Exploring the genetic causal inference between plasma lipidome and lung carcinoma: a bidirectional mendelian randomization study

May 23, 2025Discover oncology

Genetic links between blood fat molecules and lung cancer risk in both directions

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Abstract

Positive associations were found between several plasma lipid levels and the risk of lung carcinoma, with odds ratios ranging from 1.094 to 1.180.

Specific plasma lipids, such as Sterol ester 27:1/20:5 and various forms of Phosphatidylcholine, are positively associated with lung carcinoma risk.
Conversely, certain other forms of Phosphatidylcholine showed an inverse association with lung carcinoma risk.
The analysis suggests that lung carcinoma does not significantly affect the levels of the investigated plasma lipids.
These findings provide preliminary genetic evidence for the relationship between plasma lipids and lung cancer.

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BACKGROUND: Clinical observational studies have highlighted differences in plasma lipid profiles between lung carcinoma patients and healthy individuals. However, the causal relationship underlying these differences remains unclear. This study aims to investigate the bidirectional causal relationship between 179 plasma lipids and lung carcinoma.

METHODS: A bivariate two-sample (MR) study was conducted using data from public genome-wide association studies (GWAS). The primary analytical technique employed was the inverse variance weighting method (IVW), with MR-Egger, weighted-median, and weighted mode as supplementary methods. Sensitivity analyses including Cochran's Q test and MR-Egger intercept test were performed to ensure the robustness of the results.

RESULTS: Mendelian randomization analysis revealed positive associations between levels of certain plasma lipidome-Sterol ester 27:1/20:5 levels (OR 1.162, 95% confidence interval (CI) 1.077-1254, P 1.15e), Phosphatidylcholine (PC) 20:4_0:0 levels (OR 1.112, 95%CI 1.051-1.176, P 2.33e), PC 17:0_20:4 levels (OR 1.108, 95%CI 1.051-1.167, P 1.33e, PC 18:0_20:4 levels (OR 1.094, 95%CI 1.046-1.144, P 8.08e), PC O-16:0:4 levels (OR 1.180, 95%CI 1.089-1.277, P4.61e), PC O-16:1_20:4 levels (OR 1.155, 95%CI 1.077-1.239, P 5.00e)-with the risk of lung carcinoma. Conversely, PC 15:0_18:2 levels (OR 0.823, 95%CI 0.760-0.892, P1.95e), PC 16:0_18:2 levels (OR 0.863, 95%CI 0.801-0.931, P 1.28e), PC 16:1_18:2 levels (OR 0.856, 95%CI 0.791-0.926, P 1.13e), PC 18:1_18:2 levels (OR 0.847, 95%CI 0.77-0.911, P 9.15e) were inversely associated with the risk of lung carcinoma. Reverse Mendelian randomization analysis indicated that lung carcinoma did not have a significant causal effect on the 179 plasma lipids. -4 -4 -4 -5 -5 -5 -6 -4 -4 -6

CONCLUSION: Our study reveals the causal relationship between plasma lipidome and lung cancer, provides preliminary genetic evidence, and provides a new idea for understanding the pathogenesis of lung cancer and finding promising therapeutic targets.

Key numbers

1.112

Increase in Lung Cancer Risk

Odds ratio from analysis of plasma lipids linked to lung carcinoma.

0.823

Decrease in Lung Cancer Risk

Odds ratio indicating protective effect from specific plasma lipids.

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Exploring the genetic causal inference between plasma lipidome and lung carcinoma: a bidirectional mendelian randomization study

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