical intractable epilepsy.
  • The cells were transplanted into the posterior periventricular region above the hippocampus in the brains of either healthy adult rats (control) or rats with selective injury of the hippocampal CA1 region (global ischemia).
  • Cell survival at 10 weeks was 4.7 +/- 0.3% (control, n = 3) and 3.7 +/- 1.1% (ischemia, n = 3); at 16 weeks, cell survival was 3.4 +/- 0.6% (control, n = 2) and 7.2 +/- 1.5% (ischemia, n = 2), i.e., comparable to what has been observed earlier when transplanting embryonic tissue into the human brain or progenitor cells between inbred rats.
  • We did not observe signs of tumor formation or aberrant cell morphology.
  • CONCLUSION: The present study shows that adult human NPCs survive, show targeted migration, proliferate, and differentiate after grafting into the adult rat brain.
  • [MeSH-major] Brain Ischemia / therapy. Stem Cell Transplantation. Stem Cells / cytology. Stem Cells / physiology. Transplantation, Heterologous
  • [MeSH-minor] Adult. Animals. Cell Differentiation. Cell Movement. Cell Proliferation. Humans. Male. Rats. Rats, Sprague-Dawley

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  • (PMID = 17538384.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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12. Fang JS, Deng YW, Li MC, Chen FH, Wang YJ, Lu M, Fang F, Wu J, Yang ZY, Zhou XY, Wang F, Chen C: [Isolation and identification of brain tumor stem cells from human brain neuroepithelial tumors]. Zhonghua Yi Xue Za Zhi; 2007 Jan 30;87(5):298-303
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  • [Title] [Isolation and identification of brain tumor stem cells from human brain neuroepithelial tumors].
  • OBJECTIVE: To establish a simplified culture system for the isolation of brain tumor stem cells (BTSCs) from the tumors of human neuroepithelial tissue, to observe the growth and differentiation pattern of BTSCs, and to investigate their expression of the specific markers.
  • METHODS: Twenty-six patients with brain neuroepithelial tumors underwent tumor resection.
  • Two pieces of tumor tissues were taken from each tumor to be dissociated, triturated into single cells in sterile DMEM-F12 medium, and then filtered.
  • The tumor cells were seeded at a concentration of 200,000 viable cells per mL into serum-free DMEM-F12 medium simply supplemented with B27, human basic fibroblast growth factor (20 microg/L), human epidermal growth factor (20 microg /L), insulin (4 U/L), L-glutamine, penicillin and streptomycin.
  • After the primary brain tumor spheres (BTSs) were generated, they were triturated again and passed in fresh medium.
  • The rate of CD133 positive cells in the tumor specimens was (21 +/- 6.2)% - (38 +/- 7.0)%.
  • The tumors of human neuroepithelial tissue contain CD133 and nestin positive tumor stem cells which can be isolated, proliferate and differentiate in vitro and give rise to brain tumor spheres.
  • This tumorigenic subset may provide both a platform for brain tumor research and a target for clinical treatment.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplasms, Neuroepithelial / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adolescent. Adult. Cell Proliferation / drug effects. Child. Culture Media, Serum-Free / pharmacology. Female. Humans. Male. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 17456355.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Culture Media, Serum-Free
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13. Jackson EL, Alvarez-Buylla A: Characterization of adult neural stem cells and their relation to brain tumors. Cells Tissues Organs; 2008;188(1-2):212-24
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  • [Title] Characterization of adult neural stem cells and their relation to brain tumors.
  • The adult mammalian brain contains neural stem cells that are capable of generating new neurons and glia over the course of a lifetime.
  • Neural stem cells reside in 2 germinal niches, the subventricular zone (SVZ) and the dentate gyrus subgranular zone.
  • Recent studies have shown that adult SVZ stem cells are derived from radial glia, the stem cells in the developing brain, which in turn are derived from the neuroepithelum, the earliest brain progenitors.
  • Thus, SVZ stem cells are a continuum from neuroepithelium to radial glia to astrocytes, and are contained within what has been considered the lineage for astrocytes.
  • However, it seems that only a small subset of the astrocytes present in the adult brain have stem cell properties.
  • Recent findings have shown that SVZ stem cell astrocytes express a receptor for platelet-derived growth factor (PDGF), suggesting that the ability to respond to specific growth factor stimuli, such as PDGF, epidermal growth factor and others, may be unique to these stem cell astrocytes.
  • Intriguingly, activation of these same signaling pathways is widely implicated in brain tumor formation.
  • Since the adult brain has very few proliferating cells capable of accumulating the numerous mutations required for transformation, the adult neural stem and/or progenitor cells may be likely candidates for the brain tumor cell of origin.
  • Indeed, activation of the PDGF or epidermal growth factor pathways in adult neural stem or progenitor cells confers tumor-like properties on these cells, lending support to this hypothesis.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Neurons / pathology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18223308.001).
  • [ISSN] 1422-6421
  • [Journal-full-title] Cells, tissues, organs
  • [ISO-abbreviation] Cells Tissues Organs (Print)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 116
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4. Yao Y, Tang X, Li S, Mao Y, Zhou L: Brain tumor stem cells: view from cell proliferation. Surg Neurol; 2009 Mar;71(3):274-9
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  • [Title] Brain tumor stem cells: view from cell proliferation.
  • A small population of TSCs, which form neurospheres and possess the capacity for self-renewal, has been recently identified in adult and pediatric brain tumors.
  • The understanding of brain TSCs has been greatly advanced by the knowledge of cell proliferation, which contributes to initiate and sustain the malignant phenotype.
  • In this article, the authors summarized the evidence of the presence of TSCs in human brain tumors and emphasized the significance of the proliferative status of TSCs.
  • Finally, the preliminary evidence that TSCs in malignant brain tumors have more proliferative capacity than stem/progenitor cells in benign brain tumors was discussed.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology

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  • (PMID = 19249579.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 40
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15. Sgubin D, Aztiria E, Perin A, Longatti P, Leanza G: Activation of endogenous neural stem cells in the adult human brain following subarachnoid hemorrhage. J Neurosci Res; 2007 Jun;85(8):1647-55
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  • [Title] Activation of endogenous neural stem cells in the adult human brain following subarachnoid hemorrhage.
  • In the adult human brain, the presence of neural stem cells has been documented in the subgranular layer of the dentate gyrus of the hippocampus and in the subventricular zone of the lateral ventricles.
  • Neurogenesis has also been reported in rodent models of ischemic stroke, traumatic brain injury, epileptic seizures, and intracerebral or subarachnoid hemorrhage.
  • However, only sparse information is available about the occurrence of neurogenesis in the human brain under similar pathological conditions.
  • In the present report, we describe neural progenitor cell proliferation in the brain of patients suffering from subarachnoid hemorrhage (SAH) resulting from ruptured aneurysm.
  • Ten cerebral samples from both SAH and control patients obtained, respectively, during aneurysm clipping and deep brain tumor removal were analyzed by reverse transcription followed by polymerase chain reaction (RT-PCR) and/or immunohistochemistry (IHC).
  • Thus, activation of neural progenitor cell proliferation may occur in adult human brain following subarachnoid hemorrhage, possibly contributing to the promotion of spontaneous recovery, in this pathological condition.
  • [MeSH-major] Cerebral Cortex / metabolism. Neurons / metabolism. Stem Cells / metabolism. Subarachnoid Hemorrhage / pathology
  • [MeSH-minor] Adult. Aged. Aneurysm, Ruptured / complications. Biomarkers / metabolism. Cell Proliferation. Female. Gene Expression Profiling. Humans. Immunohistochemistry. Intracranial Aneurysm / complications. Male. Microscopy, Confocal. Microscopy, Fluorescence. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17455304.001).
  • [ISSN] 0360-4012
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
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16. Galli R, Gritti A, Vescovi AL: Adult neural stem cells. Methods Mol Biol; 2008;438:67-84
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  • [Title] Adult neural stem cells.
  • Neural stem cells (NSCs) have been identified in the mature central nervous system (CNS), and they reside in specific areas.
  • The proper application of this method to the cells allows the establishment of long-term expanding stable NSC lines, starting from different neural tissues as the adult rodent CNS and human brain tumor specimens.
  • [MeSH-major] Cell Culture Techniques / methods. Neurons / cytology. Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Differentiation. Cell Separation. Cells, Cultured. Central Nervous System / cytology. Central Nervous System / pathology. Dissection. Humans. Neoplastic Stem Cells / cytology. Rodentia

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  • (PMID = 18369750.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Varghese M, Olstorn H, Sandberg C, Vik-Mo EO, Noordhuis P, Nistér M, Berg-Johnsen J, Moe MC, Langmoen IA: A comparison between stem cells from the adult human brain and from brain tumors. Neurosurgery; 2008 Dec;63(6):1022-33; discussion 1033-4
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  • [Title] A comparison between stem cells from the adult human brain and from brain tumors.
  • OBJECTIVE: To directly compare stem cells from the normal adult human brain (adult human neural stem cells [AHNSC]), Grade II astrocytomas (AC II), and glioblastoma multiforme (GBM), with respect to proliferative and tumor-forming capacity and differentiation potential.
  • METHODS: Cells were isolated from tissue obtained during epilepsy surgery (AHNSCs) or tumor surgery (glioma stem cells [GSC]).
  • 1) GBM stem cells formed tumors after orthotopic transplantation; AHNSCs showed no sign of tumor formation;.
  • 5) both AHNSCs and stem cells from AC II and GBM responded to differentiation cues with a dramatic decrease in the proliferation index (Ki-67);.
  • CONCLUSION: AHNSCs and stem cells from AC II and GBM differ with respect to proliferation, tumor-forming capacity, and rate and pattern of differentiation.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / physiopathology. Neurons / pathology. Neurons / physiology. Stem Cells / pathology. Stem Cells / physiology
  • [MeSH-minor] Adult. Cell Differentiation. Cell Proliferation. Cells, Cultured. Female. Humans. Male

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  • (PMID = 19057315.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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18. Jasmin JF, Yang M, Iacovitti L, Lisanti MP: Genetic ablation of caveolin-1 increases neural stem cell proliferation in the subventricular zone (SVZ) of the adult mouse brain. Cell Cycle; 2009 Dec;8(23):3978-83
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  • [Title] Genetic ablation of caveolin-1 increases neural stem cell proliferation in the subventricular zone (SVZ) of the adult mouse brain.
  • Adult neural stem cells are self-renewing multipotent cells that have the potential to replace dysfunctional and/or dying neuronal cells at the site of brain injury or degeneration.
  • Caveolins are well-known tumor-suppressor genes that were recently found to be involved in the regulation of stem cell proliferation.
  • For instance, ablation of the caveolin-1 (Cav-1) gene in mice markedly increases the proliferation of intestinal and mammary stem cells.
  • However, the roles of caveolins in the proliferation of adult neural stem cells still remain unknown.
  • In this study, dual-label immunofluorescence analysis of the proliferation marker, Ki67, and the stem cell markers, nestin and Sox2, was performed on brains of 8 week-old wild-type (WT) and Cav-1 knockout (KO) mice.
  • Remarkably similar results were also obtained with Cav-2 and Cav-3 KO mouse brains as well, with increased proliferation of adult neural stem cells.
  • Thus, the SVZ of caveolin KO mouse brains displays an increased proliferation of adult neural stem cells.
  • Caveolin proteins might represent new crucial regulators of adult neural stem cell proliferation.
  • [MeSH-major] Brain / metabolism. Caveolin 1 / metabolism. Cerebral Ventricles / cytology. Neurons / cytology. Stem Cells / cytology

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  • (PMID = 19923909.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA098779; United States / NCI NIH HHS / CA / R01-CA120876
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caveolin 1; 0 / Intermediate Filament Proteins; 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / SOXB1 Transcription Factors; 0 / Sox2 protein, mouse
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19. Hide T, Kuratsu J: [Progress in the study of brain tumor stem cells as treatment targets]. Brain Nerve; 2009 Jul;61(7):781-9
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  • [Title] [Progress in the study of brain tumor stem cells as treatment targets].
  • The study of cancer stem cells (CSCs) is on the cutting edge of cancer research.
  • Following the discovery of neural stem cells (NSCs), extensive studies on their characteristics led to the discovery of cancer stem cells (CSCs) in brain tumors: these cells are termed brain tumor stem cells (BTSCs).
  • Adult NSCs exist in the subventricular zone (SVZ) of the lateral ventricle and in the subgranular zone (SGZ) of the hippocampal dentate gyrus.
  • Specific genes referred to as "stemness genes," combined with a specific microenvironment called the "stem cell niche" are important in maintaining NSC characteristics.
  • Identification of BTSCs yielded new insights regarding the chemo- and radio-resistant properties that facilitate their selective survival and ability to initiate tumor recurrence.
  • Moreover, treatment with drugs that affect the stem cell niche in brain tumor-bearing mice prolonged their survival.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / therapy. Glioblastoma / pathology. Glioblastoma / therapy. Neoplastic Stem Cells
  • [MeSH-minor] Adult. Animals. Cerebral Ventricles / cytology. Dentate Gyrus / cytology. Hippocampus / cytology. Humans. Mice. Stem Cell Niche / physiology

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  • (PMID = 19618855.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 35
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20. Miyagawa T, Mochizuki Y, Nakahara Y, Kawamura T, Sasaki S, Tsukamoto H, Tabata H, Okada H, Kobashi Y: [A case of chronic aspiration pneumonia caused by juvenile brain stem tumor]. Nihon Kokyuki Gakkai Zasshi; 2009 Mar;47(3):222-6

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  • [Title] [A case of chronic aspiration pneumonia caused by juvenile brain stem tumor].
  • A brain stem tumor was detected on his brain magnetic resonance imaging, which was thought to be the cause of his mis-swallowing.
  • [MeSH-major] Brain Stem Neoplasms / complications. Pneumonia, Aspiration / etiology
  • [MeSH-minor] Adult. Chronic Disease. Humans. Male

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  • (PMID = 19348270.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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21. Evers P, Lee PP, DeMarco J, Agazaryan N, Sayre JW, Selch M, Pajonk F: Irradiation of the potential cancer stem cell niches in the adult brain improves progression-free survival of patients with malignant glioma. BMC Cancer; 2010 Jul 21;10:384
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  • [Title] Irradiation of the potential cancer stem cell niches in the adult brain improves progression-free survival of patients with malignant glioma.
  • BACKGROUND: Glioblastoma is the most common brain tumor in adults.
  • The mechanisms leading to glioblastoma are not well understood but animal studies support that inactivation of tumor suppressor genes in neural stem cells (NSC) is required and sufficient to induce glial cancers.
  • This suggests that the NSC niches in the brain may harbor cancer stem cells (CSCs), Thus providing novel therapy targets.
  • METHODS: 55 adult patients with Grade 3 or Grade 4 glial cancer treated with radiotherapy at UCLA between February of 2003 and May of 2009 were included in this retrospective study.
  • CONCLUSIONS: Our study leads us to hypothesize that in glioma targeted radiotherapy of the stem cell niches in the adult brain could yield significant benefits over radiotherapy of the primary tumor mass alone and that damage caused by smaller fractions of radiation maybe less efficiently detected by the DNA repair mechanisms in CSCs.

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  • (PMID = 20663133.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA137110; United States / NCI NIH HHS / CA / R01CA137110-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2918578
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22. Qu Q, Shi Y: Neural stem cells in the developing and adult brains. J Cell Physiol; 2009 Oct;221(1):5-9
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  • [Title] Neural stem cells in the developing and adult brains.
  • Neural stem cells exist in the mammalian developing and adult nervous system.
  • Recently, tremendous interest in the potential of neural stem cells for the treatment of neurodegenerative diseases and brain injuries has substantially promoted research on neural stem cell self-renewal and differentiation.
  • Multiple cell-intrinsic regulators coordinate with the microenvironment through various signaling pathways to regulate neural stem cell maintenance, self-renewal, and fate determination.
  • This review focuses on essential intracellular regulators that control neural stem cell maintenance and self-renewal in both embryonic brains and adult nervous system.
  • These factors include the orphan nuclear receptor TLX, the high-mobility-group DNA binding protein Sox2, the basic helix-loop-helix transcription factor Hes, the tumor suppressor gene Pten, the membrane-associated protein Numb, and its cytoplasmic homolog Numblike.
  • The aim of this review is to summarize our current understanding of neural stem cell regulation through these important stem cell regulators.

