Evidence map›Paper›PMID 40527815›Full record

ArticleMedicine2025

Liposomes, immune cells, and lung cancer subtypes: A bidirectional Mendelian randomization study.

Kang Tian, Zhaofei Pang, Qiang Liu, Deyu Guo, Hui Jiang, Hongchang Shen, Jiajun Du

Abstract read
In one paragraph

Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Kang TianInstitute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Zhaofei PangInstitute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Qiang LiuInstitute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Deyu GuoInstitute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Hui JiangInstitute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Hongchang ShenInstitute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Jiajun DuInstitute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in lipid metabolism and immune cell functions have gained attention for their impact on the tumor microenvironment. However, the causal relationships between lipids and immune cells in lung cancer subtypes remain unclear. This study utilized plasma lipidomics summary data from genome-wide association studies, immune phenotypic data from the European Bioinformatics Institute, and comprehensive statistics of different lung cancer subtypes from the International Lung Cancer Consortium and the Transdisciplinary Research in Cancer of the Lung (TRICL). Two-sample Mendelian randomization and Bayesian weighted Mendelian randomization were applied to explore causal links between lipids and lung cancer subtypes. Sensitivity tests ensured robustness, and mediation analysis assessed immune cell roles. We identified causal relationships between 12 lipids, 59 immune cells, and lung cancer subtypes. Further mediation analysis showed that phosphatidylcholine (O-16:1_18:0) significantly reduced the risk of lung cancer through the CD14- CD16+ monocyte mediator (International Lung Cancer Consortium [ILCCO]: 11.11%, TRICL: 6.03%); the risk reduction through the CD16+ monocyte mediator was (ILCCO: 6.43%, TRICL: 6.67%). In squamous cell lung cancer, this lipid mediated a risk reduction via CD14- CD16+ monocyte (ILCCO: 8.30%, TRICL: 5.89%), via CD123 on plasmacytoid dendritic cell (ILCCO: 5.93%, TRICL: 4.48%), and via CD123 on CD62L+ plasmacytoid dendritic cell (ILCCO: 5.86%, TRICL: 4.43%). In contrast, phosphatidylcholine (O-16:0_20:3) levels increased the risk of small cell lung cancer via CD4 on CD39+ activated regulatory T cell (ILCCO: 10.33%, TRICL: 9.98%). Phosphatidylcholine regulates lung cancer risk through immune cells, highlighting its potential as a precise nano-targeted immunotherapy for lung cancer subtypes.

Indexed as

LiposomesLung NeoplasmsBayes TheoremGenome-Wide Association StudyHumansLipid MetabolismLipidomicsMendelian Randomization AnalysisMonocytesPhosphatidylcholinesTumor MicroenvironmentLiposomesPhosphatidylcholinescausal relationshipimmune cellliposomelung cancer subtypesMendelian randomizationnano-targeted immunotherapy

Identifiers

PMID40527815
PMCPMC12173287

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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.