Evidence map›Paper›PMID 32915415›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2021

1p/19q co-deletion status is associated with distinct tumor-associated macrophage infiltration in IDH mutated lower-grade gliomas.

Yanyu Zhang, Yuan Xie, Liqun He, Jiefu Tang, Qiyuan He, Qingze Cao, Langjun Cui, Wei Guo, Kai Hua, Anna Dimberg and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

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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

12 authors at 7 institutions in 2 countries.

Yanyu Zhang *Key Laboratory of Ministry of Education for Medicinal Plant Resource and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Developing of Endangered Chinese Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China.
Yuan Xie *Key Laboratory of Ministry of Education for Medicinal Plant Resource and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Developing of Endangered Chinese Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China.
Liqun He *Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin Neurological Institute, Key Laboratory of Post-Neuro-injury Neuro-Repair and Regeneration in Central Nervous System, Ministry of Education and Tianjin City, Tianjin, 300052, China.
Jiefu TangDepartment of Spine Surgery, Huaihua No.2 Hospital, Hunan University of Medicine, Huaihua, 418000, China.
Qiyuan HeKey Laboratory of Ministry of Education for Medicinal Plant Resource and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Developing of Endangered Chinese Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China.
Qingze CaoKey Laboratory of Ministry of Education for Medicinal Plant Resource and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Developing of Endangered Chinese Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China.
Langjun CuiKey Laboratory of Ministry of Education for Medicinal Plant Resource and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Developing of Endangered Chinese Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China.
Wei GuoDepartment of Neurosurgery, Tangdu Hospital, Air Force Medical University of PLA (the Fourth Military Medical University), 569 Xinsi Road, Xi'an, 710038, China.
Kai HuaThe College of Life Sciences, Northwest University, Xi'an, 710069, China.
Anna DimbergDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Rudbeck Laboratory, 75185, Uppsala, Sweden.
Liang WangDepartment of Neurosurgery, Tangdu Hospital, Air Force Medical University of PLA (the Fourth Military Medical University), 569 Xinsi Road, Xi'an, 710038, China. drwangliang@126.com.
Lei ZhangKey Laboratory of Ministry of Education for Medicinal Plant Resource and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Developing of Endangered Chinese Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China. lei.zhang@snnu.edu.cn.ORCID http://orcid.org/0000-0001-7438-0489
Shaanxi Normal University · CNHuaihua University · CNUppsala University · SEAir Force Medical University · CNNorthwest University · CNScience for Life Laboratory · SETang Du Hospital · CN

Funding

Ministry of Science and Technology of the People's Republic of China 2018YFC1313003National Natural Science Foundation of China 81702489, 81911530166, 81772661,81402081,81870978Shaanxi Normal University GK202003048,GK202003050,GK201603110, cx2019013,s201910718084
6 · The paper itself

Abstract

backgroundTumor-associated macrophages (TAM)s are critical regulators of glioma progression. As yet, however, TAMs in isocitrate dehydrogenase (IDH) mutated lower-grade gliomas (LGGs) have not been thoroughly investigated. The aim of this study was to determine whether 1p/19q co-deletion status affects the TAM phenotype or its prevalence in IDH mutated LGGs.

methodsTAMs in IDH mutated LGGs were analyzed using transcriptome data from 230 samples in the TCGA database in combination with transcriptome data from single-cell RNA sequencing of IDH-mutated LGGs. Proteins potentially involved in TAM regulation were examined by immuno-staining in primary LGG samples harboring IDH mutations. Essential signaling pathways regulating TAM phenotypes were investigated in a glioma mouse model using small molecule inhibitors.

resultsMost of the TAMs in IDH-mutated LGGs expressed the M1 activation markers CD86 and TNF, whereas a subset of individual TAMs co-expressed both M1 and M2-related markers. Bioinformatics analysis in combination with immuno-staining of IDH-mutated patient samples revealed higher amounts of TAMs expressing M2-related markers in 1p/19q non-codeletion IDH-mutated LGGs compared to 1p/19q codeletion LGGs. The levels of transforming growth factor beta 1 (TGFβ1) and macrophage colony-stimulating factor (M-CSF) were significantly higher in 1p/19q non-codeletion LGGs than in 1p/19q codeletion LGGs. M-CSF and TGFβ1 signal inhibition decreased tumor growth and modulated the TAM phenotype in a glioma mouse model.

conclusionsOur data indicate that 1p/19q co-deletion status relates to distinct TAM infiltration in gliomas, which is likely mediated by M-CSF and TGFβ1 signaling. M-CSF and TGFβ1 signaling may play a pivotal role in regulating the TAM phenotype in glioma.

Indexed as

Chromosome DeletionAnimalsBrain NeoplasmsChromosomes, Human, Pair 1Chromosomes, Human, Pair 19Disease ProgressionFemaleGliomaHumansIsocitrate DehydrogenaseMacrophage Colony-Stimulating FactorMiceMice, Inbred C57BLMonocytesMutationNeoplasm GradingCSF1R protein, humanIsocitrate DehydrogenaseMacrophage Colony-Stimulating FactorReceptor, Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating FactorTransforming Growth Factor beta11p/19qGliomaLGGTumor-associated macrophage

Identifiers

PMID32915415
PMCPMC12980690
OpenAlexW3085348277

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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.