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
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  • (PMID = 19562676.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS059546-01; United States / NINDS NIH HHS / NS / R01 NS059546; United States / NINDS NIH HHS / NS / R01 NS059546-02S1; United States / NINDS NIH HHS / NS / NS059546-02S1; United States / NINDS NIH HHS / NS / R01 NS059546-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
  • [Number-of-references] 70
  • [Other-IDs] NLM/ NIHMS200546; NLM/ PMC2869301
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23. Zhang C, Yao Y, Wang Y, Chen Z, Wu J, Mao Y, Zhou L: Temozolomide for adult brain stem glioblastoma: case report of a long-term survivor. Int J Neurosci; 2010 Dec;120(12):787-91
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  • [Title] Temozolomide for adult brain stem glioblastoma: case report of a long-term survivor.
  • Brain stem gliomas are rare intracranial tumors, especially in adults.
  • Malignant or high-grade brain stem gliomas are usually associated with a very poor prognosis.
  • This case report documents an adolescent harboring brain stem glioblastoma who had complete radiological response to temozolomide after partial tumor resection and survived for more than 3 years.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Brain Stem Neoplasms / drug therapy. Brain Stem Neoplasms / mortality. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Glioblastoma / mortality
  • [MeSH-minor] Fatal Outcome. Humans. Male. Survival Rate / trends. Treatment Outcome. Young Adult

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  • (PMID = 20946086.001).
  • [ISSN] 1563-5279
  • [Journal-full-title] The International journal of neuroscience
  • [ISO-abbreviation] Int. J. Neurosci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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24. Lasky JL 3rd, Choe M, Nakano I: Cancer stem cells in pediatric brain tumors. Curr Stem Cell Res Ther; 2009 Dec;4(4):298-305
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  • [Title] Cancer stem cells in pediatric brain tumors.
  • Although recent studies have focused on molecular mechanisms that underlie the initiation and progression of adult glioblastoma multiforme (GBM), these tumors differ phenotypically and at a molecular level from pediatric brain tumors.
  • Recent investigations have identified a stem cell population, termed "brain tumor stem cells" (BTSC) within the heterogeneous cell populations that comprise malignant brain tumors which may be partly responsible for the resistance to current therapies.
  • By exploiting molecular differences present within these heterogeneous populations of brain tumor cells, we may be able to achieve specific eradication of BTSC and long-lasting remissions, while causing less toxicity to normal tissues.
  • In this review, we describe the issues surrounding the identification and characterization of BTSC, the molecular biology of BTSC for different pediatric brain tumors, and suggest future avenues for the development of treatments for this devastating disease.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Optic Nerve Glioma / pathology
  • [MeSH-minor] Adult Stem Cells / pathology. Biomarkers / metabolism. Cell Differentiation. Chemotherapy, Adjuvant. Child. Humans. Surgical Procedures, Operative


25. Covacu R, Arvidsson L, Andersson A, Khademi M, Erlandsson-Harris H, Harris RA, Svensson MA, Olsson T, Brundin L: TLR activation induces TNF-alpha production from adult neural stem/progenitor cells. J Immunol; 2009 Jun 1;182(11):6889-95
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  • [Title] TLR activation induces TNF-alpha production from adult neural stem/progenitor cells.
  • Adult neural stem cells (NSCs) are believed to facilitate CNS repair and tissue regeneration.
  • Primary cultures of neural stem/progenitor cells isolated from the subventricular zone of brains from adult Dark Agouti rats were exposed to 1) supernatants from activated macrophages;.
  • [MeSH-major] Neurons / metabolism. Stem Cells / metabolism. Toll-Like Receptor 2 / agonists. Toll-Like Receptor 4 / agonists. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Brain / cytology. Cells, Cultured. Cytokines / pharmacology. Interferon-gamma / pharmacology. Macrophages / secretion. Paracrine Communication. RNA, Messenger / drug effects. Rats. Rats, Inbred Strains

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  • (PMID = 19454685.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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26. Liu D, Ou L, Clemenson GD Jr, Chao C, Lutske ME, Zambetti GP, Gage FH, Xu Y: Puma is required for p53-induced depletion of adult stem cells. Nat Cell Biol; 2010 Oct;12(10):993-8
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  • [Title] Puma is required for p53-induced depletion of adult stem cells.
  • The knock-in mice exhibit constitutive p53 activation and segmental progeria that is correlated with the depletion of adult stem cells in multiple tissues, including bone marrow, brain and testes.
  • Furthermore, a deficiency of Puma, which is required for p53-dependent apoptosis after DNA damage, rescues segmental progeria and prevents the depletion of adult stem cells.
  • These findings suggest a key role of p53-dependent apoptosis in depleting adult stem cells after the accumulation of DNA damage, which leads to a decrease in tissue regeneration.


27. Kang SK, Park JB, Cha SH: Multipotent, dedifferentiated cancer stem-like cells from brain gliomas. Stem Cells Dev; 2006 Jun;15(3):423-35
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  • [Title] Multipotent, dedifferentiated cancer stem-like cells from brain gliomas.
  • In modern cancer biology, external factors and niches can act on differentiated tissue cells to cause cancer by inducing dedifferentiation of mature adult cells.
  • Recently, we discovered that dedifferentiation of glioma cancer cells alters the expression of mature and neural stem cell (NSC)-related genes, in that cancer cells adjust to the serum-deprived environment and cell-to-cell interaction by down-regulating genes associated with neural mature markers and up-regulating genes that are primitive NSC markers.
  • After grafting to severe combined immunodeficient (SCID) mouse brains, dedifferentiated cancer stem cells migrated and continued active proliferation for more than 4 weeks.
  • We also performed microarray analysis and characterized the gene expression patterns in control cancer cells with dedifferentiated cancer stem-like cells.
  • In this report, we propose that the dedifferentiation process of brain tumor and normal tissue may contribute to the malignancy and aggressiveness of the brain cancer.
  • [MeSH-major] Brain / pathology. Brain Neoplasms / pathology. Cell Differentiation. Glioma / pathology. Multipotent Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Movement. Cell Proliferation. DNA, Complementary / genetics. Drug Resistance. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes / genetics. Humans. Mice. Mice, SCID. Neoplasm Metastasis. Neurons / cytology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tumor Cells, Cultured

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  • [ErratumIn] Stem Cells Dev. 2006 Oct;15(5):749
  • (PMID = 16846378.001).
  • [ISSN] 1547-3287
  • [Journal-full-title] Stem cells and development
  • [ISO-abbreviation] Stem Cells Dev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / RNA, Messenger
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28. Matsunaga S, Fujitsu K, Yagishita S, Ichikawa T, Takemoto Y, Takeda Y, Miyahara K, Niino H, Shiina T: Endodermal cyst ventral to the lower brain stem. Neurol Med Chir (Tokyo); 2006 Dec;46(12):614-8

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  • [Title] Endodermal cyst ventral to the lower brain stem.
  • A 28-year-old woman presented with a rare case of endodermal cyst located ventral to the lower brain stem manifesting as recurrent aseptic meningitis.
  • Computed tomography and magnetic resonance imaging demonstrated a cystic mass located ventral to the lower brain stem and extending from the prepontine to the upper cervical (C-2) cistern.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Endodermal Sinus Tumor / pathology
  • [MeSH-minor] Adult. Female. Humans

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  • (PMID = 17185890.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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29. Widera D, Mikenberg I, Kaltschmidt B, Kaltschmidt C: Potential role of NF-kappaB in adult neural stem cells: the underrated steersman? Int J Dev Neurosci; 2006 Apr-May;24(2-3):91-102
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  • [Title] Potential role of NF-kappaB in adult neural stem cells: the underrated steersman?
  • Neural stem cells are precursors of neurons and glial cells.
  • During brain development, these cells proliferate, migrate and differentiate into specific lineages.
  • Recently neural stem cells within the adult central nervous system were identified.
  • Informations are now emerging about regulation of stem cell proliferation, migration and differentiation by numerous soluble factors such as chemokines and cytokines.
  • NF-kappaB is an inducible transcription factor detected in neurons, glia and neural stem cells.
  • It has been recently shown that members of the NF-kappaB family are widely expressed by neurons, glia and neural stem cells.
  • Recent data suggest an important role of NF-kappaB on proliferation, migration and differentiation of neural stem cells.
  • In this review, we suggest a model explaining the multiple action of NF-kappaB on neural stem cells.
  • Furthermore, we discuss the potential role of NF-kappaB within the so-called brain cancer stem cells.
  • [MeSH-major] NF-kappa B / physiology. Neurons / metabolism. Signal Transduction / physiology. Stem Cells / metabolism
  • [MeSH-minor] Animals. Brain Neoplasms / pathology. Cell Differentiation. Cell Movement. Cell Proliferation. Humans. Models, Neurological. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16413989.001).
  • [ISSN] 0736-5748
  • [Journal-full-title] International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
  • [ISO-abbreviation] Int. J. Dev. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 130
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30. Mao Y, Zhou L, Zhu W, Wang X, Yang G, Xie L, Mao X, Jin K: Proliferative status of tumor stem cells may be correlated with malignancy grade of human astrocytomas. Front Biosci; 2007;12:2252-9
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  • [Title] Proliferative status of tumor stem cells may be correlated with malignancy grade of human astrocytomas.
  • Tumor stem cells are implicated in tumor initiation and maintenance.
  • Recent studies have shown that a subpopulation of cells isolated from brain tumors can form neurospheres in vitro, and have multiple characteristic properties observed in neural stem cells.
  • In vivo implantation of these cells can induce tumors that phenocopy original tumors, suggesting that tumor stem cells are involved in brain carcinogenesis.
  • We found that a population of cells in human glioblastoma multiforme expressed multiple protein markers of neural stem cells including nestin, TUC-4, doublecortin and beta III-tubulin.
  • To investigate further whether these properties of tumor stem cells are correlated with their biological behavior, immunohistochemistry was performed on brain sections from astrocytomas of different grades using antibodies against neural stem cell markers.
  • The number of cells expressing Ki67 antigen and neural stem cell markers was increased in relation to worsening histological grade of astrocytomas, indicating that the capacity for tumor stem cell proliferation may be clinically relevant.
  • Thus, tumor stem cells in astrocytomas may be involved in carcinogenesis.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Middle Aged. Neurons / metabolism. Stem Cells / metabolism

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  • (PMID = 17127461.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG21980
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen
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31. Jacques TS, Swales A, Brzozowski MJ, Henriquez NV, Linehan JM, Mirzadeh Z, O' Malley C, Naumann H, Alvarez-Buylla A, Brandner S: Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes. EMBO J; 2010 Jan 6;29(1):222-35
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  • [Title] Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes.
  • It has been suggested that intrinsic brain tumours originate from a neural stem/progenitor cell population in the subventricular zone of the post-natal brain.
  • However, the influence of the initial genetic mutation on the phenotype as well as the contribution of mature astrocytes to the formation of brain tumours is still not understood.
  • We deleted Rb/p53, Rb/p53/PTEN or PTEN/p53 in adult subventricular stem cells; in ectopically neurografted stem cells; in mature parenchymal astrocytes and in transplanted astrocytes.
  • We found that only stem cells, but not astrocytes, gave rise to brain tumours, independent of their location.
  • This suggests a cell autonomous mechanism that enables stem cells to generate brain tumours, whereas mature astrocytes do not form brain tumours in adults.
  • Our study underlines an important role of stem cells and the relevance of initial genetic mutations in the pathogenesis and phenotype of brain tumours.

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  • (PMID = 19927122.001).
  • [ISSN] 1460-2075
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD032116; United States / NICHD NIH HHS / HD / R37 HD032116; United States / NICHD NIH HHS / HD / HD-32116
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / glial fibrillary astrocytic protein, mouse; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2808375
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32. Siebzehnrubl FA, Jeske I, Müller D, Buslei R, Coras R, Hahnen E, Huttner HB, Corbeil D, Kaesbauer J, Appl T, von Hörsten S, Blümcke I: Spontaneous in vitro transformation of adult neural precursors into stem-like cancer cells. Brain Pathol; 2009 Jul;19(3):399-408
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous in vitro transformation of adult neural precursors into stem-like cancer cells.
  • Recent studies have found that cellular self-renewal capacity in brain cancer is heterogeneous, with only stem-like cells having this property.
  • A link between adult stem cells and cancer stem cells remains, however, to be shown.
  • Here, we describe the emergence of cancer stem-like cells from in vitro cultured brain stem cells.
  • Adult rat subventricular zone (SVZ) stem cells transformed into tumorigenic cell lines after expansion in vitro.
  • These cell lines maintained characteristic features of stem-like cells expressing Nestin, Musashi-1 and CD133, but continued to proliferate upon differentiation induction.
  • Karyotyping detected multiple acquired chromosomal aberrations, and syngeneic transplantation into the brain of adult rats resulted in malignant tumor formation.
  • Deficient downregulation of platelet-derived growth factor (PDGF) receptor alpha was identified as candidate mechanism for tumor cell proliferation, and its knockdown by siRNA resulted in a reduction of cell growth.
  • Our data point to adult brain precursor cells to be transformed in malignancies.
  • Furthermore, in vitro expansion of adult neural stem cells, which will be mandatory for therapeutic strategies in neurological disorders, also harbors the risk for amplifying precursor cells with acquired genetic abnormalities and induction of malignant tumors after transplantation.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Cell Transformation, Neoplastic / pathology. Neoplastic Stem Cells / pathology. Neurons / pathology
  • [MeSH-minor] Animals. Blotting, Western. Brain / cytology. Brain Tissue Transplantation / adverse effects. Cell Differentiation / physiology. Chromosome Aberrations. Immunohistochemistry. RNA, Small Interfering. Rats. Rats, Wistar. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18637011.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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33. Bayrakli F, Dinçer A, Sav A, Vardareli E, Peker S: Late brain stem radionecrosis seventeen years after fractionated radiotherapy. Turk Neurosurg; 2009 Apr;19(2):182-5
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  • [Title] Late brain stem radionecrosis seventeen years after fractionated radiotherapy.
  • The appearance of a new lesion several years after radiation treatment for a primary brain tumor may represent different kind of pathologies.
  • His cranial MRI study showed heterogeneous signal intensity of brain stem radionecrosis in the pons spreading through the mesencephalon and left brachium pontis.
  • The leading diagnosis was high-grade glial tumor.
  • [MeSH-major] Astrocytoma / radiotherapy. Brain Neoplasms / radiotherapy. Brain Stem / pathology. Radiation Injuries / pathology
  • [MeSH-minor] Biopsy. Humans. Magnetic Resonance Imaging. Male. Necrosis. Time Factors. Young Adult

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  • (PMID = 19431132.001).
  • [ISSN] 1019-5149
  • [Journal-full-title] Turkish neurosurgery
  • [ISO-abbreviation] Turk Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
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34. Okamoto K, Furusawa T, Ishikawa K, Sasai K, Tokiguchi S: Focal T2 hyperintensity in the dorsal brain stem in patients with vestibular schwannoma. AJNR Am J Neuroradiol; 2006 Jun-Jul;27(6):1307-11
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  • [Title] Focal T2 hyperintensity in the dorsal brain stem in patients with vestibular schwannoma.
  • BACKGROUND AND PURPOSE: The vestibular nucleus cannot be visualized on MR imaging, but some patients with vestibular schwannoma show a tiny area of hyperintensity in the dorsal brain stem on T2-weighted images.
  • METHODS: We retrospectively reviewed the postoperative MR images of 53 patients with cerebellopontine angle tumor.
  • If such hyperintensity is seen in a patient with a large cerebellopontine angle tumor, a diagnosis of vestibular schwannoma is suggested.
  • [MeSH-major] Brain Stem / pathology. Magnetic Resonance Imaging. Neuroma, Acoustic / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Cerebellar Neoplasms / diagnosis. Cerebellar Neoplasms / pathology. Cerebellar Neoplasms / surgery. Cerebellopontine Angle. Female. Humans. Male. Middle Aged

