{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Neuro-Oncology, Research, NNI"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA156711"],"scientific_name":["Homo sapiens"],"tag":["xref:PubMed:22927677"],"long_description":["Gliomas are the most devastating of primary adult malignant brain tumors. These tumors are highly infiltrative and can arise from cells with extensive self-renewal capability and chemoresistance, frequently termed glioma-propagating cells (GPCs). GPCs are thus the plausible culprits of tumor recurrence. Treatment strategies that eradicate GPCs will greatly improve disease outcome. Such findings support the use of GPCs as in vitro cellular systems for small molecule screening. However, the nuances in utilizing GPCs as a cellular screening platform are not trivial. These slow-growing cells are typically cultured as suspension, spheroid structures in serum-free condition supplemented with growth factors. Consequently, replenishment of growth factors throughout the screening period must occur to maintain cells in their undifferentiated state, as the more lineage-committed, differentiated cells are less tumorigenic. We will present a case study of a small molecule screen conducted with GPCs and explain how unique sphere activity assays were implemented to distinguish drug efficacies against the long-term, self-renewing fraction, as opposed to transient-amplifying progenitors, latter of which are detected in conventional viability assays. We identified Pololike kinase 1 as a regulator of GPC survival. Finally, we leveraged on public glioma databases to illustrate GPC contribution to disease progression and patient survival outcome. Overall design: Total RNA from primary neurosphere culture of brain tumor specimens were hybridized in baseline condition. Specimens were obtained from 11 patients and replicate arrays were performed for all 11 neurosphere cultures."],"repository":["ENA"],"name_synonyms":["Human, Modern., human being, Man (Taxonomy), Homo sapiens, man, Man, human, Modern Man"],"description_synonyms":["Glioma 1, Glioma NOS, l(3)01673, Glioma (except Nasal glioma, GLM, glial tumors, Polo kinase, malignant, neuroglial tumor, obsolete_glioma, Mixed Glioma, Malignant Glioma, Neuroglial Tumor, tumour of the neuroglia, Tumor, Malignant, Cell, neoplasm of neuroglia, serine/threonine-protein kinase 13, l(3)S025604, [M]Glioma NOS (morphologic abnormality), POLO/PLK1, tumor of the neuroglia, [M]Gliomas (morphologic abnormality), Case Study., Gliomas, Mixed, Glial Cell Tumor, [M]Glioma NOS, Case Studies, Mixed Gliomas, Glial Tumor, NOS (except Nasal glioma, Polo, Neuroglial Neoplasm, glioma (morphologic abnormality), Neuroglial Neoplasms, Glioma NOS (morphologic abnormality), PLK, Plk, neuroglial tumour, Glial Cell, Malignant glioma, Neoplasm of the Neuroglia, Tumor of Neuroglia, Glial Neoplasm, STPK13, anon-WO0172774.3, neuroglial neoplasm, tumor of neuroglia, Neoplasm of Neuroglia, 1324/08, glial tumor, no ICD-O subtype, PLK1, POLO, CG12306, l(3)77Aa, Tumor of the Neuroglia, plk, tumour of neuroglia, glial tumour, Glial Cell Tumors, Case Histories, not neoplastic), Gliomas (morphologic abnormality), 0256/04, Malignant Gliomas, DmelCG12306, Glioma, glial neoplasm, [M]Gliomas, malignant (morphologic abnormality), glioma, Tumors of Neuroglia, neoplasm of the neuroglia, Neoplasms of Neuroglia, l(3)S132408, Tumors"],"additional_accession":[]},"is_claimable":false,"name":"Homo sapiens","description":"Glioma-propagating cells as an in vitro screening platform: PLK1 as a case study","dates":{"last_updated":"2025-09-24","first_public":"2014-02-11"},"accession":"PRJNA156711","cross_references":{"GEO":["GSE36782"],"taxon":["9606"],"PubMed":["22927677"]}}