Evidence map›Paper›PMID 27013192›Full record

ArticleCancer research2016

CSF1 Overexpression Promotes High-Grade Glioma Formation without Impacting the Polarization Status of Glioma-Associated Microglia and Macrophages.

Ishani De, Megan D Steffen, Paul A Clark, Clayton J Patros, Emily Sokn, Stephanie M Bishop, Suzanne Litscher, Vilena I Maklakova, John S Kuo, Fausto J Rodriguez and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
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  7. Role of Innate Immunity in Cancer.Advances in experimental medicine and biology · 2025
    Review
  8. Piezo1-related physiological and pathological processes in glioblastoma.Frontiers in cell and developmental biology · 2025
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Ishani DeSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin.
Megan D SteffenSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin.
Paul A ClarkDepartment of Neurological Surgery and Carbone Cancer Center, University of Wisconsin-Madison, Madison, Wisconsin.
Clayton J PatrosSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin.
Emily SoknSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin.
Stephanie M BishopSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin.
Suzanne LitscherSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin.
Vilena I MaklakovaSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin.
John S KuoDepartment of Neurological Surgery and Carbone Cancer Center, University of Wisconsin-Madison, Madison, Wisconsin.
Fausto J RodriguezDivision of Neuropathology, Department of Pathology, Johns Hopkins University, Baltimore, Maryland.
Lara S CollierSchool of Pharmacy, Carbone Cancer Center and the Molecular and Cellular Pharmacology Graduate Program, University of Wisconsin-Madison, Madison, Wisconsin. lcollier@wisc.edu.
University of Wisconsin Carbone Cancer Center · USJohns Hopkins University · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Institutional Clinical and Translational Science AwardUL1TR000427 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$32.2M
INSTITUTIONAL CTSA (UW-MADISON): CLINICAL TRIALSUL1RR025011 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$29.5M
Na-K-Cl cotransporter in Glioblastoma MultiformeR01NS075995 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SUN, DANDAN · 2011 to 2015
$1.8M
CSF1 signaling in gliomagenesisR01NS085364 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI COLLIER, LARA S · 2014 to 2019
$1.6M
PET/CT Imaging of Malignant Brain Tumors with 124I-NM404R01CA158800 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI HALL, LANCE T, WEICHERT, JAMEY P · 2011 to 2014
$1.2M
NCATS NIH HHS UL1 TR000427NCI NIH HHS HHSN261201000130CNCI NIH HHS P30 CA014520NCI NIH HHS R01 CA158800NCRR NIH HHS UL1 RR025011NINDS NIH HHS R01 NS075995NINDS NIH HHS R01 NS085364
6 · The paper itself

Abstract

Current therapies for high-grade gliomas extend survival only modestly. The glioma microenvironment, including glioma-associated microglia/macrophages (GAM), is a potential therapeutic target. The microglia/macrophage cytokine CSF1 and its receptor CSF1R are overexpressed in human high-grade gliomas. To determine whether the other known CSF1R ligand IL34 is expressed in gliomas, we examined expression array data of human high-grade gliomas and performed RT-PCR on glioblastoma sphere-forming cell lines (GSC). Expression microarray analyses indicated that CSF1, but not IL34, is frequently overexpressed in human tumors. We found that while GSCs did express CSF1, most GSC lines did not express detectable levels of IL34 mRNA. We therefore studied the impact of modulating CSF1 levels on gliomagenesis in the context of the GFAP-V12Ha-ras-IRESLacZ (Ras*) model. Csf1 deficiency deterred glioma formation in the Ras* model, whereas CSF1 transgenic overexpression decreased the survival of Ras* mice and promoted the formation of high-grade gliomas. Conversely, CSF1 overexpression increased GAM density, but did not impact GAM polarization state. Regardless of CSF1 expression status, most GAMs were negative for the M2 polarization markers ARG1 and CD206; when present, ARG1(+) and CD206(+) cells were found in regions of peripheral immune cell invasion. Therefore, our findings indicate that CSF1 signaling is oncogenic during gliomagenesis through a mechanism distinct from modulating GAM polarization status. Cancer Res; 76(9); 2552-60. ©2016 AACR.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorGliomaHumansImmunohistochemistryMacrophage Colony-Stimulating FactorMacrophagesMiceMice, TransgenicMicrogliaMicroscopy, ConfocalPolymerase Chain ReactionReceptor, Macrophage Colony-Stimulating FactorTissue Array AnalysisUp-RegulationMacrophage Colony-Stimulating FactorReceptor, Macrophage Colony-Stimulating Factor

Identifiers

PMID27013192
PMCPMC4873447
OpenAlexW2303329342

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.