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  • (PMID = 16775286.001).
  • [ISSN] 0195-6108
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Betschinger J, Mechtler K, Knoblich JA: Asymmetric segregation of the tumor suppressor brat regulates self-renewal in Drosophila neural stem cells. Cell; 2006 Mar 24;124(6):1241-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Asymmetric segregation of the tumor suppressor brat regulates self-renewal in Drosophila neural stem cells.
  • How stem cells generate both differentiating and self-renewing daughter cells is unclear.
  • Here, we show that Drosophila larval neuroblasts-stem cell-like precursors of the adult brain-regulate proliferation by segregating the growth inhibitor Brat and the transcription factor Prospero into only one daughter cell.
  • In brat or prospero mutants, both daughter cells grow and behave like neuroblasts leading to the formation of larval brain tumors.
  • We have identified a molecular mechanism that may control self-renewal and prevent tumor formation in other stem cells as well.
  • [MeSH-major] Cell Division. Neoplasms / pathology. Neurons / metabolism. Stem Cells / metabolism
  • [MeSH-minor] Animals. Brain / cytology. Cell Cycle Proteins / metabolism. Cell Nucleus / drug effects. DNA-Binding Proteins / genetics. DNA-Binding Proteins / pharmacology. DNA-Binding Proteins / physiology. Drosophila / embryology. Drosophila Proteins / genetics. Drosophila Proteins / metabolism. Drosophila Proteins / pharmacology. Drosophila Proteins / physiology. Gene Expression Regulation. Genes, Tumor Suppressor. Genes, myc / physiology. Humans. Larva / cytology. Mutation. Nerve Tissue Proteins / metabolism. Nerve Tissue Proteins / physiology. Nuclear Proteins / metabolism. Nuclear Proteins / physiology. Transcription Factors / metabolism. Transcription Factors / physiology


41. Quiñones-Hinojosa A, Sanai N, Gonzalez-Perez O, Garcia-Verdugo JM: The human brain subventricular zone: stem cells in this niche and its organization. Neurosurg Clin N Am; 2007 Jan;18(1):15-20, vii
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The human brain subventricular zone: stem cells in this niche and its organization.
  • The human brain harbors stem cells in the subventricular zone (SVZ).
  • The authors have collected postmortem and intraoperative tissue from adult human patients and found that it contains a unique ribbon of astrocytes that proliferate in vivo and can function as neural stem cells in vitro.
  • In this article, the authors report on four main types of SVZ walls in the human brain.
  • Understanding the organization of the adult human SVZ represents a necessary first step in understanding cellular proliferation, precursor migration, and the neurogenic niche of the largest known germinal region in the adult human brain.
  • [MeSH-major] Adult Stem Cells / cytology. Cerebral Ventricles / cytology

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  • (PMID = 17244550.001).
  • [ISSN] 1042-3680
  • [Journal-full-title] Neurosurgery clinics of North America
  • [ISO-abbreviation] Neurosurg. Clin. N. Am.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 1F32NS047011; United States / NINDS NIH HHS / NS / K08NS055851
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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42. Schmidt NO, Przylecki W, Yang W, Ziu M, Teng Y, Kim SU, Black PM, Aboody KS, Carroll RS: Brain tumor tropism of transplanted human neural stem cells is induced by vascular endothelial growth factor. Neoplasia; 2005 Jun;7(6):623-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brain tumor tropism of transplanted human neural stem cells is induced by vascular endothelial growth factor.
  • The transplantation of neural stem cells (NSCs) offers a new potential therapeutic approach as a cell-based delivery system for gene therapy in brain tumors.
  • This is based on the unique capacity of NSCs to migrate throughout the brain and to target invading tumor cells.
  • We analyzed the in vitro and in vivo effects of angiogenic growth factors and protein extracts from surgical specimens of brain tumor patients on NSC migration.
  • Here, we demonstrate that vascular endothelial growth factor (VEGF) is able to induce a long-range attraction of transplanted human NSCs from distant sites in the adult brain.
  • Our results indicate that tumor-upregulated VEGF and angiogenic-activated microvasculature are relevant guidance signals for NSC tropism toward brain tumors.
  • [MeSH-major] Brain Neoplasms / pathology. Neurons / cytology. Stem Cells / cytology. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Movement. Cell Transplantation. Cells, Cultured. Culture Media, Conditioned / pharmacology. Dose-Response Relationship, Drug. Endothelium, Vascular / cytology. Enzyme-Linked Immunosorbent Assay. Humans. Microscopy, Fluorescence. Neovascularization, Pathologic. Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Swine. Tropism. Umbilical Veins / cytology. Up-Regulation. Vascular Endothelial Growth Factor Receptor-1 / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • (PMID = 16036113.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC1501284
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43. Demeter K, Zádori A, Agoston VA, Madarász E: Studies on the use of NE-4C embryonic neuroectodermal stem cells for targeting brain tumour. Neurosci Res; 2005 Nov;53(3):331-42
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  • [Title] Studies on the use of NE-4C embryonic neuroectodermal stem cells for targeting brain tumour.
  • Neural stem cells were suggested to migrate to and invade intracranial gliomas.
  • In the presented studies, interactions of NE-4C embryonic neural stem cells were investigated with C6 and Gl261, LL and U87, glioblastoma cells or with primary astrocytes.
  • Glioma-derived humoral factors did not influence the proliferation of stem cells.
  • In chimera-aggregates, all types of glioma cells co-aggregated with astrocytes, but most of them segregated from stem cells.
  • Complete intercalation of stem and tumour cells was detected only in chimera-aggregates of Gl261 glioma and NE-4C cells.
  • If mixed suspensions of NE-4C and Gl261 cells were injected into the brain, stem cells survived and grew inside the tumour mass.
  • NE-4C stem cells, however, did not migrate towards the tumour, if implanted near to Gl261 tumours established in the adult mouse forebrain.
  • The observations indicate that not all types of stem cells could be used for targeting all sorts of brain tumours.
  • [MeSH-major] Brain Neoplasms / therapy. Brain Tissue Transplantation / methods. Ectoderm / transplantation. Stem Cell Transplantation / methods. Stem Cells / physiology
  • [MeSH-minor] Animals. Astrocytes / physiology. Cell Aggregation / physiology. Cell Communication / physiology. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cell Movement / physiology. Cell Proliferation / drug effects. Coculture Techniques. Glioblastoma / physiopathology. Glioblastoma / therapy. Graft Survival / physiology. Growth Substances / metabolism. Growth Substances / pharmacology. Humans. Mice. Neoplasm Invasiveness / physiopathology. Rats

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  • (PMID = 16183159.001).
  • [ISSN] 0168-0102
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Growth Substances
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44. Butovsky O, Ziv Y, Schwartz A, Landa G, Talpalar AE, Pluchino S, Martino G, Schwartz M: Microglia activated by IL-4 or IFN-gamma differentially induce neurogenesis and oligodendrogenesis from adult stem/progenitor cells. Mol Cell Neurosci; 2006 Jan;31(1):149-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microglia activated by IL-4 or IFN-gamma differentially induce neurogenesis and oligodendrogenesis from adult stem/progenitor cells.
  • Cell renewal in the adult central nervous system (CNS) is limited, and is blocked in inflammatory brain conditions.
  • We show that both neurogenesis and oligodendrogenesis of adult neural progenitor cells in mice are blocked by inflammation-associated (endotoxin-activated) microglia, but induced by microglia activated by cytokines (IL-4 or low level of IFN-gamma) associated with T-helper cells.
  • Blockage was correlated with up-regulation of microglial production of tumor necrosis factor-alpha.
  • It thus appears that microglial phenotype critically affects their ability to support or impair cell renewal from adult stem cell.
  • [MeSH-major] Interferon-gamma / pharmacology. Interleukin-4 / pharmacology. Microglia / cytology. Oligodendroglia / cytology. Stem Cells / cytology


45. Shiras A, Chettiar ST, Shepal V, Rajendran G, Prasad GR, Shastry P: Spontaneous transformation of human adult nontumorigenic stem cells to cancer stem cells is driven by genomic instability in a human model of glioblastoma. Stem Cells; 2007 Jun;25(6):1478-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous transformation of human adult nontumorigenic stem cells to cancer stem cells is driven by genomic instability in a human model of glioblastoma.
  • The presence of a CD133+/nestin+ population in brain tumors suggests that a normal neural stem cell may be the cell of origin for gliomas.
  • We have identified human CD133-positive NSCs from adult glioma tissue and established them as long-term in vitro cultures human neuroglial culture (HNGC)-1.
  • Replicative senescence in HNGC-1 led to a high level of genomic instability and emergence of a spontaneously immortalized clone that developed into cell line HNGC-2 with features of cancer stem cells (CSCs), which include the ability for self-renewal and the capacity to form CD133-positive neurospheres and develop intracranial tumors.
  • The activated forms of Notch and Hes isoforms were expressed in both non-neoplastic neural stem cells and brain tumor stem cells derived from it.
  • Importantly, a significant overexpression of these molecules was found in the brain tumor stem cells.
  • These findings suggest that this model comprised of HNGC-1 and HNGC-2 cells would be a useful system for studying pathways involved in self-renewal of stem cells and their transformation to cancer stem cells.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Cell Transformation, Neoplastic / genetics. Genomic Instability / physiology. Glioblastoma / pathology. Models, Biological. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Cell Aging / genetics. Cell Proliferation. Humans. Mice. Mice, Nude. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Telomerase / metabolism. Tumor Cells, Cultured

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  • (PMID = 17332509.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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46. Schrot RJ, Ma JH, Greco CM, Arias AD, Angelastro JM: Organotypic distribution of stem cell markers in formalin-fixed brain harboring glioblastoma multiforme. J Neurooncol; 2007 Nov;85(2):149-57
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  • [Title] Organotypic distribution of stem cell markers in formalin-fixed brain harboring glioblastoma multiforme.
  • The role of stem cells in the origin, growth patterns, and infiltration of glioblastoma multiforme is a subject of intense investigation.
  • One possibility is that glioblastoma may arise from transformed stem cells in the ventricular zone.
  • To explore this hypothesis, we examined the distribution of two stem cell markers, activating transcription factor 5 (ATF5) and CD133, in an autopsy brain specimen from an individual with glioblastoma multiforme.
  • The brain was harvested within several hours after death.
  • After formalin fixation, sectioning, and mapping of tumor location in the gross specimen, histologic specimens were prepared from tumor-bearing and grossly normal hemispheres.
  • Both markers co-localized to the ependymal and subependymal zones on the side of the tumor, but not in the normal hemisphere or more rostrally in the affected hemisphere.
  • To our knowledge, this is the first in situ demonstration of stem cell markers in whole human brain.
  • The robust staining for ATF5 and CD133 in histologically normal ventricular zone suggests that an increase in periventricular stem cell activity occurred in this patient on the side of the tumor, either as a localized response to brain injury or as an integral component of oncogenesis and tumor recurrence.
  • [MeSH-major] Activating Transcription Factors / metabolism. Antigens, CD / metabolism. Brain / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Glycoproteins / metabolism. Peptides / metabolism
  • [MeSH-minor] Adult. Biomarkers / metabolism. Cerebral Ventricles / metabolism. Fatal Outcome. Humans. Immunohistochemistry. Male. Tissue Distribution

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  • [CommentIn] J Neurooncol. 2008 Sep;89(2):247-8; author reply 249 [18568293.001]
  • (PMID = 17516028.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / ATF5 protein, human; 0 / Activating Transcription Factors; 0 / Antigens, CD; 0 / Biomarkers; 0 / Glycoproteins; 0 / Peptides
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47. Yoshimura J, Nishiyama K, Fukuda M, Watanabe M, Igarashi H, Fujii Y: Adult cerebellopontine angle medulloblastoma originating in the pons mimicking focal brainstem tumor. J Neuroimaging; 2009 Oct;19(4):385-7
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  • [Title] Adult cerebellopontine angle medulloblastoma originating in the pons mimicking focal brainstem tumor.
  • We herein report a rare case of cerebellopontine angle (CPA) medulloblastoma originating in the brainstem that demonstrated a very unusual clinical presentation and radiological appearances.
  • MR spectroscopic imaging is considered to be quite useful for the management of this rare type of brainstem tumor.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Cerebellopontine Angle / pathology. Infratentorial Neoplasms / pathology. Medulloblastoma / pathology. Pons / pathology
  • [MeSH-minor] Adult. Aspartic Acid / analogs & derivatives. Aspartic Acid / metabolism. Choline / metabolism. Diagnosis, Differential. Female. Follow-Up Studies. Functional Laterality. Humans. Magnetic Resonance Imaging. Magnetic Resonance Spectroscopy

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  • (PMID = 19021841.001).
  • [ISSN] 1552-6569
  • [Journal-full-title] Journal of neuroimaging : official journal of the American Society of Neuroimaging
  • [ISO-abbreviation] J Neuroimaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; N91BDP6H0X / Choline
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48. Govindan A, Mahadevan A, Bhat DI, Arivazhagan A, Chakraborti S, Suja MS, Phalguni AA, Sampath S, Chandramouli BA, Shankar SK: Papillary glioneuronal tumor-evidence of stem cell origin with biphenotypic differentiation. J Neurooncol; 2009 Oct;95(1):71-80
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  • [Title] Papillary glioneuronal tumor-evidence of stem cell origin with biphenotypic differentiation.
  • Co-localization of glial and neuronal markers was demonstrable on confocal microscopy with expression of stem cell markers (Nestin and CD133) suggesting possible origin from neuroepithelial stem cell with biphenotypic differentiation.
  • [MeSH-major] Brain Neoplasms / pathology. Carcinoma, Papillary / pathology. Neoplastic Stem Cells / pathology. Neuroglia / pathology. Neurons / pathology
  • [MeSH-minor] AC133 Antigen. Adult. Antigens, CD / metabolism. Glycoproteins / metabolism. Humans. Male. Meningioma. Middle Aged. Nerve Tissue Proteins / metabolism. Peptides / metabolism

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  • (PMID = 19404583.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 Antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Nerve Tissue Proteins; 0 / PROM1 protein, human; 0 / Peptides
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49. Chernov MF, Skvortzova TY, Brodskaya ZL: Reduction of blood flow in the brain stem and cerebellum caused by petroclival tumors. Neurol Med Chir (Tokyo); 2005 Jan;45(1):31-5; discussion 36

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  • [Title] Reduction of blood flow in the brain stem and cerebellum caused by petroclival tumors.
  • Blood flow in the brain stem (BSBF) and cerebellum (CerBF) was investigated by positron emission tomography in 12 patients with petroclival tumors (study group) and 14 healthy volunteers (control group). (15)O-labeled water was used as the radioisotope tracer.
  • Five of 12 patients in the study group exhibited more than 20% reduction of CerBF ipsilateral to the tumor, whereas no such asymmetry was disclosed in any subject in the control group (p < 0.01).
  • Sex, age, and tumor histology had no statistically significant association with the level of BSBF.
  • No statistically significant association between BSBF and the type of postoperative course was found, whereas four of the five patients with more than 20% reduction of CerBF ipsilateral to the tumor had prominently increased cerebellar ataxia after removal of the neoplasm.
  • [MeSH-major] Brain Stem / blood supply. Cerebellum / blood supply. Cerebrovascular Circulation / physiology. Cranial Fossa, Posterior. Skull Base Neoplasms / physiopathology
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 15699618.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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50. Taupin P: Potential of neural stem cells for the treatment of brain tumors. Clin Med Oncol; 2008;2:451-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential of neural stem cells for the treatment of brain tumors.
  • Neural stem cells (NSCs) are self-renewing multipotent cells that generate the main phenotypes of the nervous system, neurons, astrocytes and oligodendrocytes.
  • Neural progenitor and stem cells have been isolated and characterized in vitro, from adult, fetal and post-mortem tissues, providing sources of material for cellular therapy.
  • Neural progenitor and stem cells, isolated and cultured in vitro, can be genetically modified and when transplanted migrate to tumor sites in the brain.
  • These intrinsic properties of neural progenitor and stem cells provide tremendous potential to bolster the translation of NSC research to therapy.
  • It is proposed to combine gene therapy and cellular therapy to treat brain cancers.
  • Hence, neural progenitor and stem cells provide new opportunities for the treatment of brain cancers.

