ArticleBMC cancer2024
Systematic druggable genome-wide Mendelian randomization identifies therapeutic targets for lung cancer.
Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- SMAD7 Downregulation Promotes Ferroptosis in Pulmonary Arterial Hypertension Via the TGF-β1-SMAD2/3 Pathway.Shock (Augusta, Ga.) · 2026Article
- Identifying druggable gene-related biomarkers in intervertebral disc degeneration through transcriptome sequencing and mendelian randomization analysis.Frontiers in genetics · 2026Article
- Unveiling novel potential drug targets for lung cancer through Mendelian randomization analysis.Scientific reports · 2025Article
- Systematic druggable genome-wide mendelian randomization identifies therapeutic targets for childhood asthma.Medicine · 2025Article
- Multi-omics and comprehensive multi-trait analysis identify shared genetic etiology of heart failure and related cancers.Human genomics · 2025Article
- DNA methylation-mediated ADA overexpression drives pancreatic cancer progression.Discover oncology · 2025Article
- Mendelian Randomization-Based Discovery of Novel Protein Biomarkers and Drug Targets in Colorectal Cancer: Validation Through Prognostic Modeling, Single-Cell Analysis, and In Vitro Cell Experiments.Applied biochemistry and biotechnology · 2025Article
- Druggable genome-wide Mendelian randomization integrating GWAS and eQTL/pQTL data identifies targets for lung squamous cell carcinoma.Scientific reports · 2025Article
- Identification of therapeutic targets in lung adenocarcinoma using Mendelian randomization and multi-omics.Discover oncology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundDrug repurposing provides a cost-effective approach to address the need for lung cancer prevention and therapeutics. We aimed to identify actionable druggable targets using Mendelian randomization (MR).
methodsSummary-level data of gene expression quantitative trait loci (eQTLs) were sourced from the eQTLGen resource. We procured genetic associations with lung cancer and its subtypes from the TRICL, ILCCO studies (discovery) and the FinnGen study (replication). We implemented Summary-data-based Mendelian Randomization analysis to identify potential therapeutic targets for lung cancer. Colocalization analysis was further conducted to assess whether the identified signal pairs shared a causal genetic variant.
findingsIn the main analysis dataset, we identified 55 genes that demonstrate a causal relationship with lung cancer and its subtypes. However, in the replication cohort, only three genes were found to have such a causal association with lung cancer and its subtypes, and of these, HYKK (also known as AGPHD1) was consistently present in both the primary analysis dataset and the replication cohort. Following HEIDI tests and colocalization analyses, it was revealed that HYKK (AGPHD1) is associated with an increased risk of squamous cell carcinoma of the lung, with an odds ratio and confidence interval of OR = 1.28,95%CI = 1.24 to 1.33.
interpretationWe have found that the HYKK (AGPHD1) gene is associated with an increased risk of squamous cell carcinoma of the lung, suggesting that this gene may represent a potential therapeutic target for both the prevention and treatment of lung squamous cell carcinoma.
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