ArticleFrontiers in oncology2026
Genetic associations link lung cancer liability to brain imaging phenotypes and nominate an FN1-associated tumor-oligodendrocyte program in small-cell lung cancer.
Article in Frontiers in oncology, 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
Background: Brain metastasis is a major cause of mortality in lung cancer, particularly in small-cell lung cancer (SCLC). Whether genetic susceptibility to lung cancer is associated with brain structural and functional traits relevant to metastatic vulnerability remains unclear. We investigated subtype-specific genetic associations with brain imaging phenotypes and explored the biological context of the SCLC-associated white-matter signal. Methods: Bidirectional two-sample Mendelian randomization (MR) was performed using European genome-wide association study summary statistics for three lung cancer subtypes, 3,935 structural MRI phenotypes, and 191 resting-state functional MRI traits. MR findings were evaluated using genetic-correlation and sensitivity analyses. Public single-cell and spatial transcriptomic datasets from brain metastases, computational ligand-receptor inference, and virtual perturbation modeling were used to explore the SCLC-related findings. Results: SCLC genetic liability showed the clearest white-matter-related pattern, involving the superior cerebellar peduncle and cerebellar-related functional connectivity, whereas lung squamous cell carcinoma was mainly associated with frontal and parietal traits. Single-cell analysis identified mature-like, intermediate, and reactive-like oligodendrocyte states. Reactive-like cells exhibited reduced myelination-associated genes and enhanced stress-response programs. Computational analyses prioritized an FN1-associated tumor-oligodendrocyte interaction program, with neuronal-like malignant SCLC cells as the major predicted sender population. Cross-dataset, spatial, and virtual perturbation analyses provided additional exploratory support for tumor-derived FN1 as a candidate niche-organizing signal associated with reactive oligodendrocyte remodeling. Conclusions: Lung cancer subtypes show distinct genetic associations with brain phenotypes. The SCLC findings and exploratory multi-omics analyses support an FN1-centered tumor-oligodendrocyte model that warrants experimental validation.
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