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  • (PMID = 21892316.001).
  • [ISSN] 1177-9314
  • [Journal-full-title] Clinical medicine. Oncology
  • [ISO-abbreviation] Clin Med Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3161643
  • [Keywords] NOTNLM ; cancer / cellular therapy / gene therapy / nervous system
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51. Molcanyi M, Riess P, Haj-Yasein NN, Bentz K, Loehr M, Kuchta J, Zivcak J, Stenzel W, Miletic H, Hescheler J, Neugebauer E, Hampl JA, Ernestus RI, Schafer U: Developmental potential of the murine embryonic stem cells transplanted into the healthy rat brain--novel insights into tumorigenesis. Cell Physiol Biochem; 2009;24(1-2):87-94
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  • [Title] Developmental potential of the murine embryonic stem cells transplanted into the healthy rat brain--novel insights into tumorigenesis.
  • Although engraftment of undifferentiated pluripotent embryonic stem cells (ESCs) into the injured central nervous system (CNS) may lead to targeted cell replacement of lost/damaged cells, sustained proliferative activity combined with uncontrolled differentiation of implanted cells presents a risk of tumor formation.
  • As tumorigenic potential is thought to be associated with pluripotency of embryonic stem cells, pre-differentiation may circumvent this problem.
  • Recently, it has been demonstrated that tumorigenesis occurs despite pre-differentiation if the neural precursor cells are implanted into the brain of a homologous animal (e.g., mouse to mouse).
  • However, xenotransplantation (e.g., mouse to rat) without pre-differentiation, lead to the development of healthy neuronal cells, in absence of tumor formation, suggesting that tumor-suppressive effects of host tissue on engrafted ESCs may play a role in transplant tumorigenesis.
  • We critically investigated tumorigenesis and possible mechanisms of anticipated tumor-suppressive effect under conditions analogous to previously published studies.
  • Xenotransplantation of D-3 murine ESCs into uninjured adult rat brains lacking any preliminary inflammatory potential was found to lead to tumor formation in 5 out of 8 of animals within 2 weeks postimplantation.
  • Tumor-suppressive effects, reflected by Erdo et. al could possibly be ascribed to immunomodulatory activity of macrophages scavenging the tumorigenic fraction of the implanted cells.
  • [MeSH-major] Brain / pathology. Brain Neoplasms / pathology. Embryonic Stem Cells / transplantation

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  • [Copyright] 2009 S. Karger AG, Basel.
  • (PMID = 19590196.001).
  • [ISSN] 1421-9778
  • [Journal-full-title] Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
  • [ISO-abbreviation] Cell. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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52. Caussinus E, Gonzalez C: Induction of tumor growth by altered stem-cell asymmetric division in Drosophila melanogaster. Nat Genet; 2005 Oct;37(10):1125-9
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  • [Title] Induction of tumor growth by altered stem-cell asymmetric division in Drosophila melanogaster.
  • In stem cells, loss of polarity and impairment of asymmetric cell division could alter cell fates and thereby render daughter cells unable to respond to the mechanisms that control proliferation.
  • To test this hypothesis, we generated Drosophila melanogaster larval neuroblasts containing mutations in various genes that control asymmetric cell division and then assayed their proliferative potential after transplantation into adult hosts.
  • We found that larval brain tissue carrying neuroblasts with mutations in raps (also called pins), mira, numb or pros grew to more than 100 times their initial size, invading other tissues and killing the hosts in 2 weeks.
  • Increasing evidence suggests that some tumors may be of stem cell origin.
  • Our results show that loss of function of any of several genes that control the fate of a stem cell's daughters may result in hyperproliferation, triggering a chain of events that subverts cell homeostasis in a general sense and leads to cancer.
  • [MeSH-major] Drosophila melanogaster / cytology. Genomic Instability. Neoplasms / genetics. Stem Cells / cytology


53. An JH, Lee SY, Jeon JY, Cho KG, Kim SU, Lee MA: Identification of gliotropic factors that induce human stem cell migration to malignant tumor. J Proteome Res; 2009 Jun;8(6):2873-81
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  • [Title] Identification of gliotropic factors that induce human stem cell migration to malignant tumor.
  • Neural stem cells are mobile, are attracted to regions of brain damage, and can migrate a considerable distance to reach a glioma site.
  • This research is expected to provide clues to the molecular mechanisms underlying the migration of neural stem cells (F3 cell) to glioma sites.
  • These results reveal that this novel molecular approach to the monitoring of glioma may provide clinically relevant information regarding tumor malignancy, and should also prove appropriate for high-throughput clinical screening applications.
  • [MeSH-major] Cell Movement. Glioma / genetics. Glioma / metabolism. Neurons / cytology. Stem Cells / physiology
  • [MeSH-minor] Adult. Aged. Annexin A2 / genetics. Annexin A2 / metabolism. Blotting, Western. Cell Line. Electrophoresis, Gel, Two-Dimensional. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Proteomics / methods. Reproducibility of Results. Tumor Cells, Cultured

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  • (PMID = 19351187.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANXA2 protein, human; 0 / Annexin A2; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins
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54. Lorenzoni JG, Devriendt D, Massager N, Desmedt F, Simon S, Van Houtte P, Brotchi J, Levivier M: Brain stem metastases treated with radiosurgery: prognostic factors of survival and life expectancy estimation. Surg Neurol; 2009 Feb;71(2):188-95; discussion 195, 195-6
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  • [Title] Brain stem metastases treated with radiosurgery: prognostic factors of survival and life expectancy estimation.
  • BACKGROUND: The objective of this study is to study prognostic factors of survival and 3 stratification systems for life expectancy estimation in patients with brain stem metastases treated with radiosurgery.
  • METHODS: Between December 1999 and November 2006, 25 patients with 27 brain stem metastases were treated with Gamma Knife radiosurgery.
  • RESULTS: The primary tumor location was in the lungs in 12 patients, breast in 8, and other in 5.
  • Tumor control was achieved in all but one followed lesion (95%).
  • Median survival of patients with brain stem metastases was 11.1 months.
  • In multivariate analysis, KPS of 80 or more, control of the primary tumor, absence of radiotherapy, and a marginal dose higher than 18 Gy were associated with better survival.
  • Rather than the brain stem location of an intracranial metastasis, the patient integral clinical status seems to be more important in determining survival.
  • [MeSH-major] Brain Stem Neoplasms / secondary. Brain Stem Neoplasms / surgery. Life Expectancy. Radiosurgery
  • [MeSH-minor] Adult. Aged. Cohort Studies. Female. Humans. Male. Middle Aged. Radiotherapy Dosage. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 18439658.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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55. De Toni A, Zbinden M, Epstein JA, Ruiz i Altaba A, Prochiantz A, Caillé I: Regulation of survival in adult hippocampal and glioblastoma stem cell lineages by the homeodomain-only protein HOP. Neural Dev; 2008 May 28;3:13
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  • [Title] Regulation of survival in adult hippocampal and glioblastoma stem cell lineages by the homeodomain-only protein HOP.
  • After birth, neurogenic activities are relegated to stem cell niches, which include the subgranular layer of the dentate gyrus of the hippocampus.
  • Here, we have analyzed the function of HOP (Homeodomain only protein) in this stem cell niche and in human glioblastomas.
  • RESULTS: We find that HOP is strongly expressed by radial astrocytes of the dentate gyrus in mice, which are stem cells that give rise to hippocampal granular neurons throughout adulthood.
  • Deletion or down-regulation of HOP results in a decrease of apoptosis of these stem cells without changes in proliferation, and in an increase in the number of newly formed granule neurons.
  • CONCLUSION: These data suggest that HOP participates in the regulation of the adult mouse hippocampal stem cell niche by negatively affecting cell survival.
  • In addition, HOP may work as a tumor suppressor in a subset of glioblastomas.
  • HOP function thus appears to be critical in the adult brain in a region of continued plasticity, and its deregulation may contribute to disease.

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  • (PMID = 18507846.001).
  • [ISSN] 1749-8104
  • [Journal-full-title] Neural development
  • [ISO-abbreviation] Neural Dev
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL071546-05A1; United States / NHLBI NIH HHS / HL / R01 HL071546; United States / NHLBI NIH HHS / HL / R01 HL071546-05A1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOP protein, human; 0 / Homeodomain Proteins; 0 / Hop protein, mouse; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2416439
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56. Prabhu K, Daniel RT, Mani S, Chacko AG: Dermoid tumor with diastematobulbia. Surg Neurol; 2009 Dec;72(6):717-21; discussion 721

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dermoid tumor with diastematobulbia.
  • Dermoid tumor with diastematobulbia is very rare.
  • CASE DESCRIPTION: We report a dermoid tumor in an adult female with an unusual location and morphology.
  • The anterior part of the lesion was situated in the prepontine cistern and encircling the anterior half of the brainstem.
  • [MeSH-major] Brain Stem Neoplasms / surgery. Cerebral Ventricle Neoplasms / surgery. Cisterna Magna / surgery. Dermoid Cyst / surgery. Fourth Ventricle / surgery. Medulla Oblongata / surgery. Neoplasms, Multiple Primary / surgery. Pons / surgery
  • [MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging. Neoplasm Invasiveness. Neural Tube Defects / diagnosis. Neural Tube Defects / pathology. Neural Tube Defects / surgery. Neurologic Examination. Postoperative Complications / diagnosis

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  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • (PMID = 19608253.001).
  • [ISSN] 1879-3339
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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57. Xu Q, Yuan X, Xu M, McLafferty F, Hu J, Lee BS, Liu G, Zeng Z, Black KL, Yu JS: Chemokine CXC receptor 4--mediated glioma tumor tracking by bone marrow--derived neural progenitor/stem cells. Mol Cancer Ther; 2009 Sep;8(9):2746-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemokine CXC receptor 4--mediated glioma tumor tracking by bone marrow--derived neural progenitor/stem cells.
  • Malignant gliomas manifest frequent tumor recurrence after surgical resection and/or other treatment because of their nature of invasiveness and dissemination.
  • The recognized brain tumor-tracking property of neural progenitor/stem cells opened the possibility of targeting malignant brain tumors using neural progenitor/stem cells.
  • We and others have previously shown that fetal neural progenitor/stem cells can be used to deliver therapeutic molecules to brain tumors.
  • Our recent work has further shown that gene delivery by bone marrow-derived neural progenitor/stem cells achieves therapeutic effects in a glioma model.
  • In this study, we isolate and characterize bone marrow-derived neural progenitor/stem cells, which also express the chemokine receptor chemokine CXC receptor 4 (CXCR4).
  • Furthermore, beta-galactosidase-labeled bone marrow-derived neural progenitor/stem cells implanted in the contralateral side of the brain were shown to track gliomas as early as day 1 and increased through days 3 and 7.
  • Intracranial glioma tracking by bone marrow-derived neural progenitor/stem cells is significantly inhibited by preincubation of bone marrow-derived neural progenitor/stem cells with a blocking anti-CXCR4 antibody, suggesting a CXCR4-dependent tracking mechanism.
  • Glioma tracking bone marrow-derived neural progenitor/stem cells were found to express progenitor/stem cell markers, as well as CXCR4.
  • Although bromodeoxyuridine incorporation assays and proliferating antigen staining indicated that tumor tracking bone marrow-derived neural progenitor/stem cells were mostly nonproliferating, these cells survive in the local tumor environment with little apoptosis.
  • Elucidating the molecular mechanism of brain tumor tracking by adult source stem cells may provide basis for the development of future targeted therapy for malignant brain tumors.

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  • (PMID = 19723878.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS048959; United States / NINDS NIH HHS / NS / NS048959-01; United States / NINDS NIH HHS / NS / R21 NS048879-02; United States / NINDS NIH HHS / NS / NS048879-02; United States / NINDS NIH HHS / NS / R21 NS048879; United States / NINDS NIH HHS / NS / NS048879; United States / NINDS NIH HHS / NS / R01 NS048959-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cxcr4 protein, rat; 0 / Receptors, CXCR4
  • [Other-IDs] NLM/ NIHMS140357; NLM/ PMC2760002
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58. Carpentino JE, Hartman NW, Grabel LB, Naegele JR: Region-specific differentiation of embryonic stem cell-derived neural progenitor transplants into the adult mouse hippocampus following seizures. J Neurosci Res; 2008 Feb 15;86(3):512-24
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  • [Title] Region-specific differentiation of embryonic stem cell-derived neural progenitor transplants into the adult mouse hippocampus following seizures.
  • Embryonic stem (ES) cells can generate neural progenitors and neurons in vitro and incorporate into the adult central nervous system (CNS) following transplantation, suggesting their therapeutic potential for treating neurological disorders.
  • However, our understanding of the conditions that direct ES-derived neural progenitor (ESNP) migration and differentiation within different regions of the adult CNS is incomplete.
  • To examine the potential for ESNPs to incorporate into the adult hippocampus and differentiate into hippocampal neurons or glia following seizure-induced damage, we compared the fates of ESNPs after they were transplanted into the CA3 region or fimbria 1 week following KA-induced seizures.
  • After 4-8 weeks, ESNPs grafted into the CA3 region had migrated to the dentate gyrus (DG), where a small subset adopted neural stem cell fates and continued to proliferate, based on bromodeoxyuridine uptake.
  • Taken together, these data suggest that seizures induce molecular changes in the CA3 region and DG that promote region-specific neural differentiation and suppress tumor formation.

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17918739.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS042826; United States / NINDS NIH HHS / NS / R01 NS042826-05; United States / NINDS NIH HHS / NS / NS42826
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Convulsants; 0 / Excitatory Amino Acid Agonists; SIV03811UC / Kainic Acid
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59. Widera D, Mikenberg I, Elvers M, Kaltschmidt C, Kaltschmidt B: Tumor necrosis factor alpha triggers proliferation of adult neural stem cells via IKK/NF-kappaB signaling. BMC Neurosci; 2006;7:64
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  • [Title] Tumor necrosis factor alpha triggers proliferation of adult neural stem cells via IKK/NF-kappaB signaling.
  • BACKGROUND: Brain inflammation has been recognized as a complex phenomenon with numerous related aspects.
  • In addition to the very well-described neurodegenerative effect of inflammation, several studies suggest that inflammatory signals exert a potentially positive influence on neural stem cell proliferation, migration and differentiation.
  • Tumor necrosis factor alpha (TNF-alpha) is one of the best-characterized mediators of inflammation.
  • To date, conclusions about the action of TNF on neural stem or progenitor cells (NSCs, NPCs) have been conflicting.
  • RESULTS: Here we describe for the first time the TNF-mediated signal transduction cascade in neural stem cells (NSCs) that results in increased proliferation.
  • Understanding stem cell proliferation is crucial for future regenerative and anti-tumor medicine.
  • [MeSH-major] Cell Proliferation / drug effects. I-kappa B Kinase / metabolism. NF-kappa B / metabolism. Neurons / drug effects. Signal Transduction / drug effects. Stem Cells / drug effects. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16987412.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Tumor Necrosis Factor-alpha; 136601-57-5 / Cyclin D1; EC 2.7.11.10 / I-kappa B Kinase; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ PMC1586209
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60. Quiñones-Hinojosa A, Sanai N, Soriano-Navarro M, Gonzalez-Perez O, Mirzadeh Z, Gil-Perotin S, Romero-Rodriguez R, Berger MS, Garcia-Verdugo JM, Alvarez-Buylla A: Cellular composition and cytoarchitecture of the adult human subventricular zone: a niche of neural stem cells. J Comp Neurol; 2006 Jan 20;494(3):415-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cellular composition and cytoarchitecture of the adult human subventricular zone: a niche of neural stem cells.
  • The lateral wall of the lateral ventricle in the human brain contains neural stem cells throughout adult life.
  • With varying thickness and cell densities, four layers were observed throughout the lateral ventricular wall: a monolayer of ependymal cells (Layer I), a hypocellular gap (Layer II), a ribbon of cells (Layer III) composed of astrocytes, and a transitional zone (Layer IV) into the brain parenchyma.
  • Unlike rodents and nonhuman primates, adult human glial fibrillary acidic protein (GFAP)+ subventricular zone (SVZ) astrocytes are separated from the ependyma by the hypocellular gap.
  • However, compared to rodents, the adult human SVZ appears to be devoid of chain migration or large numbers of newly formed young neurons.
  • This work provides a basic description of the organization of the adult human SVZ.
  • [MeSH-major] Astrocytes / ultrastructure. Lateral Ventricles / cytology. Neurons / ultrastructure. Prosencephalon / cytology. Stem Cells / ultrastructure
  • [MeSH-minor] Adolescent. Adult. Cell Differentiation. Child. Ependyma / cytology. Ependyma / ultrastructure. Humans. Immunohistochemistry. Middle Aged

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16320258.001).
  • [ISSN] 0021-9967
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 1F32NS047011-01; United States / NICHD NIH HHS / HD / R01 HD032116
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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61. Talos F, Abraham A, Vaseva AV, Holembowski L, Tsirka SE, Scheel A, Bode D, Dobbelstein M, Brück W, Moll UM: p73 is an essential regulator of neural stem cell maintenance in embryonal and adult CNS neurogenesis. Cell Death Differ; 2010 Dec;17(12):1816-29
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  • [Title] p73 is an essential regulator of neural stem cell maintenance in embryonal and adult CNS neurogenesis.
  • The p53 family member p73 is essential for brain development, but its precise role and scope remain unclear.
  • Global p73 deficiency determines an overt and highly penetrant brain phenotype marked by cortical hypoplasia with ensuing hydrocephalus and hippocampal dysgenesis.
  • In this study, we define a novel essential role of p73 in the regulation of the neural stem cell compartment.
  • In both embryonic and adult neurogenesis, p73 has a critical role in maintaining an adequate neurogenic pool by promoting self-renewal and proliferation and inhibiting premature senescence of neural stem and early progenitor cells.
  • Thus, products of the p73 gene locus are essential maintenance factors in the central nervous system, whose broad action stretches across the entire differentiation arch from stem cells to mature postmitotic neurons.

