Evidence map›Paper›PMID 27165742›Full record

ArticleCancer cell2016

Olig2-Dependent Reciprocal Shift in PDGF and EGF Receptor Signaling Regulates Tumor Phenotype and Mitotic Growth in Malignant Glioma.

Fanghui Lu, Ying Chen, Chuntao Zhao, Haibo Wang, Danyang He, Lingli Xu, Jincheng Wang, Xuelian He, Yaqi Deng, Ellen E Lu and 13 more

Open access · greenAbstract read
In one paragraph

Article in Cancer cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
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  11. Killing the killers: Natural killer cell therapy targeting glioma stem cells in high-grade glioma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  12. Genes · 2025
    Article
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16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 9 institutions in 2 countries.

Fanghui LuLaboratory of Pathology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and National Collaborative Innovation Center, Chengdu 610041, China; Department of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Ying ChenSchool of Life Sciences, Xiamen University, Fujian 361102, China.
Chuntao ZhaoDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Haibo WangDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Danyang HeDepartment of Pathology & Integrative Biology Program, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Lingli XuDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Jincheng WangDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Xuelian HeDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Yaqi DengDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Ellen E LuDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Xue LiuSchool of Life Sciences, Xiamen University, Fujian 361102, China.
Ravinder VermaDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Hong BuLaboratory of Pathology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and National Collaborative Innovation Center, Chengdu 610041, China.
Rachid DrissiDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Maryam FouladiDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Anat O Stemmer-RachamimovDepartment of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Dennis BurnsDepartment of Pathology & Integrative Biology Program, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Mei XinDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA.
Joshua B RubinDepartments of Pediatrics and Anatomy and Neurobiology, Washington University School of Medicine, St Louis, MO 63110, USA.
El Mustapha BahassiDepartment of Internal Medicine, UC Brain Tumor Center, University of Cincinnati, Cincinnati, OH 45267, USA.
Peter CanollDepartment of Pathology & Cellular Biology, Columbia University Medical Center, New York, NY 10032, USA.
Eric C HollandDivision of Human Biology and Solid Tumor Translational Research, Fred Hutchinson Cancer Research Center, Alvord Brain Tumor Center, University of Washington, Seattle, WA 98109, USA.
Q Richard LuDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 25229, USA; Key Laboratory of Birth Defects, Children's Hospital of Fudan University, Shanghai 201102, China. Electronic address: richard.lu@cchmc.org.
Cincinnati Children's Hospital Medical Center · USThe University of Texas Southwestern Medical Center · USXiamen University · CNColumbia University Irving Medical Center · USFred Hutch Cancer Center · USHarvard University · USState Key Laboratory of BiotherapyUniversity of Cincinnati · USWashington University in St. Louis · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI MEINZEN-DERR, JAREEN, STRAWN, JEFFREY ROBERT · 2015 to 2024
$37.5M
Molecular Mechanisms of Oligodendrocyte Differentiation and MyelinationR01NS072427 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2010 to 2018
$3.6M
Chromatin remodeling control of myelination and remyelinationR01NS075243 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2012 to 2018
$2.6M
Hippo Signaling in Heart Development and RepairR01HL132211 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI XIN, MEI · 2016 to 2020
$1.9M
A Novel Model of Medulloblastoma to Define Cancer Pathways and Molecular TargetsR01NS078092 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2012 to 2016
$1.7M
Molecular and signaling mechanisms of peripheral nerve sheath tumorigenesisR37NS096359 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI LU, QING R · 2016 to 2018
$1.6M
NCATS NIH HHS UL1 TR001425NHLBI NIH HHS R01 HL132211NINDS NIH HHS R01 NS072427NINDS NIH HHS R01 NS075243NINDS NIH HHS R01 NS078092NINDS NIH HHS R37 NS096359
6 · The paper itself

Abstract

Malignant gliomas exhibit extensive heterogeneity and poor prognosis. Here we identify mitotic Olig2-expressing cells as tumor-propagating cells in proneural gliomas, elimination of which blocks tumor initiation and progression. Intriguingly, deletion of Olig2 resulted in tumors that grow, albeit at a decelerated rate. Genome occupancy and expression profiling analyses reveal that Olig2 directly activates cell-proliferation machinery to promote tumorigenesis. Olig2 deletion causes a tumor phenotypic shift from an oligodendrocyte precursor-correlated proneural toward an astroglia-associated gene expression pattern, manifest in downregulation of platelet-derived growth factor receptor-α and reciprocal upregulation of epidermal growth factor receptor (EGFR). Olig2 deletion further sensitizes glioma cells to EGFR inhibitors and extends the lifespan of animals. Thus, Olig2-orchestrated receptor signaling drives mitotic growth and regulates glioma phenotypic plasticity. Targeting Olig2 may circumvent resistance to EGFR-targeted drugs.

Indexed as

AnimalsAstrocytesBasic Helix-Loop-Helix ProteinsCell Line, TumorCell ProliferationCell Transformation, NeoplasticErbB ReceptorsGene Expression ProfilingGene Expression Regulation, NeoplasticGliomaHumansMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicNerve Tissue ProteinsBasic Helix-Loop-Helix ProteinsErbB ReceptorsNerve Tissue ProteinsReceptors, Platelet-Derived Growth Factor

Identifiers

PMID27165742
PMCPMC4946168
OpenAlexW2345641371

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.