Evidence map›Paper›PMID 32592484›Full record

ArticleNeuro-oncology2020

JAM-A functions as a female microglial tumor suppressor in glioblastoma.

Soumya M Turaga, Daniel J Silver, Defne Bayik, Evi Paouri, Sen Peng, Adam Lauko, Tyler J Alban, Nozha Borjini, Sarah Stanko, Ulhas P Naik and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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  13. Microglia and Brain Macrophages as Drivers of Glioma Progression.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 7 institutions in 1 country.

Soumya M TuragaDepartment of Biological, Geological, and Environmental Sciences, Cleveland State University, Cleveland, Ohio.
Daniel J SilverDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Defne BayikDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Evi PaouriDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Sen PengCancer and Cell Biology Division, TGen, Phoenix, Arizona.
Adam LaukoDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Tyler J AlbanDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Nozha BorjiniDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Sarah StankoDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Ulhas P NaikCardeza Center for Vascular Biology, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania.
Ruth A KeriCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio.
James R ConnorDepartment of Neurosurgery, Penn State College of Medicine, Hershey, Pennsylvania.
Jill S Barnholtz-SloanCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio.
Joshua B RubinDepartment of Pediatrics, Washington University School of Medicine, St Louis, Missouri.
Michael BerensCancer and Cell Biology Division, TGen, Phoenix, Arizona.
Dimitrios DavalosDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Justin D LathiaDepartment of Biological, Geological, and Environmental Sciences, Cleveland State University, Cleveland, Ohio.
Cleveland Clinic Lerner College of Medicine · USCase Western Reserve University · USCleveland State University · USTranslational Genomics Research Institute · USPenn State Milton S. Hershey Medical Center · USThomas Jefferson University · USWashington University in St. Louis · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
RESEARCH ONCOLOGY TRAINING GRANTT32CA059366 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 1993 to 2025
$5.5M
Gliovascular Mechanisms of Blood-Brain Barrier Disruption in Neuroinflammatory DiseaseR01NS112526 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI DAVALOS, DIMITRIOS · 2019 to 2023
$2.4M
Elucidating and Leveraging the mTOR Negative Feedback Pathway in Breast CancerR01CA213843 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI KERI, RUTH A. · 2017 to 2021
$2.0M
Novel adhesion mechanisms in glioblastoma stem cellsR01NS083629 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI LATHIA, JUSTIN D. · 2013 to 2017
$1.7M
Contribution of sex differences in glioblastoma immune suppression for improved immunotherapy responseF32CA243314 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI BAYIK WATSON, DEFNE · 2019 to 2020
$94k
Serotonin drives cancer stem cell maintenance and glioblastoma progressionF32CA213727 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI SILVER, DANIEL J · 2017 to 2018
$94k
NCI NIH HHS F32 CA213727NCI NIH HHS R01 CA213843NCI NIH HHS T32 CA059366NIGMS NIH HHS T32 GM007250NINDS NIH HHS R01 NS083629NINDS NIH HHS R01 NS112526
6 · The paper itself

Abstract

backgroundGlioblastoma (GBM) is the most aggressive primary brain tumor and has a dismal prognosis. Previously, we identified that junctional adhesion molecule A (JAM-A), a cell adhesion molecule, is highly elevated in human GBM cancer stem cells and predicts poor patient prognosis. While JAM-A is also highly expressed in other cells in the tumor microenvironment, specifically microglia and macrophages, how JAM-A expression in these cells affects tumor growth has yet to be determined. The goal of this study was to understand the role of microenvironmental JAM-A in mediating GBM growth.

methodsMale and female wild-type (WT) and JAM-A-deficient mice were transplanted intracranially with the syngeneic glioma cell lines GL261 and SB28 and were assessed for differences in survival and microglial activation in tumors and in vitro. RNA-sequencing was performed to identify differentially regulated genes among all genotypes, and differences were validated in vitro and in vivo.

resultsWe found that JAM-A-deficient female mice succumbed to GBM more quickly compared with WT females and JAM-A-deficient and male WT mice. Analysis of microglia in the tumors revealed that female JAM-A-deficient microglia were more activated, and RNA-sequencing identified elevated expression of Fizz1 and Ifi202b specifically in JAM-A-deficient female microglia.

conclusionsOur findings suggest that JAM-A functions to suppress pathogenic microglial activation in the female tumor microenvironment, highlighting an emerging role for sex differences in the GBM microenvironment and suggesting that sex differences extend beyond previously reported tumor cell-intrinsic differences.

Indexed as

GlioblastomaAnimalsCell Line, TumorFemaleHumansJunctional Adhesion Molecule AMaleMiceMice, Inbred C57BLMicrogliaTumor MicroenvironmentJunctional Adhesion Molecule Aglioblastomajunctional adhesion molecule Amicrogliasex differences

Identifiers

PMID32592484
PMCPMC7690368
OpenAlexW3037116814

What OpenQuestion holds

Textmetadata
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.