Evidence map›Paper›PMID 36439186›Full record

ReviewFrontiers in immunology2022

Epigenetic modifications in the accumulation and function of myeloid-derived suppressor cells.

Liangjie Xu, Cuicui Zhou, Yi Liang, Tinpan Fan, Fen Zhang, Xinxin Chen, Wei Yuan

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  8. Targeting the myeloid microenvironment in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2023
    Review
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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

7 authors at 1 institution in 1 country.

Liangjie XuDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Cuicui ZhouDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Yi LiangDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Tinpan FanDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Fen ZhangDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Xinxin ChenDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Wei YuanDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Jiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are key players under various pathologic conditions, such as cancer. Epigenetic modifications such as DNA methylation, RNA-mediated processes, and histone modification can alter gene transcription, and thus regulating pathological process. Studies have shown that epigenetic modification contributes to the accumulation and function of MDSCs. This review summarizes the crosstalk between the epigenetic alterations and MDSCs functions, and briefly introduces how the accumulation and function of MDSCs caused by epigenetic modification impact on the disease development, which represents as a promising therapeutic strategy for the related disorders.

Indexed as

Myeloid-Derived Suppressor CellsNeoplasmsDNA MethylationEpigenesis, GeneticHumansDNA methylationepigenetic modificationhistone acetylationmyeloid-derived suppressor cellsN6-methylationubiquitination

Identifiers

PMID36439186
PMCPMC9691837
OpenAlexW4308803023

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.