ArticleJournal of cardiothoracic surgery2026
Genetic evidence for a potential role of cytoskeleton-associated protein 2 in lung squamous cell carcinoma: a bidirectional mendelian randomization study.
Article in Journal of cardiothoracic surgery, 2026. 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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Abstract
backgroundCytoskeleton-associated protein 2 (CKAP2) plays a role in tumor proliferation, but its causal relationship with lung cancer remains unclear. This study employed a bidirectional two-sample Mendelian randomization (MR) analysis to investigate this association.
methodsUsing genome-wide association and FinnGen data, we assessed the potential causal relationship between genetically predicted plasma CKAP2 levels and lung cancer risk, including its subtypes. The inverse-variance weighted (IVW) method served as the primary analysis, supplemented by MR-Egger and weighted median. Sensitivity analyses included leave-one-out, Cochran's Q, MR-Egger intercept, and MR-PRESSO. To assess generalizability, we replicated the forward MR analysis using an independent deCODE pQTL dataset.
resultsForward MR showed a nominal association between elevated CKAP2 and lung squamous cell carcinoma (LUSC) risk (IVW: OR = 1.18; 95% CI = 1.01-1.38; P = 0.033). However, this did not survive Bonferroni correction (α = 0.0125) and was not replicated in an independent deCODE dataset (OR = 0.875; P = 0.493). No significant associations were found for overall lung cancer, lung adenocarcinoma, or small cell lung cancer. Sensitivity analyses revealed no heterogeneity or horizontal pleiotropy. Reverse MR found no causal effect of lung cancer on CKAP2 levels.
conclusionsThis study provides nominally significant genetic evidence for an association between elevated CKAP2 levels and LUSC risk, but the finding does not survive multiple-testing correction and was not replicated in an independent dataset. Further validation in larger cohorts with harmonized proteomic platforms is required before CKAP2 can be considered a therapeutic target.
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