Evidence map›Paper›PMID 38140790›Full record

ArticleCancer medicine2024

MDSC suppresses T cell antitumor immunity in CAC via GPNMB in a MyD88-dependent manner.

Bo Wang, Lu Wang, Runshi Shang, Lin Xie

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. LDLRJournal of clinical and translational hepatology · 2026
    Article
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  4. Review
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  9. Observational
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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

4 authors at 2 institutions in 2 countries.

Bo WangDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Lu WangInstitute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Organ Transplantation, Ministry of Education; NHC Key Laboratory of Organ Transplantation; Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, China.
Runshi ShangInstitute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Organ Transplantation, Ministry of Education; NHC Key Laboratory of Organ Transplantation; Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, China.
Lin XieInstitute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Organ Transplantation, Ministry of Education; NHC Key Laboratory of Organ Transplantation; Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, China.ORCID 0000-0002-7058-0851
Ministry of Education of the People's Republic of China · CNTongji Hospital · CN

Funding

Open Project of the Key Laboratory of Organ Transplantation, Ministry of Education, and NHC 2020QYKF02the Hubei Province health and family planning scientific research project WJ2023M014the Hubei Provincial Natural Science Foundation of China 2021CFB401the National Natural Science Foundations of China #82273309
6 · The paper itself

Abstract

backgroundMyeloid-derived suppressor cells (MDSCs) played an essential role in tumor microenvironment to suppress host antitumor immunity and help cancer cells escape immune surveillance. However, the molecular mechanism behind tumor evasion mediated by MDSCs is not fully understood. Glycoprotein nonmetastatic melanoma protein B (GPNMB) is considered to associate with tumor initiation, metastasis and angiogenesis. Blocking GPNMB function is a potentially valuable therapy for cancer by eliminating GPNMB

methodsWe here focus on the underlying the relationship between GPNMB function and MyD88 signaling pathway activation in MDSCs' antitumor activity in CAC.

resultsCAC development in the mouse model is associated with expanded GPNMB

conclusionMyD88 signaling pathway plays an essential role in GPNMB

Indexed as

Membrane GlycoproteinsMyeloid-Derived Suppressor CellsMyeloid Differentiation Factor 88Signal TransductionTumor MicroenvironmentAnimalsCell Line, TumorCell ProliferationDisease Models, AnimalEye ProteinsHumansMiceMice, Inbred C57BLT-LymphocytesTumor EscapeEye ProteinsGpnmb protein, mouseMembrane GlycoproteinsMyd88 protein, mouseMyeloid Differentiation Factor 88colitis‐associated colorectal cancerGPNMBMDSCMyD88 signalingT cell immunity

Identifiers

PMID38140790
PMCPMC10807660
OpenAlexW4390144025

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.