| SKIP001185 | |
| SKIP ID | SKIP001185 |
| Organism(En) | - |
| Organism(Ja) | - |
| Cell Type(En) | - |
| Cell Type(Ja) | - |
| Cell Tissue(En) | CNS |
| Cell Tissue(Ja) | 中枢神経 |
| Cell Origin | Diseased |
| Cell Name 1(En) | GNS 362 |
| Cell Name 1(Ja) | GNS 362 |
| Cell Name 2(En) | G362 |
| Cell Name 2(Ja) | G362 |
| Disease Name 1(Ja) | 再発多形膠芽腫 |
| ICD Code 1 | C719 |
| Disease Name 1(En) | Recurrent 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 | 71 |
| Age Range | 70-79 |
| 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) | 再発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 | Immunocytochemistry |
| 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 | - |
| 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 | Information Only |
| Provider 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 |
| Provider 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 |
| Provider Email | peter[dot]dirks[at]sickkids[dot]ca |
| Provider URL | http://www.cell.com/action/showMethods?pii=S1934-5909%2809%2900149-0 |
| Ethical Statement(En) | - |
| Ethical Statement(Ja) | - |
| Terms of Use(En) | - |
| Terms of Use(Ja) | - |
| PubMed ID | 27300435 -- 19497285 -- 23108137 |
| DOI | 10.1016/j.ccell.2016.05.002 -- 10.1016/j.stem.2009.03.014 -- 10.1158/0008-5472.CAN-12-1881 |
| Title | Inhibition of Dopamine Receptor D4 Impedes Autophagic Flux, Proliferation, and Survival of Glioblastoma Stem Cells. -- Glioma stem cell lines expanded in adherent culture have tumor-specific phenotypes and are suitable for chemical and genetic screens. -- A tumorigenic MLL-homeobox network in human glioblastoma stem cells. |
| Authors | 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 -- 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 -- Gallo M, Ho J, Coutinho FJ, Vanner R, Lee L, Head R, Ling EK, Clarke ID, Dirks PB |
| Journal | Cancer Cell -- Cell Stem Cell -- Cancer Res |
| Year | 2016 -- 2009 -- 2012 |
| Volume | 29 -- 4 -- 73 |
| Issue | 6 -- 6 -- 1 |
| Pages | 859-73 -- 568-80 -- 417-27 |
| URL | http://www.ncbi.nlm.nih.gov/pubmed/27300435 -- http://www.ncbi.nlm.nih.gov/pubmed/19497285 -- http://www.ncbi.nlm.nih.gov/pubmed/23108137 |
| Free input | Abstract 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. -- -- |
| Note | G362 is positive for both SOX2 and nestin. G362 is susceptible for the dopamine receptor DRD4 antagonists composed of PNU 96415E and L-741,742. |