Evidence map›Paper›PMID 41239138›Full record

ArticleDiscover oncology2025

Integrative Mendelian randomization and spatial transcriptomics analysis reveals causal links between plasma lipidome and non-small cell lung cancer.

Baiquan Zhang, Jintao Liu, Qian Guo, Huanqin Wang, Lijun Miao, Lu Zhou

Abstract read
In one paragraph

Article in Discover oncology, 2025. 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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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Baiquan ZhangDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Jintao LiuDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Qian GuoDepartment of Rhinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Huanqin WangDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Lijun MiaoDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Lu ZhouDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. sqzhoulu@163.com.

Funding

the Medical Science and Technology Research Project of Henan Province LHGJ20200363the National Natural Science Foundation of China Youth Fund Project No.82100048
6 · The paper itself

Abstract

backgroundThis study aimed to investigate the potential causal relationship between plasma lipidome and non-small cell lung cancer (NSCLC) using a two-sample Mendelian randomization (MR) approach based on large-scale genome-wide association study (GWAS) data.

methodsA two-sample bidirectional MR analysis was conducted using summary-level data from the GeneRISK and FinnGen GWAS. Genetic instruments were selected for 179 plasma lipid traits. Causal effects were estimated using inverse variance weighting (IVW), MR-Egger, weighted median, and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO) methods. Spatial transcriptomic profiling and machine learning-based gene prioritization were further employed to explore potential mechanistic links.

resultsMR identified 30 lipid species significantly associated with NSCLC risk, of which 17 demonstrated consistent causal effects across multiple sensitivity analyses. A subset of phosphatidylcholine and phosphatidylethanolamine species exhibited inverse associations, indicating potential protective effects, while specific sterol esters, sphingomyelins, and triacylglycerols were positively associated with disease susceptibility. Plasmacytoma Variant Translocation 1 (PVT1) was first prioritized as a key lipid-associated gene by three machine learning algorithms and was subsequently validated by spatial transcriptomics, showing elevated expression in tumor-dense regions.

conclusionThis study reveals a causal link between distinct plasma lipid species and NSCLC risk, emphasizing the role of lipid structural diversity. PVT1 may act as a critical mediator connecting lipid dysregulation to lung tumorigenesis, offering novel biomarker and therapeutic target potential.

Indexed as

Causal inferenceGWASMendelian randomizationNon-small cell lung cancerPlasma lipidome

Identifiers

PMID41239138
PMCPMC12618756

What Socratic holds

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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 Socratic graph.