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  • (PMID = 21076477.001).
  • [ISSN] 1476-5403
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS042168; United States / NCI NIH HHS / CA / CA093853-10; United States / NCI NIH HHS / CA / CA93853; United States / NIGMS NIH HHS / GM / T32 GM007518; United States / NCI NIH HHS / CA / R01 CA093853; United States / NCI NIH HHS / CA / R01 CA093853-10; United States / NINDS NIH HHS / NS / NS42168
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Receptors, Notch; 0 / SOXB1 Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
  • [Other-IDs] NLM/ NIHMS338733; NLM/ PMC3260880
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62. Fomchenko EI, Holland EC: Platelet-derived growth factor-mediated gliomagenesis and brain tumor recruitment. Neurosurg Clin N Am; 2007 Jan;18(1):39-58, viii
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  • [Title] Platelet-derived growth factor-mediated gliomagenesis and brain tumor recruitment.
  • Many researchers view brain tumors as clonal entities derived from the cancer stem cell; however, recent documentation of the importance of the tumor microenvironment for glioma initiation and progression as well as the ability of neural stem or progenitor cells to migrate toward the sites of injury or tumor formation reveals additional complexities in brain tumorigenesis.
  • Paracrine effects of PDGF in animal models of gliomagenesis, continued adult neurogenesis capable of increasing in response to brain injury, and the growth factor-rich environment of brain tumors suggest that recruitment may play a role in gliomagenesis.
  • In this view, glioma formation involves recruitment of cells from the adjacent brain and possibly other sites.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / physiopathology. Glioma / pathology. Glioma / physiopathology. Platelet-Derived Growth Factor / metabolism. Stem Cells / pathology

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  • (PMID = 17244553.001).
  • [ISSN] 1042-3680
  • [Journal-full-title] Neurosurgery clinics of North America
  • [ISO-abbreviation] Neurosurg. Clin. N. Am.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA099489; United States / NCI NIH HHS / CA / R01 CA100688; United States / NCI NIH HHS / CA / U01 CA894314-1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor
  • [Number-of-references] 179
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63. Moviglia GA, Carrizo AG, Varela G, Gaeta CA, Paes de Lima A, Farina P, Molina H: Preliminary report on tumor stem cell/B cell hybridoma vaccine for recurrent glioblastoma multiforme. Hematol Oncol Stem Cell Ther; 2008 Jan-Mar;1(1):3-13
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  • [Title] Preliminary report on tumor stem cell/B cell hybridoma vaccine for recurrent glioblastoma multiforme.
  • BACKGROUND: Glioblastoma multiforme (GBM), the most aggressive glioma, presents with a rapid evolution and relapse within the first year, which is attributed to the persistence of tumor stem cells (TSC) and the escape of immune surveillance.
  • Tumor B-cell hybridoma (TBH) vaccines have been shown to function as antigen-presenting cells.
  • RESULTS: Treatment with MLC had strong and rapid therapeutic effects, but was limited in duration and induced various degrees of brain inflammation.
  • Treatment with MLC+TBH acted synergistically, provoking a rapid, strong and lasting therapeutic response but also generating different degrees of brain inflammation.
  • A lasting therapeutic effect without generating high degrees of brain inflammation occurred in patients treated with TBH vaccine alone.
  • CONCLUSION: TSC vaccine consisting of TBH alone seems to have potent adjuvant reactions overcoming both persistence of tumor stem cells and immune escape of GBM without provoking an encephalitic reaction.
  • [MeSH-major] B-Lymphocytes / transplantation. Brain Neoplasms / therapy. Cancer Vaccines / therapeutic use. Glioblastoma / therapy. Hybridomas / transplantation. Neoplastic Stem Cells / transplantation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Leukocytes, Mononuclear / immunology. Leukocytes, Mononuclear / transplantation. Lymphocyte Culture Test, Mixed. Male. Middle Aged. Neoplasm Recurrence, Local / therapy

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  • (PMID = 20063522.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Cancer Vaccines
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64. Xu Q, Yuan X, Liu G, Black KL, Yu JS: Hedgehog signaling regulates brain tumor-initiating cell proliferation and portends shorter survival for patients with PTEN-coexpressing glioblastomas. Stem Cells; 2008 Dec;26(12):3018-26
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  • [Title] Hedgehog signaling regulates brain tumor-initiating cell proliferation and portends shorter survival for patients with PTEN-coexpressing glioblastomas.
  • The identification of brain tumor stem-like cells (BTSCs) has implicated a role of biological self-renewal mechanisms in clinical brain tumor initiation and propagation.
  • The molecular mechanisms underlying the tumor-forming capacity of BTSCs, however, remain unknown.
  • BTSC proliferation could be abrogated in a pathway-dependent fashion in vitro and in an intracranial tumor model in athymic mice.
  • Both SHH-dependent and -independent brain tumor growth required phosphoinositide 3-kinase-mammalian target of rapamycin signaling.
  • [MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. Hedgehog Proteins / metabolism. PTEN Phosphohydrolase / metabolism. Signal Transduction
  • [MeSH-minor] Adult. Aged. Animals. Cell Proliferation. Humans. Mice. Mice, Nude. Middle Aged. Neoplastic Stem Cells. Phosphatidylinositol 3-Kinases / metabolism

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  • (PMID = 18787206.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS048879; United States / NINDS NIH HHS / NS / NS048959
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hedgehog Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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65. Pfenninger CV, Roschupkina T, Hertwig F, Kottwitz D, Englund E, Bengzon J, Jacobsen SE, Nuber UA: CD133 is not present on neurogenic astrocytes in the adult subventricular zone, but on embryonic neural stem cells, ependymal cells, and glioblastoma cells. Cancer Res; 2007 Jun 15;67(12):5727-36
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  • [Title] CD133 is not present on neurogenic astrocytes in the adult subventricular zone, but on embryonic neural stem cells, ependymal cells, and glioblastoma cells.
  • Human brain tumor stem cells have been enriched using antibodies against the surface protein CD133.
  • An antibody recognizing CD133 also served to isolate normal neural stem cells from fetal human brain, suggesting a possible lineage relationship between normal neural and brain tumor stem cells.
  • Whether CD133-positive brain tumor stem cells can be derived from CD133-positive neural stem or progenitor cells still requires direct experimental evidence, and an important step toward such investigations is the identification and characterization of normal CD133-presenting cells in neurogenic regions of the embryonic and adult brain.
  • Here, we present evidence that CD133 is a marker for embryonic neural stem cells, an intermediate radial glial/ependymal cell type in the early postnatal stage, and for ependymal cells in the adult brain, but not for neurogenic astrocytes in the adult subventricular zone.
  • Our findings suggest two principal possibilities for the origin of brain tumor stem cells: a derivation from CD133-expressing cells, which are normally not present in the adult brain (embryonic neural stem cells and an early postnatal intermediate radial glial/ependymal cell type), or from CD133-positive ependymal cells in the adult brain, which are, however, generally regarded as postmitotic.
  • Alternatively, brain tumor stem cells could be derived from proliferative but CD133-negative neurogenic astrocytes in the adult brain.
  • In the latter case, brain tumor development would involve the production of CD133.
  • [MeSH-major] Antigens, CD / metabolism. Brain Neoplasms / metabolism. Embryonic Stem Cells / metabolism. Ependyma / metabolism. Glioblastoma / metabolism. Glycoproteins / metabolism. Peptides / metabolism. Prosencephalon / metabolism
  • [MeSH-minor] Adult. Animals. Astrocytes / metabolism. Blotting, Western. Epithelial Cells / metabolism. Flow Cytometry. Fluorescent Antibody Technique. Humans. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplastic Stem Cells / metabolism. Neuroglia / metabolism

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  • (PMID = 17575139.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501838
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides
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66. Park HJ, Kim JK, Jeon HM, Oh SY, Kim SH, Nam DH, Kim H: The neural stem cell fate determinant TLX promotes tumorigenesis and genesis of cells resembling glioma stem cells. Mol Cells; 2010 Nov;30(5):403-8
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  • [Title] The neural stem cell fate determinant TLX promotes tumorigenesis and genesis of cells resembling glioma stem cells.
  • A growing body of evidence indicates that deregulation of stem cell fate determinants is a hallmark of many types of malignancies.
  • The neural stem cell fate determinant TLX plays a pivotal role in neurogenesis in the adult brain by maintaining neural stem cells.
  • Here, we report a tumorigenic role of TLX in brain tumor initiation and progression.
  • Increased TLX expression was observed in a number of glioma cells and glioma stem cells, and correlated with poor survival of patients with gliomas.
  • Ectopic expression of TLX in the U87MG glioma cell line and Ink4a/Arf-deficient mouse astrocytes (Ink4a/Arf(-/-) astrocytes) induced cell proliferation with a concomitant increase in cyclin D expression, and accelerated foci formation in soft agar and tumor formation in in vivo transplantation assays.
  • Furthermore, overexpression of TLX in Ink4a/Arf(-/-) astrocytes inhibited cell migration and invasion and promoted neurosphere formation and Nestin expression, which are hallmark characteristics of glioma stem cells, under stem cell culture conditions.
  • Our results indicate that TLX is involved in glioma stem cell genesis and represents a potential therapeutic target for this type of malignancy.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Transformation, Neoplastic / pathology. Glioma / pathology. Neoplastic Stem Cells / pathology. Neural Stem Cells / pathology. Receptors, Cytoplasmic and Nuclear / physiology
  • [MeSH-minor] Adult. Animals. Astrocytes / metabolism. Astrocytes / pathology. Astrocytoma / genetics. Cell Growth Processes / physiology. Cell Line, Tumor. Cell Movement / physiology. Central Nervous System Neoplasms. Cyclin D / genetics. Humans. Intermediate Filament Proteins / genetics. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Metastasis. Nerve Tissue Proteins / genetics. Nestin. Neurogenesis. Prognosis. Up-Regulation

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  • [ErratumIn] Mol Cells. 2011 Feb ;31(2):199. Park, Myung-Jin [removed]; Soeda, Akio [removed]
  • (PMID = 20814749.001).
  • [ISSN] 0219-1032
  • [Journal-full-title] Molecules and cells
  • [ISO-abbreviation] Mol. Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin D; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / NR2E1 protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Receptors, Cytoplasmic and Nuclear
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67. Rhee W, Ray S, Yokoo H, Hoane ME, Lee CC, Mikheev AM, Horner PJ, Rostomily RC: Quantitative analysis of mitotic Olig2 cells in adult human brain and gliomas: implications for glioma histogenesis and biology. Glia; 2009 Apr 1;57(5):510-23
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  • [Title] Quantitative analysis of mitotic Olig2 cells in adult human brain and gliomas: implications for glioma histogenesis and biology.
  • The capacity of adult human glial progenitor cells (AGPs), to proliferate and undergo multipotent differentiation, positions them as ideal candidate cells of origin for human gliomas.
  • To investigate this potential role we identified AGPs as mitotically active Olig2 cells in nonneoplastic adult human brain and gliomas.
  • Extrapolating from a mean Olig2/Mib-1 labeling index (LI) of 52% and total cell number of 100 billion, we estimated the overall prevalence of mitotic Olig2 AGPs in nonneoplastic human brain parenchyma at 10 million.
  • The novel framework provided by this quantitative and comparative analysis supports future studies to examine the histogenetic role of Olig2 AGPs in adult gliomas, their potential contribution to the tumor stroma and the molecular role of Olig2 in glioma pathogenesis.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18837053.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / T32 NS007144; United States / NINDS NIH HHS / NS / T32 NS007144-25; United States / NINDS NIH HHS / NS / T32 NS007144-28; United States / NINDS NIH HHS / NS / T32 NS 0007144
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / MIB-1 antibody; 0 / Nerve Growth Factors; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human
  • [Other-IDs] NLM/ NIHMS77469; NLM/ PMC4415884
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68. Mimeault M, Batra SK: Recent insights into the molecular mechanisms involved in aging and the malignant transformation of adult stem/progenitor cells and their therapeutic implications. Ageing Res Rev; 2009 Apr;8(2):94-112
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  • [Title] Recent insights into the molecular mechanisms involved in aging and the malignant transformation of adult stem/progenitor cells and their therapeutic implications.
  • Recent advancements in tissue-resident adult stem/progenitor cell research have revealed that enhanced telomere attrition, oxidative stress, ultraviolet radiation exposure and oncogenic events leading to severe DNA damages and genomic instability may occur in these immature and regenerative cells during chronological aging.
  • Particularly, the alterations in key signaling components controlling their self-renewal capacity and an up-regulation of tumor suppressor gene products such as p16(INK4A), p19(ARF), ataxia-telangiectasia mutated (ATM) kinase, p53 and/or the forkhead box O (FOXOs) family of transcription factors may result in their dysfunctions, growth arrest and senescence or apoptotic death during the aging process.
  • These molecular events may culminate in a progressive decline in the regenerative functions and the number of tissue-resident adult stem/progenitor cells, and age-related disease development.
  • Conversely, the telomerase re-activation and accumulation of numerous genetic and/or epigenetic alterations in adult stem/progenitor cells with advancing age may result in their immortalization and malignant transformation into highly leukemic or tumorigenic cancer-initiating cells and cancer initiation.
  • Therefore, the cell-replacement and gene therapies and molecular targeting of aged and dysfunctional adult stem/progenitor cells including their malignant counterpart, cancer-initiating cells, hold great promise for treating and even curing diverse devastating human diseases.

