SKIP001187
SKIP ID SKIP001187
Organism(En) -
Organism(Ja) -
Cell Type(En) -
Cell Type(Ja) -
Cell Tissue(En) -
Cell Tissue(Ja) -
Cell Origin Diseased
Cell Name 1(En) GNS144
Cell Name 1(Ja) GNS144
Cell Name 2(En) G144
Cell Name 2(Ja) G144
Disease Name 1(Ja) 多形膠芽腫
ICD Code 1 C719
Disease Name 1(En) Glioblastoma multiforme
OMIM1 131550
Disease Name 2(Ja) -
ICD Code 2 -
Disease Name 2(En) -
OMIM 2 -
Disease Name 3(Ja) -
ICD Code 3 -
Disease Name 3(En) -
OMIM 3 -
Age 51
Age Range 50-59
Sex Male
Race(En) -
Race(Ja) -
Genetic Diagnosis Yes
Not Detected No
Description(En) Tumors were dissociated into single cells by placing in Accutase (Sigma) or an enzyme cocktail for 15-20 min at room temperature. For those tumors with excess debris, cells were initially allowed to form spheres or aggregates in suspension culture, and these were then transferred to a fresh laminin-coated flask. They subsequently attached and began to outgrow over the course of a week.
GNS cells were patient-derived tumour cells established and maintained as an adherent monolayer.
Description(Ja) 多形膠芽腫患者の腫瘍細胞由来の神経膠芽腫幹細胞
Cell Morphology fibroblast-like
Grade Research Grade
Vector --
Transgene -
Adhesiveness -
Feeder --
Feeder Cell -
Medium serum-free medium with epidermal growth factor (EGF) and basic fibroblast growth factor (FGF)
Genome Editing -
CO2 -
Mycoplasma -
Detection of Contaminants Mycoplasma -
Pluripotent Markers Yes
Pluripotent Markers Assay Immunostaining
in vitro Differentiation -
in vitro Differentiation Assay -
in vivo Differentiation Yes
in vivo Differentiation Assay intracranial transplantation into immunocompromised mice
Other 1 Assay -
Other 1 Assay Method -
Other 2 Assay -
Other 2 Assay Method -
Other 3 Assay -
Other 3 Assay Method -
Karyotype Yes
Karyotype Assay -
Remaining Vector Detection -
Remaining Vector Detection Assay -
STR -
HLA -
Stem Cell Transcriptome analysis -
Stem Cell Transcriptome analysis Assay -
Author Name(En) Steven M. Pollard, Peter Dirks et al.
Author Name(Ja) Steven M. Pollard, Peter Dirks et al.
Author Organization(En) Arthur and Sonia Labatt Brain Tumor Research Center, Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, University of Toronto
Author Organization(Ja) Arthur and Sonia Labatt Brain Tumor Research Center, Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, University of Toronto
Author Contact Email peter[dot]dirks[at]sickkids[dot]ca
PI Organization(En) -
PI Organization(Ja) -
PI Name(En) -
PI Name(Ja) -
PI Contact Email -
Availability Available
Provider Organization(En) Integrated Systems Engineering Srl
Provider Organization(Ja) Integrated Systems Engineering Srl
Provider Email info[at]isenet[dot]it
Provider URL http://www.isenet.it/index.php/eu
Ethical Statement(En) -
Ethical Statement(Ja) -
Terms of Use(En) -
Terms of Use(Ja) -
PubMed ID 19497285
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27300435
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23108137
DOI 10.1016/j.stem.2009.03.014
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10.1016/j.ccell.2016.05.002
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10.1158/0008-5472.CAN-12-1881
Title Glioma stem cell lines expanded in adherent culture have tumor-specific phenotypes and are suitable for chemical and genetic screens.
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Inhibition of Dopamine Receptor D4 Impedes Autophagic Flux, Proliferation, and Survival of Glioblastoma Stem Cells.
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A tumorigenic MLL-homeobox network in human glioblastoma stem cells.
Authors Pollard SM, Yoshikawa K, Clarke ID, Danovi D, Stricker S, Russell R, Bayani J, Head R, Lee M, Bernstein M, Squire JA, Smith A, Dirks P
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Dolma S, Selvadurai HJ, Lan X, Lee L, Kushida M, Voisin V, Whetstone H, So M, Aviv T, Park N, Zhu X, Xu C, Head R, Rowland KJ, Bernstein M, Clarke ID, Bader G, Harrington L, Brumell JH, Tyers M, Dirks PB
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Gallo M, Ho J, Coutinho FJ, Vanner R, Lee L, Head R, Ling EK, Clarke ID, Dirks PB
Journal Cell Stem Cell
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Cancer Cell
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Cancer Res
Year 2009
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2016
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2012
Volume 4
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29
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73
Issue 6
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6
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1
Pages 568-80
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859-73
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417-27
URL http://www.ncbi.nlm.nih.gov/pubmed/19497285
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http://www.ncbi.nlm.nih.gov/pubmed/27300435
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http://www.ncbi.nlm.nih.gov/pubmed/23108137
Free input
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Summary
Glioblastomas (GBM) grow in a rich neurochemical milieu, but the impact of neurochemicals on GBM growth is largely unexplored. We interrogated 680 neurochemical compounds in patient-derived GBM neural stem cells (GNS) to determine the effects on proliferation and survival. Compounds that modulate dopaminergic, serotonergic, and cholinergic signaling pathways selectively affected GNS growth. In particular, dopamine receptor D4 (DRD4) antagonists selectively inhibited GNS growth and promoted differentiation of normal neural stem cells. DRD4 antagonists inhibited the downstream effectors PDGFRβ, ERK1/2, and mTOR and disrupted the autophagy-lysosomal pathway, leading to accumulation of autophagic vacuoles followed by G0/G1 arrest and apoptosis. These results demonstrate a role for neurochemical pathways in governing GBM stem cell proliferation and suggest therapeutic approaches for GBM.
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Note By striking contrast to all the other GBM-derived cancer stem cells, G144 does not express dopamine receptor DRD4.