ArticleCell reports2016
Lineage-Restricted OLIG2-RTK Signaling Governs the Molecular Subtype of Glioma Stem-like Cells.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Loss of oligodendrocyte transcription factor 2 protein expression in metabolically stressed oligodendrocytes.Acta neuropathologica · 2026Article
- Immunophenotypic characterization of canine oligodendroglioma cells cultured in an oligodendrocyte precursor cell-tailored medium.The Journal of veterinary medical science · 2026Article
- Interplay between Epigenetic and Transcription Factors Mediating Drug Resistance via Stem Cells in Breast Cancer.ACS omega · 2025Review
- Olig1/2 Orchestrates Progenitor Cell Fates during Mammalian Cortical Gliogenesis and Gliomagenesis.Nature communications · 2025Article
- Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.Journal of translational medicine · 2025Review
- Article
- Comprehensive analysis of angiogenesis and stemness-related genes in chemotherapy and immunotherapy of bladder cancer.Biomolecules & biomedicine · 2025Article
- Identifying Diffuse Glioma Subtypes Based on Pathway Enrichment Evaluation.Interdisciplinary sciences, computational life sciences · 2024Article
- CREB5 promotes the proliferation and self-renewal ability of glioma stem cells.Cell death discovery · 2024Article
- Review
- Deciphering the Action of Neuraminidase in Glioblastoma Models.International journal of molecular sciences · 2023Article
- Single-cell RNA sequencing reveals changes in glioma-associated macrophage polarization and cellular states of malignant gliomas with high AQP4 expression.Cancer gene therapy · 2023Article
- Neural Stem Cells as Potential Glioblastoma Cells of Origin.Life (Basel, Switzerland) · 2023Review
- Systematic in vitro analysis of therapy resistance in glioblastoma cell lines by integration of clonogenic survival data with multi-level molecular data.Radiation oncology (London, England) · 2023Article
- Biological functions of the Olig gene family in brain cancer and therapeutic targeting.Frontiers in neuroscience · 2023Review
- OLIG2 expression level could be used as an independent prognostic factor for patients with cerebellar Glioblastoma (cGBM).Clinics (Sao Paulo, Brazil) · 2023Article
- OLIG2 Is a Determinant for the Relapse of MYC-Amplified Medulloblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Survivin Inhibition by Piperine Sensitizes Glioblastoma Cancer Stem Cells and Leads to Better Drug Response.International journal of molecular sciences · 2022Article
- PNJ scaffolds promote microenvironmental regulation of glioblastoma stem-like cell enrichment and radioresistance.Biomaterials science · 2022Article
- The Effects of the Olig Family on the Regulation of Spinal Cord Development and Regeneration.Neurochemical research · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The basic helix-loop-helix (bHLH) transcription factor OLIG2 is a master regulator of oligodendroglial fate decisions and tumorigenic competence of glioma stem-like cells (GSCs). However, the molecular mechanisms underlying dysregulation of OLIG2 function during gliomagenesis remains poorly understood. Here, we show that OLIG2 modulates growth factor signaling in two distinct populations of GSCs, characterized by expression of either the epidermal growth factor receptor (EGFR) or platelet-derived growth factor receptor alpha (PDGFRα). Biochemical analyses of OLIG2 function in normal and malignant neural progenitors reveal a positive feedforward loop between OLIG2 and EGFR to sustain co-expression. Furthermore, loss of OLIG2 function results in mesenchymal transformation in PDGFRα(HIGH) GSCs, a phenomenon that appears to be circumscribed in EGFR(HIGH) GSCs. Exploitation of OLIG2's dual and antithetical, pro-mitotic (EGFR-driven), and lineage-specifying (PDGFRα-driven) functions by glioma cells appears to be critical for sustaining growth factor signaling and GSC molecular subtype.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.