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  • (PMID = 19114129.001).
  • [ISSN] 1872-9649
  • [Journal-full-title] Ageing research reviews
  • [ISO-abbreviation] Ageing Res. Rev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA111294; United States / NCI NIH HHS / CA / CA133774; United States / NCI NIH HHS / CA / R01 CA078590; United States / NCI NIH HHS / CA / R01 CA131944; United States / NCI NIH HHS / CA / CA78590; United States / NCI NIH HHS / CA / R01 CA133774; United States / NCI NIH HHS / CA / CA131944; United States / NCI NIH HHS / CA / CA111294
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] England
  • [Number-of-references] 212
  • [Other-IDs] NLM/ NIHMS526851; NLM/ PMC3828651
  •  go-up   go-down


69. Casalbore P, Budoni M, Ricci-Vitiani L, Cenciarelli C, Petrucci G, Milazzo L, Montano N, Tabolacci E, Maira G, Larocca LM, Pallini R: Tumorigenic potential of olfactory bulb-derived human adult neural stem cells associates with activation of TERT and NOTCH1. PLoS One; 2009;4(2):e4434
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumorigenic potential of olfactory bulb-derived human adult neural stem cells associates with activation of TERT and NOTCH1.
  • BACKGROUND: Multipotent neural stem cells (NSCs) have been isolated from neurogenic regions of the adult brain.
  • METHODOLOGY/PRINCIPAL FINDINGS: Using serum-free medium supplemented with epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF), we established clonally derived NS/progenitor cell (NS/PC) cultures from the olfactory bulb (OB) of five adult patients.
  • CONCLUSIONS/SIGNIFICANCE: Using culturing techniques described in current literature, NS/PCs arise from the OB of adult patients which in vivo either integrate in the CNS parenchyma showing neuron-like features or initiate tumor formation.
  • [MeSH-major] Adult Stem Cells / pathology. Cell Transformation, Neoplastic / pathology. Neurons / pathology. Olfactory Bulb / enzymology. Olfactory Bulb / pathology. Receptors, Notch / metabolism. Telomerase / metabolism
  • [MeSH-minor] Adult. Animals. Enzyme Activation / drug effects. Humans. Meningioma / pathology. Mice. Mitogens / pharmacology. Rats. Serum. Stem Cell Transplantation

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  • (PMID = 19209236.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mitogens; 0 / Receptors, Notch; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2637538
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70. Ogden AT, Waziri AE, Lochhead RA, Fusco D, Lopez K, Ellis JA, Kang J, Assanah M, McKhann GM, Sisti MB, McCormick PC, Canoll P, Bruce JN: Identification of A2B5+CD133- tumor-initiating cells in adult human gliomas. Neurosurgery; 2008 Feb;62(2):505-14; discussion 514-5
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  • [Title] Identification of A2B5+CD133- tumor-initiating cells in adult human gliomas.
  • OBJECTIVE: Several studies have shown that human gliomas contain a small population of cells with stem cell-like features.
  • It has been proposed that these "cancer stem cells" may be uniquely responsible for glioma formation and recurrence.
  • METHODS: To investigate the contributions of stem-like and progenitor-like cells in human gliomas, we used flow cytometry to characterize the expression of a cancer stem cell marker (CD133) and a glial progenitor marker (A2B5) in 25 tumors.
  • RESULTS: We found that the capacity for these different populations to form tumors varied depending on the human tumor specimen from which they were isolated.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Gangliosides / metabolism. Glioma / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adult. Animals. Antigens, CD / metabolism. Flow Cytometry. Glycoproteins / metabolism. Humans. Peptides / metabolism. Rats. Rats, Nude


71. Hara A, Niwa M, Kumada M, Aoki H, Kunisada T, Oyama T, Yamamoto T, Kozawa O, Mori H: Intraocular injection of folate antagonist methotrexate induces neuronal differentiation of embryonic stem cells transplanted in the adult mouse retina. Brain Res; 2006 Apr 26;1085(1):33-42
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  • [Title] Intraocular injection of folate antagonist methotrexate induces neuronal differentiation of embryonic stem cells transplanted in the adult mouse retina.
  • Transplanted embryonic stem (ES) cells can be integrated into the retinas of adult mice as well-differentiated neuronal cells.
  • Mouse ES cells carrying the sequence for the green fluorescent protein (GFP) gene were transplanted into adult mouse retinas by intravitreal injections 20 h after intravitreal N-methyl-d-aspartate (NMDA) administration.
  • [MeSH-major] Cell Differentiation / drug effects. Folic Acid Antagonists / administration & dosage. Methotrexate / administration & dosage. Neurons / drug effects. Retina. Stem Cell Transplantation / methods

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  • (PMID = 16584710.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin; 0 / Excitatory Amino Acid Agonists; 0 / Folic Acid Antagonists; 0 / Nerve Tissue Proteins; 0 / alpha-Fetoproteins; 147336-22-9 / Green Fluorescent Proteins; 6384-92-5 / N-Methylaspartate; EC 2.7.11.13 / Protein Kinase C; EC 3.1.3.1 / Alkaline Phosphatase; YL5FZ2Y5U1 / Methotrexate
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72. Kumabe T, Fujimura M, Jokura H, Tominaga T: Surgical treatment for choroid plexus tumors in the fourth ventricle: brain stem infiltration hinders total extirpation. Neurosurg Rev; 2008 Apr;31(2):165-72; discussion 172
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  • [Title] Surgical treatment for choroid plexus tumors in the fourth ventricle: brain stem infiltration hinders total extirpation.
  • Preoperative T2-weighted magnetic resonance imaging showed a diffuse high-intensity lesion in the brain stem in four patients.
  • No patient suffered tumor progression within the follow-up of 24-129 months (mean 64 months).
  • Adjuvant therapy for choroid plexus tumors with brain stem infiltration must be established.
  • [MeSH-major] Brain Stem / pathology. Carcinoma / surgery. Cerebral Ventricle Neoplasms / surgery. Choroid Plexus Neoplasms / surgery. Fourth Ventricle / surgery. Neurosurgical Procedures. Papilloma, Choroid Plexus / surgery
  • [MeSH-minor] Adult. Cerebral Hemorrhage / therapy. Child, Preschool. Female. Humans. Intraoperative Complications / therapy. Laminectomy. Magnetic Resonance Imaging. Male. Pregnancy

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  • [Cites] J Neurooncol. 2002 Apr;57(2):123-6 [12125972.001]
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  • (PMID = 17912563.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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73. Khanna A, Reddy SS, Jan M, Totey S, Rao TV, Rao SA, Naik AL, Totey S, Venkataramana NK: Establishment of a brain tumor tissue repository in India: maintaining quality standards. J Stem Cells; 2010;5(2):89-101
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  • [Title] Establishment of a brain tumor tissue repository in India: maintaining quality standards.
  • Tumor tissue repositories (TTRs) play a pivotal role in both basic and translational research by acting as a conduit to facilitate innovative research, thereby providing solutions to treat the incurable disease--'Cancer'.
  • One of the fundamental requirements to achieve this goal would be the acquisition of high quality tumor tissue specimens that are stored in such a manner that its integrity is preserved.
  • To address this, we have initiated an effort to build a tumor tissue repository of brain tumor tissues in the Southern part of the Indian sub-continent.
  • One of the cardinal features of brain tumors is the heterogeneity, both phenotypically and genotypically.
  • Moreover, significant gaps exist in current understanding of the molecular pathways involved in the genesis, progression, and biological and clinical behavior of brain tumors.
  • To our knowledge, such a structured initiative to store brain tumor samples is the first of its kind in the India.
  • [MeSH-major] Biomedical Research / organization & administration. Brain Neoplasms / pathology. Quality Control. Tissue Banks / organization & administration. Tissue Banks / standards
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Child. Cryopreservation. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Specimen Handling. Tissue Donors. Young Adult

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  • (PMID = 22049619.001).
  • [ISSN] 1556-8539
  • [Journal-full-title] Journal of stem cells
  • [ISO-abbreviation] J Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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74. Mangiola A, Lama G, Giannitelli C, De Bonis P, Anile C, Lauriola L, La Torre G, Sabatino G, Maira G, Jhanwar-Uniyal M, Sica G: Stem cell marker nestin and c-Jun NH2-terminal kinases in tumor and peritumor areas of glioblastoma multiforme: possible prognostic implications. Clin Cancer Res; 2007 Dec 1;13(23):6970-7
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  • [Title] Stem cell marker nestin and c-Jun NH2-terminal kinases in tumor and peritumor areas of glioblastoma multiforme: possible prognostic implications.
  • PURPOSE: It has been hypothesized that brain tumors are derived from stem cell or transiently dividing precursor transformation.
  • This study analyzes stem cell marker nestin and JNK expression in glioblastoma multiforme (GBM) and peritumor tissue and assesses their possible prognostic implications.
  • Samples were derived from tumors (first area), from tissues at a distance <1 cm (second area), and between 1 and 3.5 cm (third area) from the macroscopic tumor border.
  • RESULTS: Nestin cytoplasmic immunoreactivity was observed in the majority of cells in tumor but infrequently in peritumor areas. tJNK, observed in the nucleus and cytoplasm, was widely expressed in the three areas; pJNK, mostly located in the nuclei, was found in a variable percentage of cells in the tumor and peritumor tissue.
  • [MeSH-minor] Adult. Aged. Enzyme Activation. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Nestin. Prognosis. Stem Cells / metabolism. Stem Cells / pathology

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  • [ErratumIn] Clin Cancer Res. 2008 Aug 1;14(15):4995-6
  • (PMID = 18056172.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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75. Malakootian M, Mowla SJ, Saberi H, Asadi MH, Atlasi Y, Shafaroudi AM: Differential expression of nucleostemin, a stem cell marker, and its variants in different types of brain tumors. Mol Carcinog; 2010 Sep;49(9):818-25
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  • [Title] Differential expression of nucleostemin, a stem cell marker, and its variants in different types of brain tumors.
  • Nucleostemin (NS) is implicated in the control of stem and cancer cell proliferation.
  • In the present study, we have examined the expression of NS and its spliced variants in various brain tumors.
  • Total RNA was extracted from 59 brain tumor samples, and the expression of different NS spliced variants was measured by semi-quantitative RT-PCR.
  • The subcellular distribution of NS protein in brain tumors was further examined by immunohistochemistry.
  • Furthermore, to decipher the potential involvement of NS in brain tumorogenesis, its expression was knocked-down by means of RNA interference (RNAi) in two malignant glioma (U-87MG and A172), one astrocytoma (1321N1) and one medulloblastoma (DAOY) cell lines.
  • Our data revealed that NS and its variants are widely expressed in different types of brain tumors.
  • Among the NS spliced variants, variant "1" and variant "3" were detected in the majority of tumor samples, whereas variant "2" was only detectable in few samples.
  • As expected, a nucleolar/nucleoplasmic localization of NS protein was observed in the examined tumor samples.
  • All in all, our data suggest a potential role for NS in tumorogenesis of brain cancers.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Glioma / metabolism
  • [MeSH-minor] Adult. Brain / metabolism. Cell Cycle / genetics. Cell Line. Cell Proliferation. Female. Humans. Immunohistochemistry. Male. Medulloblastoma / genetics. Medulloblastoma / metabolism. Medulloblastoma / pathology. Middle Aged. Proteins / genetics. Proteins / metabolism. RNA Interference. RNA Splicing. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / metabolism. Stem Cells / pathology

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20572164.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins; 0 / RNA, Small Interfering
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76. Stecca B, Ruiz i Altaba A: Brain as a paradigm of organ growth: Hedgehog-Gli signaling in neural stem cells and brain tumors. J Neurobiol; 2005 Sep 15;64(4):476-90
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  • [Title] Brain as a paradigm of organ growth: Hedgehog-Gli signaling in neural stem cells and brain tumors.
  • In particular, it controls neural cell precursor proliferation in dorsal brain structures and regulates the number of neural stem cells in distinct embryonic, perinatal, and adult niches, such as the developing neocortex, the subventricular zone of the lateral ventricle of the forebrain, and the hippocampus.
  • We have proposed that Hh-Gli signaling regulates dorsal brain growth during ontogeny and that its differential regulation underlays evolutionary change in the morphology (size and shape) of dorsal brain structures.
  • It is also critically involved in sporadic brain tumorigenesis--as well as several other human cancer--suggesting that tumors derive from stem cells or progenitors maintaining an inappropriate active Hh-Gli pathway.
  • Importantly, we and others have demonstrated that human sporadic tumors from the brain and other organs require sustained HH-GLI signaling for sustained growth and survival.
  • Modulating HH-GLI signaling thus represents a novel rational avenue to treat, on one hand, brain degeneration and injury by inducing controlled HH-GLI-mediated regeneration and growth, and on the other hand, to combat cancer by blocking its abnormal activity in tumor cells.
  • [MeSH-major] Brain Neoplasms / physiopathology. Neurons / physiology. Oncogene Proteins / physiology. Stem Cells / physiology. Trans-Activators / physiology. Transcription Factors / physiology

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  • (PMID = 16041742.001).
  • [ISSN] 0022-3034
  • [Journal-full-title] Journal of neurobiology
  • [ISO-abbreviation] J. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gli protein; 0 / Hedgehog Proteins; 0 / Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors
  • [Number-of-references] 150
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77. Soltysova A, Altanerova V, Altaner C: Cancer stem cells. Neoplasma; 2005;52(6):435-40
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  • [Title] Cancer stem cells.
  • There is an increasing evidence supporting the cancer stem cell hypothesis.
  • Normal stem cells in the adult organism are responsible for tissue renewal and repair of aged or damaged tissue.
  • A substantial characteristic of stem cells is their ability for self-renewal without loss of proliferation capacity with each cell division.
  • The stem cells are immortal, and rather resistant to action of drugs.
  • Stem cells divide asymmetrically producing two daughter cells -- one is a new stem cell and the second is progenitor cell, which has the ability for differentiation and proliferation, but not the capability for self-renewal.
  • Cancer stem cells are in many aspects similar to the stem cells.
  • It has been proven that tumor cells are heterogeneous comprising rare tumor initiating cells and abundant non-tumor initiating cells.
  • Tumor initiating cells -- cancer stem cells have the ability of self-renewal and proliferation, are resistant to drugs, and express typical markers of stem cells.
  • It is not clear whether cancer stem cells originate from normal stem cells in consequence of genetic and epigenetic changes and/or by redifferentiation from somatic tumor cells to the stem-like cells.
  • Probably both mechanisms are involved in the origin of cancer stem cells.
  • Dysregulation of stem cell self-renewal is a likely requirement for the development of cancer.
  • Isolation and identification of cancer stem cells in human tumors and in tumor cell lines has been successful.
  • To date, the existence of cancer stem cells has been proven in acute and chronic myeloid leukemia, in breast cancer, in brain tumors, in lung cancer and gastrointestinal tumors.
  • Cancer stem cell model is also consistent with some clinical observations.
  • Although standard chemotherapy kills most cells in a tumor, cancer stem cells remain viable.
  • Despite the small number of such cells, they might be the cause of tumor recurrence, sometimes many years after the "successful" treatment of primary tumor.
  • Growth of metastases in distinct areas of body and their cellular heterogeneity might be consequence of cancer stem cell differentiation and/or dedifferentiation and asymmetric division of cancer stem cells.
  • Further characterization of cancer stem cells is needed in order to find ways to destroy them, which might contribute significantly to the therapeutic management of malignant tumors.
  • [MeSH-major] Neoplastic Stem Cells

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  • (PMID = 16284686.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Slovakia
  • [Number-of-references] 43
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78. Hsu YC, Lee DC, Chen SL, Liao WC, Lin JW, Chiu WT, Chiu IM: Brain-specific 1B promoter of FGF1 gene facilitates the isolation of neural stem/progenitor cells with self-renewal and multipotent capacities. Dev Dyn; 2009 Feb;238(2):302-14
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  • [Title] Brain-specific 1B promoter of FGF1 gene facilitates the isolation of neural stem/progenitor cells with self-renewal and multipotent capacities.
  • Fibroblast growth factor 1 (FGF1) has been shown to maintain proliferation and self-renewal capacities of neural stem/progenitor cells (NSPCs) in vitro.
  • We have previously identified FGF1B as the major transcript of FGF1 gene expressed exclusively in brain areas that are known to be abundant for NSPCs in vivo.
  • The F1B-GFP reporter could facilitate the isolation of NSPCs with self-renewal and multipotent capacities from human glioblastoma tissues, developing or adult mouse brains by fluorescence-activated cell sorting.
  • [MeSH-major] Brain / cytology. Fibroblast Growth Factor 1 / metabolism. Multipotent Stem Cells / cytology. Neurons / cytology. Stem Cells / cytology
  • [MeSH-minor] Animals. Base Sequence. Cell Differentiation. Cell Line, Tumor. Flow Cytometry. Gene Expression Regulation. Genes, Reporter. Glioblastoma / pathology. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Mice. Molecular Sequence Data. Promoter Regions, Genetic

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  • (PMID = 18855895.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 104781-85-3 / Fibroblast Growth Factor 1; 147336-22-9 / Green Fluorescent Proteins
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79. Ricci-Vitiani L, Pallini R, Larocca LM, Lombardi DG, Signore M, Pierconti F, Petrucci G, Montano N, Maira G, De Maria R: Mesenchymal differentiation of glioblastoma stem cells. Cell Death Differ; 2008 Sep;15(9):1491-8
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  • [Title] Mesenchymal differentiation of glioblastoma stem cells.
  • Glioblastoma multiforme is a severe form of cancer most likely arising from the transformation of stem or progenitor cells resident in the brain.
  • Although the tumorigenic population in glioblastoma is defined as composed by cancer stem cells (CSCs), the cellular target of the transformation hit remains to be identified.
  • Glioma stem cells (SCs) are thought to have a differentiation potential restricted to the neural lineage.
  • Subcutaneous injection of CSCs or single CSC clones from two of seven patients produced tumor xenografts containing osteo-chondrogenic areas in the context of glioblastoma-like tumor lesions.
  • Interestingly, mesenchymal differentiation of the tumor xenografts was associated with reduction of both growth rate and mitotic index.
  • These findings suggest that in a subclass of glioblastomas the tumorigenic hit occurs on a multipotent stem cell, which may reveal its plasticity under specific environmental stimuli.
  • The discovery of such biological properties might provide considerable information to the development of new therapeutic strategies aimed at forcing glioblastoma stem cell differentiation.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Mesoderm / cytology. Neoplastic Stem Cells / cytology
  • [MeSH-minor] Adult. Aged. Animals. Cell Differentiation. Clone Cells. Female. Humans. Male. Mice. Mice, SCID. Middle Aged. Neurons / cytology. Xenograft Model Antitumor Assays

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  • (PMID = 18497759.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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80. Medrano S, Burns-Cusato M, Atienza MB, Rahimi D, Scrable H: Regenerative capacity of neural precursors in the adult mammalian brain is under the control of p53. Neurobiol Aging; 2009 Mar;30(3):483-97
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  • [Title] Regenerative capacity of neural precursors in the adult mammalian brain is under the control of p53.
  • The question of whether or not stem cell loss drives aging in the brain has not been fully resolved.
  • Here, we used mice over-expressing the short isoform of p53 (DeltaNp53 or p44) as a model of aging to gain insight into the cellular mechanisms underlying age-related functional deficits in the brain.
  • A 2-3-fold reduction in the number of slowly dividing stem cells was evident in the subventricular zone of 9-12-month-old p44Tg mice, but not in younger p44Tg mice or in normal mice.
  • This phenotype is driven by constitutive activation of p53 and constitutive expression of p21(Cip1/waf1) in neural stem cells.
  • Our results demonstrate that p53 plays a crucial role in the maintenance of the regenerative capacity of the brain by regulating the proliferation of stem and progenitor cells.

