Evidence map›Paper›PMID 42241991›Full record

ArticleTranslational oncology2026

A pan-cancer landscape of LILRB4 identifies it as a context-dependent marker of the myeloid and antigen-presentation axis.

Jiabin Li, Xuhui He, Yueyue Guo, Longsheng Zhang, Waiming Cheng, Chaoshun Zheng

Abstract read
In one paragraph

Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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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

6 authors.

Jiabin LiRadiotherapy Department, Jieyang People's Hospital, Jieyang, China.
Xuhui HeDepartment of Orthopedics, Jieyang People's Hospital, Jieyang, China.
Yueyue GuoDepartment of Orthopedics, Jieyang People's Hospital, Jieyang, China.
Longsheng ZhangDepartment of Anesthesiology, Jieyang People's Hospital, Jieyang, China.
Waiming ChengDepartment of Discovery Research, Bio-Thera Solutions, Ltd.. Electronic address: miguelcheng20230301@gmail.com.
Chaoshun ZhengDepartment of Orthopedics, Jieyang People's Hospital, Jieyang, China. Electronic address: Cszhengderek@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibitory receptors modulate antigen presentation and myeloid responses within the tumor microenvironment, yet the cross-cancer landscape and clinical significance of LILRB4 remain incompletely defined. By integrating public multi-omics resources, we systematically profiled LILRB4 across expression, genetic alterations, DNA methylation, phosphorylation, and immune infiltration, and examined their associations with clinical outcomes. LILRB4 is enriched in immune tissues and in monocytes, macrophages, and dendritic cells, and is upregulated in multiple cancers, with occasional discordance between transcript and protein levels. Its association with survival is cancer-type dependent-protective in cervical cancer, skin cutaneous melanoma, and uterine carcinosarcoma, but associated with higher risk in lower-grade glioma and recurrence-related metrics of prostate adenocarcinoma. Genetic alterations are dominated by amplification and missense mutations clustering within immunoglobulin domains, including a P184 hotspot, yet carriers do not show consistent survival differences. LILRB4 expression positively correlates with tumor mutational burden, microsatellite instability, and homologous recombination deficiency in several cancers. In lower-grade glioma, hypermethylation at a promoter-proximal CpG site associates with longer survival, and multiple cancers display site- and cancer-specific phosphorylation differences. LILRB4 correlates strongly with macrophage infiltration, and co-expression and interaction analyses converge on antigen processing and presentation pathways, with HLA-DRA emerging as a shared node. Collectively, these findings support LILRB4 as a context-dependent marker of the myeloid and antigen-presentation axis in the tumor microenvironment and provide an integrated reference framework that warrants further functional validation.

Indexed as

Antigen presentationLILRB4Macrophage infiltrationPan-cancerPhosphorylation

Identifiers

PMID42241991
PMCPMC13266044

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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.