ArticleCancer cell international2026
A cilia-associated signature predicts resistance to anti-PD-1 immune checkpoint blockade therapy in lung adenocarcinoma.
Article in Cancer cell international, 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
backgroundTargeting immune checkpoints, specifically programmed death 1, has significantly improved clinical outcomes in non-small cell lung cancer. However, only a proportion of patients benefited from immune checkpoint blockades (ICBs) therapy. Thus, identifying novel biomarkers to better select responders to ICBs is critically important in clinical practice.
methodsThis retrospective study included two cohorts, a discovery cohort (n = 24) and a validation cohort (n = 21) of lung adenocarcinoma (LUAD) patients treated with ICB at Shanghai Pulmonary Hospital between April 2016 and November 2019. Formalin-fixed paraffin-embedded tissue samples were collected for RNA sequencing. Additionally, a TCGA dataset (GSE135222) and a clinical study dataset (POPLAR) were utilized as external validation and test sets, respectively.
resultsIn the discovery cohort, cilia-associated pathways were significantly enriched in LUAD patients with non-durable benefit. A three-gene cilia-associated signature (TMEM100, DNAH3, and NEFH) was established and effectively predicted resistance to ICB treatment (discovery cohort, Hazard Ratio [HR, 95% CI] = 0.21 [0.056-0.791], P = 3.64e-05; validation cohort, HR [95% CI] = 0.200 [0.049-0.830], P = 0.0003). This signature was further validated in an external cohort (HR [95% CI] = 0.461 [ 0.164-1.292], P = 0.067). Further analysis demonstrated that the cilia-associated signature was negatively associated with various types of tumor-infiltrating immune cells, including effector T cells, macrophages, and dendritic cells.
conclusionOur findings suggest that cilia-associated signature may serve as a potential biomarker to identify LUAD patients with reduced likelihood of benefiting from ICB therapy, though further validation in larger cohorts is warranted.
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