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  • (PMID = 17850928.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / RR11102; United States / NIA NIH HHS / AG / R01 AG026094; United States / NIA NIH HHS / AG / AG20915; United States / NCRR NIH HHS / RR / R24 RR011102; United States / NIA NIH HHS / AG / AG026094-03; United States / NIA NIH HHS / AG / R01 AG026094-03; United States / NIA NIH HHS / AG / R01 AG020915
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS95177; NLM/ PMC2662499
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81. Tunici P, Yu JS: Pituitary adenoma stem cells. Methods Mol Biol; 2009;568:195-201
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary adenoma stem cells.
  • The identification of a subpopulation of brain tumor cells with potent tumorigenic capacity strengthens the cancer stem cell hypothesis of the origin of the tumors that has recently attracted the attention of many researchers.
  • Reports have been published on the identification of tumor cells with stem cells characteristics in different types of tumors (acute myelogenic leukemia, breast cancer, prostate cancer, bone sarcomas, liver cancer, and melanomas).
  • We and other groups have previously reported the isolation of cancer stem cells from adult glioblastoma multiforme.
  • These cells express stem cell markers, and when differentiated they express glial and neuronal markers.
  • In vivo they give a tumor that recapitulates the characteristics of the tumor in the patient.
  • More recently we have isolated tumor stem-like cells also from benign tumors like pituitary adenomas.
  • Cells derived from pituitary adenomas are able to grow as floating aggregates resembling the neurospheres (typical of normal stem cells) in a medium supplemented by growth factors (EGF and bFGF).
  • The immunocytochemical analysis revealed that pituitary tumor stem-like cells are positives for nestin and, when grown for ten days in differentiation medium they express GFAP, BIII tubulin, and S-100.
  • In vitro tumor stem-like cells derived from a patient with a somatotroph adenoma showed high production of growth hormone and prolactin, while cells derived from the same patient but grown in presence of fetal bovine serum showed no production of hormones.
  • [MeSH-major] Cell Culture Techniques / methods. Neoplastic Stem Cells / pathology. Pituitary Neoplasms / pathology

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  • (PMID = 19582428.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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82. Nicolis SK: Cancer stem cells and "stemness" genes in neuro-oncology. Neurobiol Dis; 2007 Feb;25(2):217-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer stem cells and "stemness" genes in neuro-oncology.
  • The main properties of stem cells include long-term self-renewal and the capacity to give rise to one or more types of differentiated progeny.
  • Recently, much evidence was provided that leukemia and tumor maintenance and growth are sustained by a small proportion of cells exhibiting stem cell properties.
  • In neural tumors, stem cells have been detected in glioblastoma, medulloblastoma and ependymoma.
  • These observations imply that normal stem cells could be the origin of cancer stem cells; alternatively, a more differentiated progeny may revert to a "stem-like" status, and give rise to cancer stem cells.
  • In adult brain residual stem cells are located in the hippocampus, the subventricular zone and possibly the cerebellum.
  • However, evidence for the ability of more differentiated progeny (astroglia, oligodendroglia) to convert into "stem cells" in vitro has also been provided, thus greatly expanding the potential target of oncogenic mutations.
  • In the framework of the cancer stem cell hypothesis, genes originally identified as important for normal neural stem cells may be essential to support cancer stem cells as well.
  • Stem cell genes act in several ways: they stimulate stem cell self-replication, inhibit differentiation, control excessive replication that might lead to "exhaustion" of the stem cell pool.
  • Mutations in man and mouse, in spontaneous or experimental brain tumors, often target stem cell genes or genes lying in their functional pathway, the main examples being the Sonic hedgehog and the Wnt pathways.
  • Interestingly, several stem cell genes are often overexpressed in brain tumors, even if they are not mutated.
  • This suggests that these genes may be important for the generation of cancer stem cells from more differentiated precursors, or for cancer stem cell maintenance.
  • Cancer stem cells partially differentiate in vivo, and in vitro they also give rise to seemingly normal differentiated progeny, like normal stem cells: thus, their main defect, leading to cancer, may lie in the unbalance between self-replication and terminal differentiation of this minority cell population.
  • Knowledge of extrinsic diffusible factors affecting the activity of stem cell genes may help identifying tools for inducing cancer stem cell differentiation, which might be of use in therapy.
  • [MeSH-major] Brain Neoplasms / genetics. Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic / genetics. Neoplastic Stem Cells / physiology
  • [MeSH-minor] Animals. Biomarkers, Tumor / genetics. Cell Differentiation / genetics. Cell Division / genetics. Cell Lineage / genetics. Humans. Signal Transduction / genetics

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  • (PMID = 17141509.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP05122
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 133
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83. Jackson EL, Garcia-Verdugo JM, Gil-Perotin S, Roy M, Quinones-Hinojosa A, VandenBerg S, Alvarez-Buylla A: PDGFR alpha-positive B cells are neural stem cells in the adult SVZ that form glioma-like growths in response to increased PDGF signaling. Neuron; 2006 Jul 20;51(2):187-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PDGFR alpha-positive B cells are neural stem cells in the adult SVZ that form glioma-like growths in response to increased PDGF signaling.
  • Neurons and oligodendrocytes are produced in the adult brain subventricular zone (SVZ) from neural stem cells (B cells), which express GFAP and have morphological properties of astrocytes.
  • We report here on the identification B cells expressing the PDGFRalpha in the adult SVZ.
  • Conditional ablation of PDGFRalpha in a subpopulation of postnatal stem cells showed that this receptor is required for oligodendrogenesis, but not neurogenesis.
  • The work demonstrates that PDGFRalpha signaling occurs early in the adult stem cell lineage and may help regulate the balance between oligodendrocyte and neuron production.
  • Excessive PDGF activation in the SVZ in stem cells is sufficient to induce hallmarks associated with early stages of tumor formation.
  • [MeSH-major] Cell Proliferation. Glioma / metabolism. Lateral Ventricles / metabolism. Neurons / metabolism. Platelet-Derived Growth Factor / physiology. Receptor, Platelet-Derived Growth Factor alpha / biosynthesis. Signal Transduction / physiology. Stem Cells / metabolism


84. Das S, Srikanth M, Kessler JA: Cancer stem cells and glioma. Nat Clin Pract Neurol; 2008 Aug;4(8):427-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer stem cells and glioma.
  • Recent data suggest that progression of these brain tumors is driven by a small subpopulation of tumor cells, which are termed cancer stem cells (CSCs) because of their capability to self-renew, proliferate and give rise to progeny of multiple neuroepithelial lineages.
  • According to the CSC hypothesis, current therapies that are extremely cytotoxic to the bulk of highly proliferative tumor cells fail to obliterate the relatively quiescent and resistant CSC compartment, thereby allowing these cells to survive and drive tumor recurrence.
  • This Review summarizes current knowledge regarding neural stem cells in the normal adult brain and CSCs in glial tumors and discusses the implications of the CSC hypothesis for the development of future therapies for brain tumors.
  • [MeSH-major] Glioma / pathology. Neoplastic Stem Cells / pathology

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  • (PMID = 18628751.001).
  • [ISSN] 1745-8358
  • [Journal-full-title] Nature clinical practice. Neurology
  • [ISO-abbreviation] Nat Clin Pract Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 91
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85. Tanaka S, Kobayashi I, Utsuki S, Iwamoto K, Takanashi J: Biopsy of brain stem glioma using motor-evoked potential mapping by direct peduncular stimulation and individual adjuvant therapy. Case report. Neurol Med Chir (Tokyo); 2005 Jan;45(1):49-55
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  • [Title] Biopsy of brain stem glioma using motor-evoked potential mapping by direct peduncular stimulation and individual adjuvant therapy. Case report.
  • A 23-year-old man presented with a brain stem glioma manifesting as a 6-month history of right hemiparesis and diplopia.
  • Serial magnetic resonance imaging showed an intrinsic diffuse brain stem glioma that gradually localized to the left cerebral peduncle after initial adjuvant therapy.
  • Partial resection of the tumor was safely performed, with slight temporary neurological worsening.
  • Individual adjuvant therapy based on the results of real-time reverse transcription-polymerase chain reaction of O6-methylguanine-deoxyribonucleic acid methyltransferase achieved an almost complete tumor response.
  • Surgery under pyramidal tract mapping and intensive postoperative adjuvant therapy resulted in a good outcome despite the presence of a generally intractable intrinsic brain stem glioma.
  • [MeSH-major] Astrocytoma / surgery. Brain Mapping. Brain Stem Neoplasms / surgery. Evoked Potentials, Motor. Mesencephalon / physiopathology. Neurosurgical Procedures / methods
  • [MeSH-minor] Adult. Biopsy / methods. Humans. Male

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  • (PMID = 15699622.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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86. van der Meulen AA, Biber K, Lukovac S, Balasubramaniyan V, den Dunnen WF, Boddeke HW, Mooij JJ: The role of CXC chemokine ligand (CXCL)12-CXC chemokine receptor (CXCR)4 signalling in the migration of neural stem cells towards a brain tumour. Neuropathol Appl Neurobiol; 2009 Dec;35(6):579-91
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of CXC chemokine ligand (CXCL)12-CXC chemokine receptor (CXCR)4 signalling in the migration of neural stem cells towards a brain tumour.
  • AIMS: It has been shown that neural stem cells (NSCs) migrate towards areas of brain injury or brain tumours and that NSCs have the capacity to track infiltrating tumour cells.
  • As chemokines are involved in the migration of immune cells in the injured brain, they may also be involved in chemoattraction of NSCs towards a brain tumour.
  • METHODS: The expression profile of various chemokine receptors in NSCs, harvested from the subventricular zone of adult mice, was investigated by reverse transcriptase- polymerase chain reaction analysis.
  • RESULTS AND CONCLUSIONS: Adult mouse NSCs functionally express various chemokine receptors of which CXC chemokine receptor (CXCR)4 shows the highest mRNA levels and most pronounced functional responses in vitro.
  • In this mouse model for metastatic brain tumours, it is shown that NSCs express CXCR4 at their cell membranes while they migrate towards the tumour, which produces CXCL12.
  • [MeSH-major] Adult Stem Cells / physiology. Brain Neoplasms / physiopathology. Cell Movement / physiology. Chemokine CXCL12 / metabolism. Neurons / cytology. Receptors, CXCR4 / metabolism
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Line, Tumor. Chemotaxis / physiology. Melanoma / physiopathology. Mice. Mice, Inbred C57BL. Neoplasms, Experimental / physiopathology. RNA, Messenger / metabolism. Receptors, CXCR / metabolism. Signal Transduction. Stem Cell Niche / physiopathology

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  • (PMID = 19627512.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCR4 protein, mouse; 0 / Chemokine CXCL12; 0 / Cxcl12 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, CXCR; 0 / Receptors, CXCR4; SY7Q814VUP / Calcium
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87. Hambardzumyan D, Becher OJ, Holland EC: Cancer stem cells and survival pathways. Cell Cycle; 2008 May 15;7(10):1371-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer stem cells and survival pathways.
  • Gliomas and medulloblastomas are the most frequent malignant brain tumors in adult and children respectively.
  • During the last decade several reports have demonstrated the existence of cancer stem cells in brain tumors, their location and their response to treatment.
  • We have recently described the therapeutic response of medulloblastomas to radiation in their native microenvironment, illustrating how p53 and Pi3K signaling pathways lead to the evasion of cell death by the nestin-expressing cells in the perivascular stem cell niche, even while the bulk of tumor succumbs to apoptosis.(1) It remains to be determined whether this mechanism of tumor resistance applies to the more complex stem-cell niche and tumor bulk of gliomas.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Medulloblastoma / radiotherapy. Neoplastic Stem Cells / radiation effects. Signal Transduction / radiation effects
  • [MeSH-minor] Animals. Humans. Intermediate Filament Proteins / metabolism. Mice. Models, Biological. Nerve Tissue Proteins / metabolism. Nestin. Phosphatidylinositol 3-Kinases / metabolism. Receptors, Notch / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18421251.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 5R01CA100688-2; United States / NCI NIH HHS / CA / R01CA 5R01CA099489-1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Number-of-references] 112
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88. Bachstetter AD, Jernberg J, Schlunk A, Vila JL, Hudson C, Cole MJ, Shytle RD, Tan J, Sanberg PR, Sanberg CD, Borlongan C, Kaneko Y, Tajiri N, Gemma C, Bickford PC: Spirulina promotes stem cell genesis and protects against LPS induced declines in neural stem cell proliferation. PLoS One; 2010 May 05;5(5):e10496
Hazardous Substances Data Bank. BROMODEOXYURIDINE .

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  • [Title] Spirulina promotes stem cell genesis and protects against LPS induced declines in neural stem cell proliferation.
  • Adult stem cells are present in many tissues including, skin, muscle, adipose, bone marrow, and in the brain.
  • Neuroinflammation has been shown to be a potent negative regulator of stem cell and progenitor cell proliferation in the neurogenic regions of the brain.
  • Quantification of the BrdU positive cells in the subgranular zone of the dentate gyrus demonstrated a decrease in proliferation of the stem/progenitor cells in the hippocampus as a result of the LPS insult.
  • Furthermore, the diet supplemented with spirulina was able to negate the LPS induced decrease in stem/progenitor cell proliferation.
  • When examined on neural stem cells in culture spirulina increased proliferation at baseline and protected against the negative influence of TNFalpha to reduce neural stem cell proliferation.
  • These results support the hypothesis that a diet enriched with spirulina and other nutraceuticals may help protect the stem/progenitor cells from insults.

