Evidence map›Paper›PMID 30773478›Full record

ArticleEBioMedicine2019

DNA damage repair alterations modulate M2 polarization of microglia to remodel the tumor microenvironment via the p53-mediated MDK expression in glioma.

Xiangqi Meng, Chunbin Duan, Hengyuan Pang, Qun Chen, Bo Han, Caijun Zha, Magafurov Dinislam, Pengfei Wu, Ziwei Li, Shihong Zhao and 4 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 93 citations in OpenAlex.

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  13. LncRNA-Mediated TPI1 and PKM2 Promote Self-Renewal and Chemoresistance in GBM.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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9 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

14 authors at 3 institutions in 2 countries.

Xiangqi MengDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China.
Chunbin DuanDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China.
Hengyuan PangDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Qun ChenDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Bo HanDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China.
Caijun ZhaDepartment of Laboratory Diagnosis, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Magafurov DinislamDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neurosurgical department, Bashkir State Medical University, Ufa 450008, Russia.
Pengfei WuDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China.
Ziwei LiDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China.
Shihong ZhaoDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Ruijia WangDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China.
Lin LinDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China.
Chuanlu JiangDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China. Electronic address: jcl6688@163.com.
Jinquan CaiDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Neuroscience Institute, Heilongjiang Academy of Medical Sciences, Harbin 150086, China. Electronic address: caijinquan666777@126.com.
Second Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNHeilongjiang Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDNA damage repair (DDR) alterations are important events in cancer initiation, progression, and therapeutic resistance. However, the involvement of DDR alterations in glioma malignancy needs further investigation. This study aims to characterize the clinical and molecular features of gliomas with DDR alterations and elucidate the biological process of DDR alterations that regulate the cross talk between gliomas and the tumor microenvironment.

methodsIntegrated transcriptomic and genomic analyses were undertaken to conduct a comprehensive investigation of the role of DDR alterations in glioma. The prognostic DDR-related cytokines were identified from multiple datasets. In vivo and in vitro experiments validated the role of p53, the key molecule of DDR, regulating M2 polarization of microglia in glioma.

findingsDDR alterations are associated with clinical and molecular characteristics of glioma. Gliomas with DDR alterations exhibit distinct immune phenotypes, and immune cell types and cytokine processes. DDR-related cytokines have an unfavorable prognostic implication for GBM patients and are synergistic with DDR alterations. Overexpression of MDK mediated by p53, the key transcriptional factor in DDR pathways, remodels the GBM immunosuppressive microenvironment by promoting M2 polarization of microglia, suggesting a potential role of DDR in regulating the glioma microenvironment.

interpretationOur work suggests that DDR alterations significantly contribute to remodeling the glioma microenvironment via regulating the immune response and cytokine pathways. FUND: This study was supported by: 1. The National Key Research and Development Plan (No. 2016YFC0902500); 2. National Natural Science Foundation of China (No. 81702972, No. 81874204, No. 81572701, No. 81772666); 3. China Postdoctoral Science Foundation (2018M640305); 4. Special Fund Project of Translational Medicine in the Chinese-Russian Medical Research Center (No. CR201812); 5. The Research Project of the Chinese Society of Neuro-oncology, CACA (CSNO-2016-MSD12); 6. The Research Project of the Health and Family Planning Commission of Heilongjiang Province (2017-201); and 7. Harbin Medical University Innovation Fund (2017LCZX37, 2017RWZX03).

Indexed as

DNA RepairTumor MicroenvironmentAnimalsCell DifferentiationCell LineCell Line, TumorFemaleGliomaHumansMacrophagesMiceMice, Inbred C57BLMicrogliaMidkineTumor Suppressor Protein p53MidkineTumor Suppressor Protein p53DNA damage repairGlioma microenvironmentMicrogliaMidkinep53

Identifiers

PMID30773478
PMCPMC6442002
OpenAlexW2914981560

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.