SynthesisHuman molecular genetics2025
Brain multi-omic Mendelian randomisation to identify novel drug targets for gliomagenesis.
Synthesis in Human molecular genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- ARGLU1 in Glioma: A Novel Potential Regulator of Splicing, DNA Repair, and Therapeutic Resistance.Cells · 2026Review
- Single-cell multi-omic integration analysis prioritizes druggable genes and reveals cell-type-specific causal effects in glioblastomagenesis.Journal of translational medicine · 2026Article
- Genetically prioritized mitochondrial regulators of advanced renal failure: multi-omic Mendelian randomization and biological plausibility assessment in allograft fibrosis.Frontiers in immunology · 2026Article
- Transitioning from molecular methods to therapeutic methods: An in‑depth analysis of glioblastoma (Review).Oncology reports · 2025Review
- Integrative multi-omics analysis identifies TGFA as a novel glioma susceptibility gene and therapeutic target.Frontiers in neurology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundGenetic variants associated with molecular traits that are also associated with liability to glioma can provide causal evidence for the identification and prioritisation of drug targets.
methodsWe performed comprehensive two-sample Mendelian randomisation (Wald ratio and/or IVW) and colocalisation analyses of molecular traits on glioma. Instrumentable traits (QTLs P < 5 × 10-8) were identified amongst 11 985 gene expression measures, 13 285 splicing isoforms and 10 198 protein abundance measures, derived from 15 brain regions. Glioma summary-level data was extracted from a genome-wide association meta-analysis of 12 496 cases and 18 190 controls.
resultsWe found evidence for causal effect of 22 molecular traits (across 18 genes/proteins) on glioma risk. Thirteen molecular traits have been previously linked with glioma risk and five were novel; HBEGF (5q31.3) expression and all glioma [OR 1.36 (95%CI 1.19-1.55); P = 4.41 × 10-6]; a CEP192 (18p11.21) splice isoform and glioblastoma [OR 4.40 (95%CI 2.28-8.48); P = 9.78 × 10-4]; a FAIM (3q22.3) splice isoform and all glioma [OR 2.72-3.43; P = 1.03 × 10-5 to 1.09 × 10-5]; a SLC8A1 (2p22.1) splice isoform and all glioma [OR 0.37 (95%CI 0.24-0.56; P = 5.72 × 10-6]; D2HGDH (2q37.3) protein and all glioma [OR 0.86 (95%CI 0.80-0.92); P = 5.94 × 10-6)].
conclusionsWe provide robust causal evidence for prioritising genes and their protein products in glioma research. Our results highlight the importance of alternative splicing as a mechanism in gliomagenesis and as an avenue for exploration of drug targets.
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