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  • (PMID = 20463965.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / P01 AG004418; United States / NIA NIH HHS / AG / R21 AG024165; United States / NIA NIH HHS / AG / P01AG04418; United States / NIA NIH HHS / AG / R21AG024165
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ PMC2864748
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89. Dalerba P, Cho RW, Clarke MF: Cancer stem cells: models and concepts. Annu Rev Med; 2007;58:267-84
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  • [Title] Cancer stem cells: models and concepts.
  • This observation is traditionally explained by postulating variations in tumor microenvironment and coexistence of multiple genetic subclones, created by progressive and divergent accumulation of independent somatic mutations.
  • According to this second scenario, tumors act as caricatures of their corresponding normal tissues and are sustained in their growth by a pathological counterpart of normal adult stem cells, cancer stem cells.
  • This model, first developed in human myeloid leukemias, is today being extended to solid tumors, such as breast and brain cancer.
  • We review the biological basis and the therapeutic implications of the stem cell model of cancer.
  • [MeSH-major] Models, Biological. Neoplasms / etiology. Neoplasms / therapy. Neoplastic Stem Cells / physiology

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  • (PMID = 17002552.001).
  • [ISSN] 0066-4219
  • [Journal-full-title] Annual review of medicine
  • [ISO-abbreviation] Annu. Rev. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA104987-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 92
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90. Muthukrishnan A, Bajoghli M, Mountz JM: Delayed development of radiation vasculopathy of the brain stem confirmed by F-18 FDG PET in a case of anaplastic astrocytoma. Clin Nucl Med; 2007 Jul;32(7):527-31
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  • [Title] Delayed development of radiation vasculopathy of the brain stem confirmed by F-18 FDG PET in a case of anaplastic astrocytoma.
  • Magnetic resonance imaging (MRI) of the brain showed a new mass lesion in the left pontine region of the brain stem.
  • Since viable tumor recurrence was strongly suspected, a biopsy was planned, although this posed significant risk.
  • Therefore, an F-18 FDG brain PET scan was performed, which demonstrated no metabolic activity in the pontine lesion leading to the less common diagnosis of long-term postradiation vasculopathy.
  • This case illustrates the importance of considering the rare diagnosis of radiation-induced vasculopathy in the differential diagnosis when symptoms of recurrent brain tumor occur.
  • [MeSH-major] Brain Stem / radionuclide imaging. Cerebrovascular Disorders / etiology. Cerebrovascular Disorders / radionuclide imaging. Fluorodeoxyglucose F18. Radiation Injuries / etiology. Radiation Injuries / radionuclide imaging. Radiotherapy / adverse effects
  • [MeSH-minor] Adult. Astrocytoma / radionuclide imaging. Astrocytoma / radiotherapy. Female. Humans. Positron-Emission Tomography / methods. Radiopharmaceuticals. Time Factors

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  • (PMID = 17581336.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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91. Kelly JJ, Stechishin O, Chojnacki A, Lun X, Sun B, Senger DL, Forsyth P, Auer RN, Dunn JF, Cairncross JG, Parney IF, Weiss S: Proliferation of human glioblastoma stem cells occurs independently of exogenous mitogens. Stem Cells; 2009 Aug;27(8):1722-33
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  • [Title] Proliferation of human glioblastoma stem cells occurs independently of exogenous mitogens.
  • Despite identification and isolation of human brain tumor stem cells (BTSCs), characteristics that distinguish BTSCs from neural stem cells remain to be elucidated.
  • Both CD133(+) and CD133(-) adult GBM BTSCs proliferated in the absence of exogenous mitogenic stimulation and gave rise to multipotent GBM spheres that were capable of self-renewal.
  • These results demonstrate that exogenous mitogen independence, mediated in part through EGFR signaling, is one characteristic that distinguishes CD133(+) and CD133(-) GBM BTSCs from neural stem cells.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Mitogens / pharmacology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adolescent. Adult. Animals. Antigens, CD / metabolism. Cell Growth Processes / drug effects. Flow Cytometry. Glycoproteins / metabolism. Humans. Mice. Peptides / metabolism. Signal Transduction. Tumor Cells, Cultured. Young Adult

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  • (PMID = 19544433.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Mitogens; 0 / Peptides
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92. Foreman NK, Schissel D, Le T, Strain J, Fleitz J, Quinones R, Giller R: A study of sequential high dose cyclophosphamide and high dose carboplatin with peripheral stem-cell rescue in resistant or recurrent pediatric brain tumors. J Neurooncol; 2005 Jan;71(2):181-7
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  • [Title] A study of sequential high dose cyclophosphamide and high dose carboplatin with peripheral stem-cell rescue in resistant or recurrent pediatric brain tumors.
  • PURPOSE: To determine the maximum tolerated dose (MTD) of carboplatin with autologous hematopoietic stem-cell rescue, in children with poor-prognosis brain tumors.
  • PATIENTS AND METHODS: A previously determined dose of cyclophosphamide with stem-cell rescue was used as a first course.
  • In a second course, carboplatin was given for 3 days with stem-cell rescue to 20 children.
  • Toxicity and tumor response were recorded.
  • The median duration of tumor response was 10 months (range: 1.5-87 months) with two children disease free at 66 and 87 months.
  • CONCLUSION: The MTD of carboplatin with stem-cell rescue is 700 mg/m2/day for 3 days.
  • Sequential stem-cell supported cyclophosphamide and carboplatin was tolerable in children with brain tumors and produced responses in PNETs and Germinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Drug Resistance, Neoplasm. Hematopoietic Stem Cell Transplantation. Neoplasm Recurrence, Local / therapy. Salvage Therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / therapeutic use. Carboplatin / administration & dosage. Carboplatin / therapeutic use. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Cyclophosphamide / therapeutic use. Dose-Response Relationship, Drug. Female. Humans. Male

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  • (PMID = 15690136.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin
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93. Heldmann U, Thored P, Claasen JH, Arvidsson A, Kokaia Z, Lindvall O: TNF-alpha antibody infusion impairs survival of stroke-generated neuroblasts in adult rat brain. Exp Neurol; 2005 Nov;196(1):204-8
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  • [Title] TNF-alpha antibody infusion impairs survival of stroke-generated neuroblasts in adult rat brain.
  • Stroke induced by 2 h middle cerebral artery occlusion triggers increased striatal and hippocampal neurogenesis in adult rats.
  • We investigated the effect of tumor necrosis factor-alpha (TNF-alpha) inhibition on the survival of the new neurons.
  • [MeSH-major] Antibodies / administration & dosage. Brain / drug effects. Infarction, Middle Cerebral Artery / physiopathology. Neurons / drug effects. Stem Cells / drug effects. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 16157335.001).
  • [ISSN] 0014-4886
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Tumor Necrosis Factor-alpha
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94. Liu Q, Liu R, Kashyap MV, Agarwal R, Shi X, Wang CC, Yang SH: Brainstem glioma progression in juvenile and adult rats. J Neurosurg; 2008 Nov;109(5):849-55

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brainstem glioma progression in juvenile and adult rats.
  • OBJECT: Brainstem gliomas are common in children and have the worst prognosis of any brain tumor in this age group.
  • On the other hand, brainstem gliomas are rare in adults, and the authors of some clinical studies have suggested that this lesion behaves differently in adults than in children.
  • In the present study, the authors test an orthotopic C6 brainstem glioma model in juvenile and adult rats, and investigate the biological behavior of this lesion in the 2 age groups.
  • METHODS: The C6 glioma cells were stereotactically implanted into the pons of juvenile or adult male rats.
  • Tumor proliferation and the number of apoptotic cells in brainstem gliomas of young and adult rats were determined by immunohistochemical staining with Ki 67 and terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate-mediated nick-end labeling assay.
  • RESULTS: Striking differences in the onset of neurological signs, duration of symptoms, survival time, tumor growth pattern, tumor proliferation, and number of apoptotic cells were found between the gliomas in the 2 groups of rats.
  • The lesions were relatively focal in adult rats but more diffuse in young rats.
  • Furthermore, brainstem gliomas in adult rats were less proliferative and had more apoptotic cells than those in young rats.
  • CONCLUSIONS: The authors found that the C6 brainstem glioma model in young and adult rats closely imitates the course of brainstem glioma in humans both in neurological findings and histopathological characteristics.
  • Their findings also suggest that the different growth pattern and invasiveness of these lesions in children compared with that in adults could be due to different cellular environments in the 2 age groups, and warrants further investigation into the difference in the host response to brainstem gliomas in children and adults.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Age Factors. Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation. Disease Models, Animal. Disease Progression. Kaplan-Meier Estimate. Male. Neoplasm Transplantation / pathology. Rats. Rats, Sprague-Dawley

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  • (PMID = 18976074.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS054651; United States / NINDS NIH HHS / NS / R01 NS054651-01A2; United States / NINDS NIH HHS / NS / R01 NS054687; United States / NINDS NIH HHS / NS / R01 NS054687-01A2
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS75237; NLM/ PMC2693119
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95. Patru C, Romao L, Varlet P, Coulombel L, Raponi E, Cadusseau J, Renault-Mihara F, Thirant C, Leonard N, Berhneim A, Mihalescu-Maingot M, Haiech J, Bièche I, Moura-Neto V, Daumas-Duport C, Junier MP, Chneiweiss H: CD133, CD15/SSEA-1, CD34 or side populations do not resume tumor-initiating properties of long-term cultured cancer stem cells from human malignant glio-neuronal tumors. BMC Cancer; 2010;10:66
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  • [Title] CD133, CD15/SSEA-1, CD34 or side populations do not resume tumor-initiating properties of long-term cultured cancer stem cells from human malignant glio-neuronal tumors.
  • BACKGROUND: Tumor initiating cells (TICs) provide a new paradigm for developing original therapeutic strategies.
  • METHODS: We screened for TICs in 47 human adult brain malignant tumors.
  • Cells forming floating spheres in culture, and endowed with all of the features expected from tumor cells with stem-like properties were obtained from glioblastomas, medulloblastoma but not oligodendrogliomas.
  • Xenografts of fewer than 500 cells in Nude mouse brains induced a progressively growing tumor.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD15 / biosynthesis. Antigens, CD34 / biosynthesis. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioma / metabolism. Glycoproteins / biosynthesis. Neoplastic Stem Cells / cytology. Neurons / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Peptides. Proteomics / methods

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  • (PMID = 20181261.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / Peptides
  • [Other-IDs] NLM/ PMC2841664
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96. Medrano S, Scrable H: Maintaining appearances--the role of p53 in adult neurogenesis. Biochem Biophys Res Commun; 2005 Jun 10;331(3):828-33
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  • [Title] Maintaining appearances--the role of p53 in adult neurogenesis.
  • In the adult mammalian brain, neuronal turnover continues to replenish cells in existing neuronal circuits, such as those involved either in odor discrimination or in learning and memory, throughout life.
  • Altered activity of the tumor suppressor p53 can upset this balance by affecting the rate of cell proliferation, but not the rate of cell death, in neurogenic regions of the adult brain.
  • [MeSH-major] Cerebral Ventricles / cytology. Dentate Gyrus / cytology. Neurons / cytology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Aging / physiology. Animals. Cell Death / physiology. Cell Proliferation. Genes, p53. Mice. Nerve Degeneration / physiopathology. Olfactory Bulb / cytology. Stem Cells / physiology

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  • (PMID = 15865938.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 61
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97. Amthauer H, Wurm R, Kuczer D, Ruf J, Michel R, Eisenacher J, Stockhammer F, Denecke T, Felix R, Plotkin M: Relevance of image fusion with MRI for the interpretation of I-123 iodo-methyl-tyrosine scans in patients with suspected recurrent or residual brain tumor. Clin Nucl Med; 2006 Apr;31(4):189-92
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  • [Title] Relevance of image fusion with MRI for the interpretation of I-123 iodo-methyl-tyrosine scans in patients with suspected recurrent or residual brain tumor.
  • PURPOSE: The aim of the study was to investigate the impact of MR/SPECT image fusion on the interpretation of I-123 iodo-methyl-tyrosine (IMT) SPECT examinations in patients with pretreated brain tumors.
  • Tumor localization and extent were evaluated and correlated with histopathology or clinical follow up, including MR imaging.
  • RESULTS: In 10 of 45 (22%) patients, image fusion had a significant impact on the interpretation of scans: 5 suspected SPECT findings were correctly classified as physiological or therapy-related; in another 5 patients, image fusion added relevant clinical information on tumor extent (infiltration of the contralateral hemisphere n = 3, infiltration of the brain stem n = 2).
  • [MeSH-major] Brain Neoplasms / pathology. Iodine Radioisotopes. Magnetic Resonance Imaging. Methyltyrosines. Tomography, Emission-Computed, Single-Photon
  • [MeSH-minor] Adolescent. Adult. Aged. Contrast Media. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm, Residual. Retrospective Studies

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  • (PMID = 16550008.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Iodine Radioisotopes; 0 / Methyltyrosines; 14684-02-7 / 3-iodo-alpha-methyltyrosine
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98. Ehtesham M, Stevenson CB, Thompson RC: Stem cell therapies for malignant glioma. Neurosurg Focus; 2005 Sep 15;19(3):E5
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  • [Title] Stem cell therapies for malignant glioma.
  • The prognosis for patients with malignant glioma, which is the most common primary intracranial neoplasm, remains dismal despite significant progress in neurooncological therapies and technology.
  • Malignant glial cells often disseminate throughout the brain, making it exceedingly difficult to target and treat all intracranial neoplastic foci, with the result that tumor recurrence is inevitable despite aggressive surgery and adjuvant radiotherapy and/or chemotherapy.
  • The use of neural stem cells (NSCs) as delivery vehicles for tumor-toxic molecules represents the first experimental strategy aimed specifically at targeting disseminated tumor pockets.
  • Investigators have demonstrated that NSCs possess robust tropism for infiltrating tumor cells, and that they can be used to deliver therapeutic agents directly to tumor satellites, with significant therapeutic benefit.
  • With the aim of developing these findings into a clinically viable technology that would not be hindered by ethical and tissue rejection-related concerns, the use of adult tissue-derived stem cells has recently been explored.
  • These technologies represent important progress in the development of a treatment strategy that can specifically target disseminated neoplastic pockets within the brain.
  • Key among these are an inadequate understanding of the specific tropic mechanisms that govern NSC migration toward invasive tumor, and the need to refine the processes used to generate tumor-tropic stem cells from adult tissues so that this can be accomplished in a clinically practicable fashion.
  • Despite these limitations, the use of stem cell therapies for brain tumors holds significant promise and may emerge as an important therapeutic modality for patients with malignant glioma.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy. Stem Cell Transplantation / methods. Stem Cells / physiology

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  • (PMID = 16190604.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 29
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99. Chojnacki A, Weiss S: Production of neurons, astrocytes and oligodendrocytes from mammalian CNS stem cells. Nat Protoc; 2008;3(6):935-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Production of neurons, astrocytes and oligodendrocytes from mammalian CNS stem cells.
  • The discovery of neural stem cells in the adult mouse brain was made possible by the creation of a novel culture system subsequently termed the neurosphere assay.
  • Therein, the dissociated adult mouse periventricular area was plated in the presence of epidermal growth factor, but in the absence of adhesive substrates, which resulted in the generation of spheres of proliferating cells that detached from the plate bottom and remained suspended in the media.
  • Since its inception, the neurosphere culture system has been widely used in the neural precursor cell field and has been extensively adapted for the isolation and expansion of corneal, cardiac, skin, prostate, mammary and brain tumor stem cells.
  • [MeSH-major] Astrocytes / cytology. Cell Separation / methods. Embryonic Stem Cells / cytology. Neurons / cytology. Oligodendroglia / cytology
  • [MeSH-minor] Animals. Brain / cytology. Brain / embryology. Cell Culture Techniques / methods. Cell Differentiation. Female. Humans. Mice. Multipotent Stem Cells / cytology. Pregnancy

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  • (PMID = 18536641.001).
  • [ISSN] 1750-2799
  • [Journal-full-title] Nature protocols
  • [ISO-abbreviation] Nat Protoc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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100. Oh MC, Lim DA: Novel treatment strategies for malignant gliomas using neural stem cells. Neurotherapeutics; 2009 Jul;6(3):458-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel treatment strategies for malignant gliomas using neural stem cells.
  • Recent studies in stem cell biology have refined our understanding of the origin and progression of cancer.
  • Identification and characterization of endogenous neural stem cells (NSCs), especially those in the adult human brain, have inspired new ideas for selectively targeting and destroying malignant gliomas.
  • Gliomas consist of a heterogeneous population of cells, and some of these cells have characteristics of cancer stem cells.
  • These brain tumor stem cells (BTSCs) share certain characteristics with normal NSCs.
  • Nonetheless, the cellular and molecular similarities between BTSCs and normal NSCs suggest a common research landscape underlying both normal and cancer stem cell biology, wherein findings of one field are relevant to the other.
  • Furthermore, the natural tropism of NSCs to gliomas has generated the idea that modified NSCs can deliver modified genes to selectively destroy malignant brain tumor cells, and even BTSCs, while leaving healthy surrounding neurons intact.
  • [MeSH-major] Brain / physiology. Brain Neoplasms / therapy. Glioma / therapy. Neurons / physiology. Stem Cells / physiology
  • [MeSH-minor] Adult Stem Cells / physiology. Animals. Genetic Therapy. Humans. Stem Cell Transplantation. Tropism / physiology

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  • (PMID = 19560736.001).
  • [ISSN] 1933-7213
  • [Journal-full-title] Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
  • [ISO-abbreviation] Neurotherapeutics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 66
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